**Probiotics and Periodontal Diseases**

**Probiotics and Periodontal Diseases**

Alicia Morales, Joel Bravo-Bown, Javier Bedoya and Jorge Gamonal Bedoya and Jorge Gamonal Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

Alicia Morales, Joel Bravo-Bown, Javier

http://dx.doi.org/10.5772/intechopen.68814

#### **Abstract**

Probiotics are defined as live microorganisms that, when administered in adequate amounts, confer a health benefit on the host. Probiotics have been used to directly modify the resident oral microbiome and proposed to modulate immune responses. In dentistry, probiotics have been employed as useful adjuncts for the reduction of caries development, suppressing oral Candida infection and controlling halitosis. Plaque-induced gingivitis is a gingival inflammation caused by the adherent bacterial biofilm around teeth. Gingivitis and periodontitis are considered to be a continuum of the same inflammatory process, although many gingivitis lesions do not progress to periodontitis. Periodontitis is an inflammatory process that affects the attachment structures of teeth. It constitutes a second cause of tooth loss worldwide. Conventional treatment modalities of periodontal disease include non-surgical and/or surgical management, with an emphasis on mechanical debridement. However, mechanical debridement as a sole therapy is not always effective to improve clinical parameters. A growing number of studies support probiotic therapy to prevent or treat gingivitis and periodontitis. Oral administration of probiotics is an effective adjunct in reducing pathogenic bacteria and improving clinical signs of disease. Probiotics may serve as adjunct or replacement therapy substitute antibiotics in managing human periodontal infections in future.

DOI: 10.5772/intechopen.68814

**Keywords:** probiotics, periodontitis, gingivitis, periodontal diseases, dental scaling

## **1. Introduction**

In order to speak about probiotics, we have to go back to the twentieth century when the Russian scientist Elie Metchnikoff postulated the theory about the influence of gastrointestinal micro biota (gut flora) over ageing. In 1908, this Nobel Prize winner attached the longevity of some Balkans towns to the frequent consumption of fermented dairy, containing Lactobacillus, which reduced the toxins produced by intestinal bacteria, promoting health and prolonging life [1].

Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons

The discovery of Lactic Acid Bacteria (LAB) in the middle of the nineteenth century confirmed the interest in microorganism and since then many people have concluded that dairy fermented by lactobacillales provide numerous benefits to our health [2].

For a long time, microorganisms have been responsible for the production of numerous foods and drinks and also have had an important impact on human health. The discovery of a symbiotic relationship between bacteria and humans awoke the curiosity of seeing the bacteria as potentially beneficial rather than pathogenic [2].

Lilly and Stillwell coined the term "probiotics" first definition in 1965 as: "Living microorganisms that confer a benefit to the host's health when given in adequate amounts" [3]. The term "prebiotic" was defined as "a non-digestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon, and thus improves host health" by Gibson and Roberfroid [4].

Symbiotic is the relationship between probiotics and prebiotics, which benefits the host by increasing the survival and implantation of live microorganisms from dietary supplements in the gastrointestinal system [5]. This has not been deeply studied, but it could increase bacteria potential to develop their function in the colon because symbiotic products could increase the survival of probiotic in their intestinal transit phase. Also, a synergic effect has been described. Prebiotics contribute to the installation of a specific bacterial flora with beneficial effects on health because they stimulate the growth of specific strains [6].

Nowadays the term probiotic has evolved and is now described as "living microorganisms, mostly bacteria, non-pathogenic, used as nutritional supplement, which after being ingested in the right amount, improve the intestinal microbial balance and cause beneficial effects on the health of those who ingest them" [7]. They are considered safe for human health [8]. Since the 1980s scientific investigation about healthy properties of ingesting probiotics has increased considerably, which boosted their use and led to their appearance in clinical practice as treatment for diseases such as chronic diarrhea, immune regulation, allergies, inflammatory bowel disease, constipation, lactose intolerance and lipid intolerance [9]. Lately there is big concern regarding the use of probiotics to treat oral infections like dental cavities (caries) and periodontal diseases. However, available information about the effects of probiotics on periodontal health is still minimal [10].

Chronic oral infections in soft tissues cause inflammatory alterations releasing pro-inflammatory substances such as cytokines, which through the circulatory system, access any area of the body, increasing the risk of muscular, digestive and cardiovascular problems, premature birth, diabetes and sports injuries. Hence, the treatment of chronic oral diseases and the maintenance of oral health should be considered as an asset in the prevention of systemic problems for general health [11].

Periodontal diseases and dental cavities have high prevalence [12], and according to the World Health Organization, the majority of children have signs of gingivitis and among adults the initial stages of periodontal disease are highly prevalent [13]. Bacterial biofilm that forms in the hard and soft tissues of the oral cavity is considered the main etiological factor in most pathological conditions of the oral cavity. The accumulation of bacteria inside the biofilm, provided by a poor oral health, influences changes in the microbial community, leading to periodontal inflammation [14].

Several studies such as Gorbach and Goldin (1985) [15], Näse et al. (2001) [16], Grudianov et al. (2002) [17], Wei et al. [18], Von Bultzingslowen et al. [19], Hatakka et al. (2007) [20] have spoken about the relation between bacterial strains like *Lactobacillus rhamnosus, Bifidobacterium* spp, and *Lactobacillus plantarum*, which have a positive effect on tooth adhesion and their action against diseases such as dental cavities (caries) and yeast infection. In recent years, treatments of periodontal diseases have changed to an antibiotic or antimicrobial kind. Nonetheless, with the increased incidence of antibiotic resistance, probiotics may be a promising area of research in periodontal therapy [21]. Currently, there is a probiotic that can be used for oral hygiene, as it combats dental plaque, gingivitis and cariogenic bacteria through the patented combination of two strains of *Lactobacillus reuteri*. This is 100% natural due to its residence in the human gastrointestinal tract and production of an antibiotic substance of broad-spectrum called "reuterina", which administrated in the right amount, causes the desired antimicrobial effect to keep the intestinal microbiota intact [11].

Increasingly, antibiotics become complex elements to manage in medical therapies due to the increment of bacterial resistance to them. However, inversely proportional, clinical studies have shown the positive effects in human health associated with the use of probiotics. This is the reason why the World Health Organization supports the use of probiotics as microbial interference therapy. Consequently, the use of probiotics could be postulated as a useful alternative in the control of periodontal diseases, since it improves the conditions of the host, reducing periodontal pocket depth, inflammation, bleeding and halitosis.

## **2. Local mechanisms of probiotic action**

The discovery of Lactic Acid Bacteria (LAB) in the middle of the nineteenth century confirmed the interest in microorganism and since then many people have concluded that dairy fer-

For a long time, microorganisms have been responsible for the production of numerous foods and drinks and also have had an important impact on human health. The discovery of a symbiotic relationship between bacteria and humans awoke the curiosity of seeing the bacteria as

Lilly and Stillwell coined the term "probiotics" first definition in 1965 as: "Living microorganisms that confer a benefit to the host's health when given in adequate amounts" [3]. The term "prebiotic" was defined as "a non-digestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in

Symbiotic is the relationship between probiotics and prebiotics, which benefits the host by increasing the survival and implantation of live microorganisms from dietary supplements in the gastrointestinal system [5]. This has not been deeply studied, but it could increase bacteria potential to develop their function in the colon because symbiotic products could increase the survival of probiotic in their intestinal transit phase. Also, a synergic effect has been described. Prebiotics contribute to the installation of a specific bacterial flora with ben-

Nowadays the term probiotic has evolved and is now described as "living microorganisms, mostly bacteria, non-pathogenic, used as nutritional supplement, which after being ingested in the right amount, improve the intestinal microbial balance and cause beneficial effects on the health of those who ingest them" [7]. They are considered safe for human health [8]. Since the 1980s scientific investigation about healthy properties of ingesting probiotics has increased considerably, which boosted their use and led to their appearance in clinical practice as treatment for diseases such as chronic diarrhea, immune regulation, allergies, inflammatory bowel disease, constipation, lactose intolerance and lipid intolerance [9]. Lately there is big concern regarding the use of probiotics to treat oral infections like dental cavities (caries) and periodontal diseases. However, available information about the effects of probiotics

Chronic oral infections in soft tissues cause inflammatory alterations releasing pro-inflammatory substances such as cytokines, which through the circulatory system, access any area of the body, increasing the risk of muscular, digestive and cardiovascular problems, premature birth, diabetes and sports injuries. Hence, the treatment of chronic oral diseases and the maintenance of oral health should be considered as an asset in the prevention of systemic problems

Periodontal diseases and dental cavities have high prevalence [12], and according to the World Health Organization, the majority of children have signs of gingivitis and among adults the initial stages of periodontal disease are highly prevalent [13]. Bacterial biofilm that forms in the hard and soft tissues of the oral cavity is considered the main etiological factor in most pathological conditions

mented by lactobacillales provide numerous benefits to our health [2].

the colon, and thus improves host health" by Gibson and Roberfroid [4].

eficial effects on health because they stimulate the growth of specific strains [6].

potentially beneficial rather than pathogenic [2].

74 Insights into Various Aspects of Oral Health

on periodontal health is still minimal [10].

for general health [11].

Several mechanisms have been suggested to contribute to the probiotic action. Their effects at local level are mentioned as follows:

	- (a) Salivaricin A and B: Bacteriocins produced by *Streptococcus salivarius*. Salivaricin decreases the proliferation of *S. mutans* and *Streptococcus sobrinus* in carious lesions. Salivaricin B inhibits the growth of *Prevotella* spp. and *Micromonas micros* in halitosis.
	- (b) Reuterin: Bacteriocin produced by *L. reuteri*, has antibacterial activity on bacterial Gram (+) and Gram (−), fungi (*Candida albicans*) and protozoa. Among them *S. mutans* and *P. intermedia*.
	- (a) *Lactobacillus acidophilus* can participate in the production of niacin, folic acid and vitamin B6.
	- (b) *Bifidobacterium dentium* increases the absorption of iron, zinc, calcium and magnesium.
	- (c) *Streptococcus thermophilus* synthesizes polysaccharides such as hyaluronic acid and produces urease.
	- (a) *Bifidobacterium longum* has anti-oxidant effect by inhibiting the formation of linolenic acid in the form of hydrogen peroxide.
	- (b) *Lactobacillus brevis* decreases the levels of nitric oxide synthetases (NOS).

## **3. Systemic mechanisms of probiotic action**

The systemic mechanisms of probiotic action are associated with its effect on immune response. In past years, there have been an increasing number of studies linking gut health with several chronic diseases. In order to understand these mechanisms, it is necessary to review this literature.

## **3.1. Use of probiotics in medicine**

Clinical studies have demonstrated the clinical potential of probiotic against many diseases. However, generalizations concerning the potential health benefits of probiotic should not be made because its effects are strain-specific [36]. Probiotics have been used in some conditions, such as:

#### *3.1.1. Atopic dermatitis*

**5.** Production of bacteriocins (cationic peptides synthesized on ribosomes with antimicro-

(a) Salivaricin A and B: Bacteriocins produced by *Streptococcus salivarius*. Salivaricin decreases the proliferation of *S. mutans* and *Streptococcus sobrinus* in carious lesions. Salivaricin B inhibits the growth of *Prevotella* spp. and *Micromonas micros*

(b) Reuterin: Bacteriocin produced by *L. reuteri*, has antibacterial activity on bacterial Gram (+) and Gram (−), fungi (*Candida albicans*) and protozoa. Among them *S.* 

(a) *Lactobacillus acidophilus* can participate in the production of niacin, folic acid and

(b) *Bifidobacterium dentium* increases the absorption of iron, zinc, calcium and

(c) *Streptococcus thermophilus* synthesizes polysaccharides such as hyaluronic acid

**8.** Changes in the cellular envelope: *Lactobacillus paracasei* HL32 inhibits *P. gingivalis* to in-

**9.** Glucosiltransferasa enzyme inhibition. *L. rhamnosus* inhibits the glycosyl-transferase en-

(b) *Lactobacillus brevis* decreases the levels of nitric oxide synthetases (NOS). **11.** Ingested probiotics can impact resident communities through trophic interactions, a direct alteration in fitness or an indirect alteration in fitness through altered production of host-derived molecules [31]. The major changes of gastrointestinal microbiome occur in stomach and small intestine. These are important not only quantitatively; they may also

The systemic mechanisms of probiotic action are associated with its effect on immune response. In past years, there have been an increasing number of studies linking gut health

(a) *Bifidobacterium longum* has anti-oxidant effect by inhibiting the formation of lino-

zyme by reducing the synthesis of glucans in the formation of the biofilm.

lenic acid in the form of hydrogen peroxide.

alter the relative abundance of major phyla [32–35].

**3. Systemic mechanisms of probiotic action**

**6.** Production of inhibitory substances like bacteriocins: peptides synthesized on ribosomes

bial activity that have a narrow spectrum of action) [27–29].

with antimicrobial activity and broad spectrum of action.

in halitosis.

76 Insights into Various Aspects of Oral Health

vitamin B6.

magnesium.

**10.** Anti-oxidant effect.

and produces urease.

duce a change in the cellular envelope [30].

*mutans* and *P. intermedia*.

**7.** Production of vitamins and other substances.

Atopic dermatitis is a chronically relapsing skin disease that occurs most commonly during early infancy and childhood. It is associated with allergen sensitization, recurrent skin infections and abnormalities in skin barriers function [37]. Foolad et al. published a meta-analysis study aimed to find evidence about the effect of probiotics in children with atopic dermatitis [38]. They concluded that the use of probiotics, specifically *L. rhamnosus* GG [39], showed to be effective in mothers and infants in preventing the development and reducing severity of atopic dermatitis [38]. In adult patients, the use of *L. salivarius* LS01 [40] and a combination of *L. salivarius* LS01 with *Bifidobacterium breve* BR03 [41] were associated with significant improvement of clinical manifestations of atopic dermatitis.

#### *3.1.2. Antibiotic-associated diarrhea*

Diarrhea is a common side effect of antibiotic use. It can be classified as *Clostridium*-associated antibiotic diarrhea or non-*Clostridium difficile*-associated antibiotic diarrhea. The first one is benign. In contrast, the second one refers to a wide spectrum of diarrhea illnesses caused by the toxins produced by *C. difficile*, including cases of severe colitis with or without the presence of pseudomembranes [42]. A series of meta-analysis concluded that probiotics significantly reduce the risk of antibiotic-associated diarrhea in children [43] and adult patients [44]. It was associated with the use of *L. rhamnosus* GG, *B. lactis* and *S. thermophiles* [43]. *S. boulardii* was reported to be effective in *C. difficile* disease [45, 46].

#### *3.1.3. Irritable bowel syndrome (IBS)*

IBS is defined as an abdominal discomfort or pain associated with altered bowel habits for at least 3 days in the previous 3 months, with the absence of organic disease [42]. A meta-analysis demonstrated that, compared with placebo, the use *L. rhamnosus* GG was associated with a significantly higher rate of treatment responders in the overall population with abdominal pain-related functional gastrointestinal disorders and in the irritable bowel syndrome patients [47].

#### *3.1.4. Inflammatory bowel disease (IBD)*

IBD consists of two disorders: ulcerative colitis (UC) and Crohn's disease (CD). The gut mucosa suffers a chronic, uncontrolled inflammation. CD is characterized by focal transmural inflammatory lesions and ulcerations that can be present anywhere in the gastrointestinal tract. UC is more superficial and limited to colon.

A meta-analysis concluded that remission rates in patients with active UC were significantly higher in patients who were treated with probiotics, specifically, VSL#3 (a combination of probiotics containing *B. breve, B. longum, Bifidobacterium infantis, L. acidophilus, L. plantarum, L. paracasei, L. bulgaricus* and *S. thermophiles*) [48].

#### *3.1.5. Helicobacter pylori*

Probiotics do not eradicate *H. pylori*, but they can diminish the levels of this bacterium in the stomach. In association with antibiotic treatments, some probiotics increased eradication rates and/or decreased adverse effects due to the antibiotics [49].

#### *3.1.6. Necrotizing enterocolitis*

It is a severe condition occurring especially in preterm infants. A Cochrane review concluded in 2011 that enteral supplementation with probiotics prevents sever necrotizing enterocolitis in preterm infants [50].

#### *3.1.7. Hypocholesterolemic treatment*

The combinations of prebiotics and probiotics such as bifidobacteria and FOS, lactobacilli and lactitol, and bifidobacteria and galactooligosacharides were used in trials and have shown promising results in hypocholesterolemic effect [51].

#### *3.1.8. Radiation enteritis*

Pelvic malignancies are commonly treated with radiation therapy. Chronic gastrointestinal side effects occur in over 30% of patients [42]. A meta-analysis concluded that probiotic treatment with *Lactobacillus* spp could prevent chemotherapy and radiation enteritis-induced diarrhea in patients with pelvic malignancies [52].

#### **3.2. Probiotic effect on immune responses**

Probiotics help maintain gut immune homeostasis by modulating immune response, enhancing epithelial barrier function and inhibiting pathogen growth. Probiotic interaction with mucosal immune system is through the same pathways as commensal bacteria. Its effect appears to be more immune regulating than immune activating [37].

Probiotics modulate epithelial barrier function through interactions with Toll-like receptor (TLR)-2 [53]. The initiation of TLRs signalling regulates synthesis of pro-inflammatory cytokines, chemokines and antimicrobial peptides, recruitment of B cells and production of IgA [54]. Probiotics have been shown to suppress systemic inflammatory response, modulating epithelial signal transduction pathways and cytokine production [55]. For example, *Lactobacillus johnsonni* N6.2 up-regulated type-1 interferon and IFN regulators Stat1 and IRF7 in a TLR-9 dependent way, in rats [56].

Several strains of lactic acid bacteria induce *in vitro* release of pro-inflammatory cytokines TNF-α and IL-6, reflecting stimulation of nonspecific immunity [57]. *L. acidophilus* Lal enhances phagocytosis in humans [58]. *L. casei* Shirota can enhance natural killer cell activity *in vivo* and *in vitro* in humans [59]. However, there are some bacteria that can decrease pro-inflammatory molecules. For example, *L. brevis* CD2 decreases inflammatory markers in saliva from patients with periodontal disease, including prostaglandin E2 (PGE2) [60]. Also, it was reported that probiotics, specifically, *L. reuteri* ATCC PTA 5289 decreased in CGF levels of TNF-α and IL-1β in patients with chronic periodontitis [61]. *Streptococcus cristatus, S. salivarius, S. mitis* and *S. sanguinis* may decrease the release of IL-8 by the epithelial cells stimulated with *Fusobacterium nucleatum* and *A. actinomycetemcomitans* [62–64].

inflammatory lesions and ulcerations that can be present anywhere in the gastrointestinal

A meta-analysis concluded that remission rates in patients with active UC were significantly higher in patients who were treated with probiotics, specifically, VSL#3 (a combination of probiotics containing *B. breve, B. longum, Bifidobacterium infantis, L. acidophilus, L. plantarum,* 

Probiotics do not eradicate *H. pylori*, but they can diminish the levels of this bacterium in the stomach. In association with antibiotic treatments, some probiotics increased eradication rates

It is a severe condition occurring especially in preterm infants. A Cochrane review concluded in 2011 that enteral supplementation with probiotics prevents sever necrotizing enterocolitis

The combinations of prebiotics and probiotics such as bifidobacteria and FOS, lactobacilli and lactitol, and bifidobacteria and galactooligosacharides were used in trials and have shown

Pelvic malignancies are commonly treated with radiation therapy. Chronic gastrointestinal side effects occur in over 30% of patients [42]. A meta-analysis concluded that probiotic treatment with *Lactobacillus* spp could prevent chemotherapy and radiation enteritis-induced diar-

Probiotics help maintain gut immune homeostasis by modulating immune response, enhancing epithelial barrier function and inhibiting pathogen growth. Probiotic interaction with mucosal immune system is through the same pathways as commensal bacteria. Its effect appears to be

Probiotics modulate epithelial barrier function through interactions with Toll-like receptor (TLR)-2 [53]. The initiation of TLRs signalling regulates synthesis of pro-inflammatory cytokines, chemokines and antimicrobial peptides, recruitment of B cells and production of IgA [54]. Probiotics have been shown to suppress systemic inflammatory response, modulating epithelial signal transduction pathways and cytokine production [55]. For example, *Lactobacillus johnsonni* N6.2 up-regulated type-1 interferon and IFN regulators Stat1 and IRF7 in a TLR-9

tract. UC is more superficial and limited to colon.

*L. paracasei, L. bulgaricus* and *S. thermophiles*) [48].

and/or decreased adverse effects due to the antibiotics [49].

promising results in hypocholesterolemic effect [51].

rhea in patients with pelvic malignancies [52].

more immune regulating than immune activating [37].

**3.2. Probiotic effect on immune responses**

*3.1.5. Helicobacter pylori*

78 Insights into Various Aspects of Oral Health

*3.1.6. Necrotizing enterocolitis*

*3.1.7. Hypocholesterolemic treatment*

in preterm infants [50].

*3.1.8. Radiation enteritis*

dependent way, in rats [56].

Some specific strains generate an effect on maturation of dendritic cells (DC). DC has a central role in directing the T cell response. They can change to T helper cell (Th) 1, Th2, Th17 and T regulatory cells (Treg) [65]. Certain bacterial strains induce the production of Th polarizing key cytokines by DCs, such as IL-10, IL-12 and IL-23 [66, 67]. Also, some *Lactobacillus* strains have been shown to stimulate Th1 cytokine production while others have increased Th2 responses or induced a mixed Th1/Th2 response [37]. An example of this is the use of a combination of *L. salivarius* LS01 and *Bifidobacterium breve* BR03 in treatment of atopic dermatitis. This probiotic mix generated a significant reduction in microbial translocation, immune activation, improved Th17/Treg cell and Th1/Th2 [41]. Intervention with *B. bifidum, L. acidophilus, L. casei* and *L. salivarius* effectively reduced signs of atopic dermatitis and serum cytokines interleukin (IL-5, IL-6, IFN-γ and serum IgE) [68]. *L. rhamnosus* GG could up-regulate IFN-γ and IL-10 in infants with cow's milk allergy or with IgE-associated dermatitis [69]. The use of *Lactobacillus delbruekii* and *Lactobacillus fermentum* significantly reduced IL-6 concentration and expression of TNF-α and NFκB in colon of patients with ulcerative colitis [70]. *L. brevis* CD2 decreased IFN-γ levels in saliva [60]. *L. reuteri* ATCC PTA 5289 decreased in CGF levels of IL-17 in patients with chronic periodontitis [61].

Anti-inflammatory effect of probiotics has been associated with Treg. For example, oral administration of *L. casei* alleviated colitis and increased the suppressive function of Treg of colon lamina propia. Consumption of *B. infantis* drives the generation of Treg cells, which attenuate nuclear factor kappa B (NFκB) activation induced by LPS of *Salmonella typhimurium* [71].

There is evidence of the effect of some probiotics on matrix metalloproteinases (MMP). They represent a family of human zinc-dependent endopeptidases [65]. *L. brevis* CD2 decreased MMP in saliva [60]. *L. reuteri* DSM 17938 + ATCC PTA 5289 decreased GCF MMP-8 and increased tissue inhibitors of matrix metalloproteinase (TIMP)-1 levels in patients with periodontitis [72].

Current studies also mentioned the role of probiotics in modulation of cell signal transduction pathways, specifically NFκB, which monitors the inflammatory response in the host [73]. *L. reuteri* inhibited inhibitory κB (IκB) degradation and IL-8 expression in TNF-α induced T84 cells and NFκB translocation to the nucleus in HeLa cells [74]. In the same way, *L. rhamnosus* GG diminished nucleus translocation of NFκB, restored decreased cytoplasmic IκB and limited IL-8 secretion in Caco-2 cell model [75]. These actions impede the stimulation of transcription of a series of pro-inflammatory genes such as the encode cytokines, chemokines and grow factors that modulate the proliferation of immune cells [76]. In bronchial epithelial cells cocultured with *S. salivarius* K12, an immunosuppression was observed, coincident with the inhibition of activation of the NF-κB pathway.

Certain strains of *Bifidobacteria, Lactobacilli, Escherichia coli, Propionibacterium, Bacillus* and *Saccharomyces* influence gene expression of TLRs, NFκB and interleukins. *In vitro*, the interaction of probiotics with antigen presenting cells results in downregulation of pro-inflammatory genes and upregulation of anti-inflammatory genes [36].

## **4. Probiotics and gingivitis**

The adherent bacterial biofilm around the teeth produces a gingival inflammation called plaqueinduced gingivitis [77]. It is the most common form of periodontal disease worldwide and plenty of data exist, from different countries and age groups, about the prevalence, extent and severity of gingivitis. Studies on population have shown that regardless of age, gender and race, gingivitis is always associated with the level of oral hygiene [78]. Large-scale population studies on children, adolescents, adults and elderly people have reported very high prevalence of gingivitis, ranging from 50 to 100% [79–82]. Gingivitis and periodontitis are regarded as a continuum of a same inflammatory process. However, it is necessary to point out that in many cases gingivitis does not progress to periodontitis [83, 84].

Once the teeth erupt, a bacterial biofilm immediately begins to form at their surfaces exposed to the oral cavity and in intimate contact with the gingival margin. The level of biofilm accumulation, the virulence of the biofilm bacteria and the humoral and cellular immune responses to the biofilm microbiome are the factors that determine the severity of the periodontal disease [85]. Normally gingivitis in young subjects remains chronic for an extended period of time and does not cause any damage to the periodontal ligament or bone. Nevertheless, an alteration of the balance between biofilm and host can originate a loss of periodontal attachment. Chronic and aggressive periodontitis start as gingivitis. However, the biological processes involved in the progression from gingivitis to periodontitis have been difficult to determine [86]. It is probable that the following elements are implicated in the disease progression to periodontitis: microbial dysbiosis, overgrowth of pathogenic bacteria, herpes virus reactivation, immune-system disruption and acquired and/or genetic susceptibility factors [87–89].

Mechanical removal of supragingival plaque is the most effective tool to prevent gingivitis [90] but most individuals do not adequately control plaque accumulation and gingivitis continues to be prevalent. To overcome this hindrance, antimicrobial products in the form of dentifrices or mouthwashes have been tested for their adjunctive efficacy in reducing plaque and gingivitis.

Probiotic technology represents a breakthrough approach to maintain oral health by utilizing natural beneficial bacteria commonly found in healthy mouths to provide a natural defence against the bacteria thought to be harmful to teeth and gums [15]. Within dentistry, the previous studies with *lactobacilli* strains such as *L. rhamnosus, L. casei, L. reuter*i, or a *Lactobacilli* mix have revealed mixed results on oral microorganisms.

Krasse et al. conducted one of the first clinical trial randomized double-blind placebo controlled. The principal aim of the study was to assess if the probiotic *L. reuteri* could be effective in the management of gingivitis and then to evaluate the influence of the probiotic on plaque and the lactobacilli population in the saliva. Fifty-nine patients with moderate to severe gingivitis were included and given either/or specific *L. reuteri* formulations (LR-1 or LR-2) at a dose of 2 × 108 CFU/day, or a corresponding placebo. At baseline (day 0), they collected saliva to determine the lactobacilli and measured gingival index and plaque on two surfaces. They taught patients to brush and to floss their teeth carefully and the treatment began. The patients returned on day 14 for final assessment of gingivitis and saliva and plaque were collected. Twenty patients were randomly given LR-1, 21 took LR-2 and 18 received inactive substances. The gingival index decreased evenly in all three groups (*p* < 0.0001). LR-1 only (not LR-2) improved more than placebo (*p* < 0.0001). Plaque index fell evenly in LR-1 (*p* < 0.05) and in LR-2 (*p* < 0.01) between day 0 and day 14 but without significant change in the inactive substance. On day 14, 65% of the patients in the LR-1 group were colonized with *L. reuteri* and 95% in the LR-2. *L. reuteri* reduce both gingivitis and plaque in patients with moderate to severe gingivitis [91].

with *S. salivarius* K12, an immunosuppression was observed, coincident with the inhibition of

Certain strains of *Bifidobacteria, Lactobacilli, Escherichia coli, Propionibacterium, Bacillus* and *Saccharomyces* influence gene expression of TLRs, NFκB and interleukins. *In vitro*, the interaction of probiotics with antigen presenting cells results in downregulation of pro-inflamma-

The adherent bacterial biofilm around the teeth produces a gingival inflammation called plaqueinduced gingivitis [77]. It is the most common form of periodontal disease worldwide and plenty of data exist, from different countries and age groups, about the prevalence, extent and severity of gingivitis. Studies on population have shown that regardless of age, gender and race, gingivitis is always associated with the level of oral hygiene [78]. Large-scale population studies on children, adolescents, adults and elderly people have reported very high prevalence of gingivitis, ranging from 50 to 100% [79–82]. Gingivitis and periodontitis are regarded as a continuum of a same inflammatory process. However, it is necessary to point out that in many cases gingivitis

Once the teeth erupt, a bacterial biofilm immediately begins to form at their surfaces exposed to the oral cavity and in intimate contact with the gingival margin. The level of biofilm accumulation, the virulence of the biofilm bacteria and the humoral and cellular immune responses to the biofilm microbiome are the factors that determine the severity of the periodontal disease [85]. Normally gingivitis in young subjects remains chronic for an extended period of time and does not cause any damage to the periodontal ligament or bone. Nevertheless, an alteration of the balance between biofilm and host can originate a loss of periodontal attachment. Chronic and aggressive periodontitis start as gingivitis. However, the biological processes involved in the progression from gingivitis to periodontitis have been difficult to determine [86]. It is probable that the following elements are implicated in the disease progression to periodontitis: microbial dysbiosis, overgrowth of pathogenic bacteria, herpes virus reactivation, immune-system disruption and acquired and/or genetic susceptibility factors [87–89].

Mechanical removal of supragingival plaque is the most effective tool to prevent gingivitis [90] but most individuals do not adequately control plaque accumulation and gingivitis continues to be prevalent. To overcome this hindrance, antimicrobial products in the form of dentifrices or mouthwashes have been tested for their adjunctive efficacy in reducing plaque

Probiotic technology represents a breakthrough approach to maintain oral health by utilizing natural beneficial bacteria commonly found in healthy mouths to provide a natural defence against the bacteria thought to be harmful to teeth and gums [15]. Within dentistry, the previous studies with *lactobacilli* strains such as *L. rhamnosus, L. casei, L. reuter*i, or a *Lactobacilli* mix

activation of the NF-κB pathway.

80 Insights into Various Aspects of Oral Health

**4. Probiotics and gingivitis**

does not progress to periodontitis [83, 84].

have revealed mixed results on oral microorganisms.

and gingivitis.

tory genes and upregulation of anti-inflammatory genes [36].

Twetman et al. conducted a clinical trial randomized double-blind placebo controlled in patients with gingivitis (n = 42). The subjects were randomly assigned to one of three comparable arms: Group A/P (n = 15) was given one active and one test substance gum daily, Group A/A (n = 14) received two active chewing gums and Group P/P (n = 13) two placebo gums. They used chewing gum (2 times a day for 10 min in the morning and evening) with *L. reuteri* (ATCC 55730 and ATCC PTA 5289, 1×108 CFU). They taught the patients to chew the gums 10 min for 2 weeks and conducted bleeding on probing and GCF sampling at baseline and after 1, 2 and 4 weeks. The levels of IL-1β, TNFα IL-6, IL-8 and IL-10 were measured using luminex technology and multiplex immunoassay kits. Bleeding on probing improved and GCF volume decreased in all groups during the chewing period. Still, the results were statistically different (*p* < 0.05) only in Groups A/P and A/A. TNFα and IL-8 levels decreased significantly (*p* < 0.05) in Group A/A compared with baseline after 1 and 2 weeks, respectively. They also observed a non-significant tendency to decrease in IL-1β during the chewing period. The levels of IL-6 and IL-10 remained unchanged in all groups after 1 and 3 weeks. The elemental basis of the probiotic approach to confront inflammation in the oral cavity could be the decrease of pro-inflammatory cytokines in GCF [92].

Staab et al. conducted a parallel-designed non-blinded study. Fifty volunteer students took part in this study. The test group took a probiotic drink (*L. casei*, 100 billion per 100 ml everyday); the control group did not drink any product. After 8 weeks, individual mechanical plaque control was delayed for 96 h. Papilla bleeding index, interproximal plaque and Turesky plaque index were measured at baseline, after 8 weeks and again 96 h later. At the coincidence points, we collected GCF for evaluation of polymorphonuclear elastase, myeloperoxidase (MPO) and MMP-3. There was no difference in the interproximal plaque index and papillary bleeding between the groups. In the test group, the elastase activity and the amount of MMP-3 were significantly lower after the intake of the probiotic drink (*p* < 0.001 and 0.016). A significant increase of MPO activity was noted in the control group; both groups had differences at the end of the survey (*p* = 0.014). According to the data, it is suggested that the probiotic milk drink has a beneficial effect on the gingival inflammation [93].

Ierardo et al. conducted a clinical trial in patients with gingivitis: Test group (n = 21) consumed chewing gum (3 times per day for 60 days) containing probiotic *L. brevis*. Control group was used for the laboratory variables (n = 16). Measurements were taken at baseline, 30 and 60 days. It was concluded that *L. brevis* has anti-inflammatory effects showing clinical improvement. In addition, it allows to reduce the levels of immunoglobulin (Ig)-A [94].

Iniesta et al. conducted a clinical trial randomized double-blind in patients with gingivitis: Test Group (n = 20) obtained lozenges with *L. reuteri* (DSM-17938 and ATCC PTA 5289, 2 × 108 CFU) for two periods of 12 weeks (with an intermediate period of 4 weeks without measures of hygiene). Microbiological and clinical differences and the pattern of colonization of *L. reuteri* were determined again. In conclusion, no significant changes occurred between and within the groups in the clinical variables. Total anaerobic counts in saliva after 4 weeks (*p* = 0.021) and counts of *P. intermedia* after 8 weeks (*p* = 0.030) decreased in the test group. In subgingival samples, *P. gingivalis* counts reduced significantly from baseline to 4 weeks (*p* = 0.008). With PCR, the presence of *L. reuteri* ATCC-PTA-5289 was higher than *L. reuteri* DSM-17938. The administration of *L. reuteri* in tablets reduced the number of selected periodontal pathogens in the subgingival microbiota, with no associated clinical impact [95].

Hallstrom et al. conducted a clinical trial randomized double-blind controlled in patients with gingivitis: Group test (n = 18) accepted lozenges of *L. reuteri* (ATCC 55730 and PTA TM9061, 1×108 CFU), two times a day for 3 weeks (with a period of 2 weeks of experimental gingivitis). During the intervention periods, all the patients presented local plaque accumulation together with manifest gingivitis at the test sites. Both groups had an increase in the volume of GCF but it was statistically significant only in the placebo group (*p* < 0.05). The concentrations of IL1-β and IL-18 (*p* < 0.05) increased significantly, while IL-8 and macrophage inflammatory protein (MIP)1-β decreased (*p* < 0.05). No differences were found between test and inactive substance. Similarly, the microbial composition was not different between the groups. The plaque accumulation, inflammatory reaction or composition of the biofilm did not seem to be significantly affected by the daily intake of probiotic lozenges during experimental gingivitis [96].

Karuppaia et al. conducted a randomized double-blind clinical trial in patients with gingivitis (aged 14–17 years): Test group (n = 108) used curd (clump of milk) 4 weeks. The control group (n = 108) excluded curd in their diet for 30 days. Clinical differences were found, the probiotic was efficacious in reducing the plaque index and gingival index [97].

Purunaik et al. conducted a clinical trial randomized double-blind placebo controlled in patients (aged 15–16 years) (n = 90) with gingivitis: Group A (n = 30) used chlorhexidine 0.2%, Group B (n = 30) mouthwash of probiotic (*L. acidophilus, L. rhamnosus, B. longum* and *Saccharomyces boulardii*) (dose: 1.25 million mix, 2 times a day for 14 days), and Group C (n = 30) placebo (20 mL per day for 60 s.). It was found that both the chlorhexidine and the probiotic group can significantly reduce the plaque index (best chlorhexidine) and the gingival index (best probiotic) [98].

Lee et al. conducted a clinical trial randomized double-blind placebo controlled in patients (n = 34) with gingivitis: Group Test (n = 17) used lozenges of *L. brevis* (CD2, 1×109 CFU), three times per day × 2 weeks and Control group (n = 17) took placebo for the same period of time. It was found that probiotic reduced the bleeding on probing. There were no differences with respect to the gingival index. The levels of NO (nitric oxid) increased in proportional form in the placebo group. The levels of MMP-8 and PGE-2 did not change [99].

Nadkerny et al. conducted a clinical trial randomized double-blind placebo controlled in three groups of patients (n = 45) with gingivitis: Group A (Test) used a mouthwash of probiotic (*L. acidophilus, L. rhamnosus, Lactibacillus sporogenes, B. longum* and *S. boulardii*; n = 15), Group B (positive control) with chlorhexidine 0.2% (n = 15), and Group C (placebo: saline solution; n = 15) for 4 weeks. The mouthwash of probiotic and chlorhexidine was efficacious in reducing the plaque index and gingival index [100].

## **5. Probiotics and periodontitis**

Ierardo et al. conducted a clinical trial in patients with gingivitis: Test group (n = 21) consumed chewing gum (3 times per day for 60 days) containing probiotic *L. brevis*. Control group was used for the laboratory variables (n = 16). Measurements were taken at baseline, 30 and 60 days. It was concluded that *L. brevis* has anti-inflammatory effects showing clinical improvement. In addition, it allows to reduce the levels of immunoglobulin (Ig)-A [94].

Iniesta et al. conducted a clinical trial randomized double-blind in patients with gingivitis: Test Group (n = 20) obtained lozenges with *L. reuteri* (DSM-17938 and ATCC PTA 5289, 2 ×

 CFU) for two periods of 12 weeks (with an intermediate period of 4 weeks without measures of hygiene). Microbiological and clinical differences and the pattern of colonization of *L. reuteri* were determined again. In conclusion, no significant changes occurred between and within the groups in the clinical variables. Total anaerobic counts in saliva after 4 weeks (*p* = 0.021) and counts of *P. intermedia* after 8 weeks (*p* = 0.030) decreased in the test group. In subgingival samples, *P. gingivalis* counts reduced significantly from baseline to 4 weeks (*p* = 0.008). With PCR, the presence of *L. reuteri* ATCC-PTA-5289 was higher than *L. reuteri* DSM-17938. The administration of *L. reuteri* in tablets reduced the number of selected periodontal

Hallstrom et al. conducted a clinical trial randomized double-blind controlled in patients with gingivitis: Group test (n = 18) accepted lozenges of *L. reuteri* (ATCC 55730 and PTA TM9061,

 CFU), two times a day for 3 weeks (with a period of 2 weeks of experimental gingivitis). During the intervention periods, all the patients presented local plaque accumulation together with manifest gingivitis at the test sites. Both groups had an increase in the volume of GCF but it was statistically significant only in the placebo group (*p* < 0.05). The concentrations of IL1-β and IL-18 (*p* < 0.05) increased significantly, while IL-8 and macrophage inflammatory protein (MIP)1-β decreased (*p* < 0.05). No differences were found between test and inactive substance. Similarly, the microbial composition was not different between the groups. The plaque accumulation, inflammatory reaction or composition of the biofilm did not seem to be significantly

pathogens in the subgingival microbiota, with no associated clinical impact [95].

affected by the daily intake of probiotic lozenges during experimental gingivitis [96].

was efficacious in reducing the plaque index and gingival index [97].

gingival index (best probiotic) [98].

Karuppaia et al. conducted a randomized double-blind clinical trial in patients with gingivitis (aged 14–17 years): Test group (n = 108) used curd (clump of milk) 4 weeks. The control group (n = 108) excluded curd in their diet for 30 days. Clinical differences were found, the probiotic

Purunaik et al. conducted a clinical trial randomized double-blind placebo controlled in patients (aged 15–16 years) (n = 90) with gingivitis: Group A (n = 30) used chlorhexidine 0.2%, Group B (n = 30) mouthwash of probiotic (*L. acidophilus, L. rhamnosus, B. longum* and *Saccharomyces boulardii*) (dose: 1.25 million mix, 2 times a day for 14 days), and Group C (n = 30) placebo (20 mL per day for 60 s.). It was found that both the chlorhexidine and the probiotic group can significantly reduce the plaque index (best chlorhexidine) and the

Lee et al. conducted a clinical trial randomized double-blind placebo controlled in patients

times per day × 2 weeks and Control group (n = 17) took placebo for the same period of time. It was found that probiotic reduced the bleeding on probing. There were no differences with

CFU), three

(n = 34) with gingivitis: Group Test (n = 17) used lozenges of *L. brevis* (CD2, 1×109

108

82 Insights into Various Aspects of Oral Health

1×108

Periodontitis is an inflammatory process caused by an infection, and it implicates the interaction of biofilm and immuno-inflammatory response of host [101]. Its consequence is the destruction of attachment structures of teeth, or periodontium. There are three signs of disease: clinical attachment loss, alveolar bone resorption and presence of periodontal pocket [102].

Periodontitis constitutes the second cause of tooth loss worldwide [103–105]. Moreover, studies [106, 107] performed in South and Central America have shown that the prevalence of severe disease is high (>30%) in these populations.

Periodontitis is caused by complex subgingival microbial communities, which are in a dysbiotic state [108]. However, a few bacteria in the subgingival biofilm have been associated with disease. Strong evidence concluded that *P. gingivalis, A. actinomycetemcomitans* and *T. forsythia* are periodontal pathogens [65]. Although the tooth-associated biofilm plays a role in the development of periodontitis, it is primarily the host inflammatory response that inflicts the irreversible damage on the periodontium [108]. T helper 1 and Th17 lymphocyte have been described in the pathogenesis of disease [65].

The aim of periodontal treatment is mechanical debridement of root surface. When periodontal pathogens are effectively reduced after therapy and higher proportions of hostcompatible microorganisms is established, improvements in clinical parameters are achieved [109]. However, mechanical debridement as a sole therapy is not always effective to improve clinical parameters [110]. Therefore, systemic antibiotics were introduced as an adjunct to mechanical treatment [111]. This treatment modality eliminates the entire microbiota, irrespective of its pathogenicity. Also, it could generate antibiotic resistance and recolonization of treated sites with pathogenic bacteria is frequent [112, 113]. Hence, there is a need of new treatment paradigms in periodontal disease management.

Several clinical trials were conducted in order to study the effect of administration of probiotics in initial treatment of periodontitis [114–117]. The bacteria most frequently used as probiotic are *L. reuteri* (DSM 17938 + ATCC PTA 5289) [72, 118–120], *Lactibacillus salivarius* WB21 [121, 122], *L. reuteri* (ATCC 55730 + ATCC PTA 5289) [123], *L. reuteri* (ATCC PTA 5289) [61], *Streptoccus oralis* KJ3 + *Streptococcus uberis* KJ2 + *Streptoccus rattus* JH145 [124] and *L. rhamnosus* SP1 [125].

Vivekananda et al. conducted a randomized, placebo-controlled, double blind, split-mouth designed clinical study to evaluate the effect of *L. reuteri* (DSM 17938 + ATCC PTA 5289) lozenges with and without scaling and root planning (SRP) on clinical and microbiological parameters of chronic periodontitis patients. The study period was 42 days. The lozenges were used two times a day for 21 days, from day 21 to day 42. Thirty systemically healthy subjects were recruited. On day 42, plaque index, gingival index and bleeding on probing decreased for all treatments. However, the level of this reduction was higher in SRP + probiotic, and lower, in placebo (*p* <0.05). Probiotic, with or without SRP, reduced significantly *P. gingivalis, A. actinomycetemcomitans* and *P. intermedia* [118].

Teughels et al. conducted a randomized, parallel, controlled and double blinded clinical, whose aim was to evaluate the effect of *L. reuteri* (DSM 17938 + ATCC PTA 5289, 1 × 108 CFU)-containing lozenges as an adjunct to full mouth disinfection protocol (FMD). Thirty systemically healthy patients were recruited (n = 15 in each group). Clinical measurements and microbiological samples were collected at baseline and 3, 6, 9 and 12 months after initial therapy with FMD. The lozenges were used two times a day for 12 weeks. At the end of intervention, i.e., 12 weeks after FMD, all clinical parameters were significantly reduced in both groups. In probiotic group, there was more pocket depth reduction and attachment gain (*p* < 0.05). Also, there was more *P. gingivalis* reduction (*p* < 0.05) [119].

Tekce et al. and Ince et al. conducted a randomized, parallel, controlled and double blinded clinical trial in order to evaluate the effect of lozenges containing *L. reuteri* (DSM 17938 + ATCC PTA 5289, 1 × 108 CFU) as an adjuvant to full mouth scaling and root planning treatment for chronic periodontitis. The lozenges were used two times a day for 3 weeks. Forty systemically healthy subjects were recruited (n = 20 in test group). Clinical measurements, microbiological and GCF samples were obtained at baseline and on days 21, 90, 180 and 360. After treatment, plaque index, gingival index, bleeding on probing and probing pocket depth were lower in test group at all times points (*p* <0.05) [120]. Attachment gain was significantly higher in the test group on days 90, 180 and 360 (*p* <0.05) [72]. Total viable cell counts and the proportions of obligate anaerobes in subgingival plaque were lower in test group at all time points (*p* <0.05), with the exception of day 360 [120]. Also, decreased GCF MMP-8 and increased TIMP-1 levels were found to be significant up to day 180 in test group (*p* <0.05) [72].

Shimauchi et al. and Mayanagi et al. conducted a randomized placebo-controlled clinical trial, whose objective was to evaluate the effect of *L. salivarius* (WB21, 6.7 × 108 CFU)-containing tablet or a placebo in treatment of mild and moderate periodontitis. The dose was three tablets taken orally every day during 8 weeks. Periodontal treatment was not performed. Sixtysix systemically healthy volunteers were recruited (n = 34 in test group). Periodontal clinical parameters, whole saliva samples and supra and subgingival plaque samples were obtained at baseline, 4 weeks, and at the end of the interventional period (8 weeks). Current smokers in the test group showed a significantly greater improvement of plaque index and probing pocket depth when compared with placebo group. Salivary lactoferrin level was also significantly decreased in the test group smokers [121]. The numerical sum of five selected periodontopathic bacteria and *T. forsythia* in subgingival plaque decreased significantly in test group (*p* <0.05) at 4 weeks of treatment [122].

Vicario et al. conducted a randomized placebo-controlled, parallel design, double-blind clinical trial. The aim was to evaluate the effect of *L. reuteri* (ATCC 55730 + ATCC PTA 5289, 2 × 108 CFU)-containing lozenges in treatment of chronic periodontitis. Twenty systemically healthy subjects were recruited. Periodontal treatment was not performed. Subjects were advised to use a lozenge every day for 30 days. Clinical measurements were performed at baseline and at the end of interventional period. Only test group demonstrated a significant reduction in plaque index, bleeding on probing and pocket depth at the end of interventional period (*p* < 0.05) [123].

Vivekananda et al. conducted a randomized, placebo-controlled, double blind, split-mouth designed clinical study to evaluate the effect of *L. reuteri* (DSM 17938 + ATCC PTA 5289) lozenges with and without scaling and root planning (SRP) on clinical and microbiological parameters of chronic periodontitis patients. The study period was 42 days. The lozenges were used two times a day for 21 days, from day 21 to day 42. Thirty systemically healthy subjects were recruited. On day 42, plaque index, gingival index and bleeding on probing decreased for all treatments. However, the level of this reduction was higher in SRP + probiotic, and lower, in placebo (*p* <0.05). Probiotic, with or without SRP, reduced significantly

Teughels et al. conducted a randomized, parallel, controlled and double blinded clinical, whose aim was to evaluate the effect of *L. reuteri* (DSM 17938 + ATCC PTA 5289, 1 × 108 CFU)-containing lozenges as an adjunct to full mouth disinfection protocol (FMD). Thirty systemically healthy patients were recruited (n = 15 in each group). Clinical measurements and microbiological samples were collected at baseline and 3, 6, 9 and 12 months after initial therapy with FMD. The lozenges were used two times a day for 12 weeks. At the end of intervention, i.e., 12 weeks after FMD, all clinical parameters were significantly reduced in both groups. In probiotic group, there was more pocket depth reduction and attachment gain (*p* <

Tekce et al. and Ince et al. conducted a randomized, parallel, controlled and double blinded clinical trial in order to evaluate the effect of lozenges containing *L. reuteri* (DSM 17938 +

ment for chronic periodontitis. The lozenges were used two times a day for 3 weeks. Forty systemically healthy subjects were recruited (n = 20 in test group). Clinical measurements, microbiological and GCF samples were obtained at baseline and on days 21, 90, 180 and 360. After treatment, plaque index, gingival index, bleeding on probing and probing pocket depth were lower in test group at all times points (*p* <0.05) [120]. Attachment gain was significantly higher in the test group on days 90, 180 and 360 (*p* <0.05) [72]. Total viable cell counts and the proportions of obligate anaerobes in subgingival plaque were lower in test group at all time points (*p* <0.05), with the exception of day 360 [120]. Also, decreased GCF MMP-8 and increased TIMP-1 levels were found to be significant up to day 180 in test group (*p* <0.05) [72].

Shimauchi et al. and Mayanagi et al. conducted a randomized placebo-controlled clinical trial,

tablet or a placebo in treatment of mild and moderate periodontitis. The dose was three tablets taken orally every day during 8 weeks. Periodontal treatment was not performed. Sixtysix systemically healthy volunteers were recruited (n = 34 in test group). Periodontal clinical parameters, whole saliva samples and supra and subgingival plaque samples were obtained at baseline, 4 weeks, and at the end of the interventional period (8 weeks). Current smokers in the test group showed a significantly greater improvement of plaque index and probing pocket depth when compared with placebo group. Salivary lactoferrin level was also significantly decreased in the test group smokers [121]. The numerical sum of five selected periodontopathic bacteria and *T. forsythia* in subgingival plaque decreased significantly in

whose objective was to evaluate the effect of *L. salivarius* (WB21, 6.7 × 108

test group (*p* <0.05) at 4 weeks of treatment [122].

CFU) as an adjuvant to full mouth scaling and root planning treat-

CFU)-containing

*P. gingivalis, A. actinomycetemcomitans* and *P. intermedia* [118].

0.05). Also, there was more *P. gingivalis* reduction (*p* < 0.05) [119].

ATCC PTA 5289, 1 × 108

84 Insights into Various Aspects of Oral Health

Szkaradkiewicz et al. conducted a clinical trial aimed to evaluate the pro-inflammatory cytokine response in patients with chronic periodontitis administered with probiotic *L. reuteri* (ATCC PTA 5289, 1 × 108 CFU)-containing lozenges. Control group did not receive lozenges. All patients were treated with SRP. They recruited 38 systemically healthy subjects (n = 24 in test group). The dose was two lozenges per day (authors did not mention the duration of intervention). Test group experimented a significant improvement of clinical measurements and a decrease in CGF levels of TNF-α, IL-1β and IL-17 (*p* <0.05) [61].

Laleman et al. conducted a double-blind, placebo-controlled, randomized clinical trial with two parallel arms in chronic periodontitis. The aim was to evaluate the adjunctive effect of probiotic (*Streptoccus oralis* KJ3 + *Streptococcus uberis* KJ2 + *Streptoccus rattus* JH145, 1 × 108 CFU)-containing lozenges after FMD. The dose was two lozenges per day during 3 months. Forty-eight subjects were recruited. Clinical parameters and microbiological samples were collected at baseline, 4, 8, 12 and 24 weeks follow-up visit. In test group, plaque index was significantly lower at the 24-week evaluation (*p* <0.05) Also, salivary *P. intermedia* counts were significantly lower at the 12-week visit in probiotic group (*p* <0.05) [124].

Morales et al. conducted a double-blind placebo controlled parallel-arm randomized clinical trial whose objective was to evaluate the clinical effect of *L. rhamnosus* (SP1, 2 × 10<sup>7</sup> CFU) containing sachet as an adjunct to non-surgical therapy (SRP) of chronic periodontitis. Twenty-eight systemically healthy subject were recruited (n = 14 in test group). The dose was one sachet of probiotic or placebo taken orally every day during 3 months. Treatment involved SRP per quadrant performed with 1-week intervals in four to six sessions. A periodontal supportive therapy was performed every 3 months. Clinical parameters were measured at baseline, 3, 6, 9 and 12 months follow-up visit. Both groups showed improvements in clinical parameters at all time points evaluated. However, there were no differences between groups in any visit [125, 126].

There are some systematic reviews whose aim was to explore the available clinical evidence on the efficacy of probiotic therapy in initial treatment of chronic periodontitis. There was a significant reduction in probing pocket depth, bleeding on probing, plaque index and attachment gain in probiotic group [116]. In the studies where *L. reuteri* was selected as probiotic, the reduction of probing pocket depth was 1.31–1.74 mm in probiotic group and 0.49–1.39 mm in placebo group. Also, the attachment gain was 0.99–1.39 mm in probiotic group and 0.29–0.76 mm in placebo group [117]. Finally, the authors concluded that oral administration of probiotics is a safe and effective adjunct to scaling and root planning in the treatment of chronic periodontitis. Their adjunctive use is likely to improve diseases indices and reduce the need for antibiotics [116].

The use of probiotics in supportive periodontal therapy (SPT) was reported in a clinical trial conducted by Iwasaki et al. The aim of this randomised, double-blind, placebo controlled clinical trial was to evaluate the effect of heat-killed *L. plantarum* L-137 on the outcome of SPT. Thirty-nine SPT subjects (n = 20 in test group) who completed active treatment for chronic periodontitis followed by SPT every 4 weeks were recruited. Subjects consumed a hard gelatine capsule of 50 mg of probiotic or placebo per day during 12 weeks. The SPT programmes and clinical examinations were performed at baseline 4, 8, and 12 weeks after start intervention. Bleeding on probing and sites with pocket probing depth ≥4 mm were significantly reduced in both groups. In test group, there was a significantly greater probing pocket depth (PPD) reduction in teeth with sites with PPD ≥ 4 mm at week 12 (*p* <0.05). This result indicates that daily intake of probiotic may be useful in SPT [127].

## **6. Conclusions**

Oral diseases are a recognized public health problem worldwide [128, 129]. Dental caries, periodontitis and oral cancer, among other oral diseases, currently occupy the health agenda, seeking to establish policies that, when integrated with other health intervention programs, will impact the oral health of our population. Along with the economic impact on governments and individuals [130], a higher cost is added in terms of pain, discomfort, social and functional limitations, and time lost and absenteeism in schools and workplaces [131, 132].

The goals of periodontal therapy are to reduce probing pocket depth, to gain attachment level and to reduce bleeding on probing suppuration. A new microbial community is needed in order to achieve the clinical results [109]. Therefore, with the aim of potentiating the effects of periodontal treatment, other protocols, such as the association of mechanical debridement with systemic antibiotics, have been used successfully in the treatment of periodontal diseases. The problems of antibiotics are in association with the elimination of the entire microflora, irrespective of their pathogenicity, and the emergence of antibiotic resistance; the shift towards a less pathogenic microbiota is only temporary with a frequent recolonization of treated sites with pathogenic bacteria; and the temporary use of antibiotics locally or systemically, does not really improve the long-term effect of periodontal therapy.

Considering the beneficial effects of probiotics, this therapy could serve as a useful adjunct or alternative to periodontal treatment. The use of probiotics in oral care applications is gaining momentum [118]. There is increasing evidence that the use of existing probiotic strains can deliver oral health benefits. Therefore, proposing a treatment involving the non-surgical treatment plus probiotic intake may result in better regulation of bacterial plaque and thus contribute to a successful periodontal treatment, and they can also exert effects on modulating immunological parameters.

## **Acknowledgements**

This study was supported by a grant provided by the Scientific and Technologic Investigation Resource, Santiago, Chile (Fondecyt Project N° 1130570) and CONICYT-PCHA/Magíster Nacional/2013-22130172. Thanks to Mr. Juan Fernandez from the Language and Translation services of the Faculty of Dentistry, University of Chile for kindly correcting the English spelling and grammar of this paper. The authors declare that there are no conflicts of interest in this study.

## **Author details**

The use of probiotics in supportive periodontal therapy (SPT) was reported in a clinical trial conducted by Iwasaki et al. The aim of this randomised, double-blind, placebo controlled clinical trial was to evaluate the effect of heat-killed *L. plantarum* L-137 on the outcome of SPT. Thirty-nine SPT subjects (n = 20 in test group) who completed active treatment for chronic periodontitis followed by SPT every 4 weeks were recruited. Subjects consumed a hard gelatine capsule of 50 mg of probiotic or placebo per day during 12 weeks. The SPT programmes and clinical examinations were performed at baseline 4, 8, and 12 weeks after start intervention. Bleeding on probing and sites with pocket probing depth ≥4 mm were significantly reduced in both groups. In test group, there was a significantly greater probing pocket depth (PPD) reduction in teeth with sites with PPD ≥ 4 mm at week 12 (*p* <0.05). This result indicates

Oral diseases are a recognized public health problem worldwide [128, 129]. Dental caries, periodontitis and oral cancer, among other oral diseases, currently occupy the health agenda, seeking to establish policies that, when integrated with other health intervention programs, will impact the oral health of our population. Along with the economic impact on governments and individuals [130], a higher cost is added in terms of pain, discomfort, social and functional

The goals of periodontal therapy are to reduce probing pocket depth, to gain attachment level and to reduce bleeding on probing suppuration. A new microbial community is needed in order to achieve the clinical results [109]. Therefore, with the aim of potentiating the effects of periodontal treatment, other protocols, such as the association of mechanical debridement with systemic antibiotics, have been used successfully in the treatment of periodontal diseases. The problems of antibiotics are in association with the elimination of the entire microflora, irrespective of their pathogenicity, and the emergence of antibiotic resistance; the shift towards a less pathogenic microbiota is only temporary with a frequent recolonization of treated sites with pathogenic bacteria; and the temporary use of antibiotics locally or systemi-

Considering the beneficial effects of probiotics, this therapy could serve as a useful adjunct or alternative to periodontal treatment. The use of probiotics in oral care applications is gaining momentum [118]. There is increasing evidence that the use of existing probiotic strains can deliver oral health benefits. Therefore, proposing a treatment involving the non-surgical treatment plus probiotic intake may result in better regulation of bacterial plaque and thus contribute to a successful periodontal treatment, and they can also exert effects on modulating

This study was supported by a grant provided by the Scientific and Technologic Investigation Resource, Santiago, Chile (Fondecyt Project N° 1130570) and CONICYT-PCHA/Magíster

limitations, and time lost and absenteeism in schools and workplaces [131, 132].

cally, does not really improve the long-term effect of periodontal therapy.

that daily intake of probiotic may be useful in SPT [127].

**6. Conclusions**

86 Insights into Various Aspects of Oral Health

immunological parameters.

**Acknowledgements**

Alicia Morales1 , Joel Bravo-Bown<sup>2</sup> , Javier Bedoya<sup>3</sup> and Jorge Gamonal1 \*

\*Address all correspondence to: jgamonal@odontologia.uchile.cl

1 Laboratory of Periodontal Biology, Department of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile

2 Faculty of Medicine and Dentistry, University of Antofagasta, Antofagasta, Chile

3 Faculty of Dentistry, University of Antioquia, Medellin, Colombia

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**Provisional chapter**

## **Cleft Lip and Palate Management from Birth to Adulthood: An Overview Adulthood: An Overview**

**Cleft Lip and Palate Management from Birth to** 

DOI: 10.5772/intechopen.68448

Maen Hussni Zreaqat, Rozita Hassan and Abdulfattah Hanoun Abdulfattah Hanoun Additional information is available at the end of the chapter

Maen Hussni Zreaqat, Rozita Hassan and

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.68448

#### **Abstract**

Cleft lip and palate (CLP) is the most common congenital deformity of the orofacial. Clefts are thought to be of multifactorial etiology due to genetic and environmental factors. Different dental abnormalities are usually seen in cleft patients, including midface deficiency, collapsed dental arches, malformation of teeth, hypodontia, and supernumerary teeth. Moreover, feeding and speech are major functional dilemmas for those patients. The goal of treatment is to restore esthetics and functional impairments associated with clefts. The nature and the extent of medical and dental problems among CLP patients dictate the need toward multidisciplinary approach where different medical and dental specialists are involved in the treatment. The purpose of this section is to codify and synthesize a literature about management of cleft lip and palate deformity from birth until adulthood so that general concepts, principles, and axioms can be formulated. In this regard, feeding plates, nasoalveolar molding (NAM), lip and palate repair, palatal expansion, alveolar bone grafting, rhinoplasty, orthodontic treatment, and orthognathic surgery will be discussed. Furthermore, the question of proper timing for each therapeutic procedure is scrutinized in this chapter. Suggested clinical tips and changes of treatment modalities are summarized and illustrated as well.

**Keywords:** cleft lip and palate, multidisciplinary management, lip repair, palate repair, orthognathic surgery

## **1. Introduction**

Cleft lip and palate (CLP) is the most common orofacial malformation affecting one in every 700–1000 newborns worldwide [1]. The anomaly is characterized by the lack continuity of tissues forming the lip, alveolus, and soft and hard palate. The severity ranges from a small

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

notch in the lip to a complete fissure extending into the roof of the mouth and nose. Due to their disturbing appearance in many cases, these deformities have attracted much attention in terms of treatment and research. The large impact of the cleft lip and palate on appearance and function renders them a major public health problem worldwide [2]. Data from human and animal studies have suggested that the etiology of cleft lip and palate results from gene-environment interaction where genes have a major influence. Current research is emphasizing on detection of location and nature of mutations in genes associated with cleft lip and palate.

In comparison with unaffected children, individuals with unilateral cleft lip and palate (UCLP) present with striking asymmetries of the soft tissues as well as the nasomaxillary and lower facial structures. The facial profile is significantly affected by the cleft anomaly; the profile is generally concave due to the maxillary retrognathia. Several studies had reported that unilateral cleft lip and palate children have increased nose width, reduced mouth width, nose asymmetry, increased nose width/mouth width ratio, reduced upper lip length [3], and reduced lip elasticity [4]. For the dentoalveolar relationships, crossbite and open bite are common findings among unilateral cleft lip and palate patients [5].

Bishara et al. suggested that differences in dentoalveolar morphology between cleft and noncleft subjects could be related to many factors. These include the morphogenetic pattern of the cleft anomaly, long-term management, and adaptive changes due to the mechanical presence of the cleft or lack of continuity of tissues [6].

**Figure 1.** Surgical instruments for cleft surgery (Heister's surgical textbook, 1731).

The management of children with cleft lip and palate is a real challenge. Intervention of cleft patients starts as early as intrauterine and continues into late adulthood. Related families are involved as well. Those patients are presented with various problems, and thus, effective therapeutic outcomes can be only through a multidisciplinary approach. The cleft team consists of different specialists work closely together, so that maximum care can be delivered in the optimum way. There is a consensus that understanding of the requirements and specialist skills of the other team members is necessary so that all members within the team can work coordinately which leads to improving outcomes.

The first proven description of treatment of a cleft lip and palate appeared in ancient China in the fourth century after Christ. Heister in 1731 described a clinical picture of cleft lip and palate management (**Figure 1**). It was Hagedorn who laid the basics of geometrical anatomical and surgical lip repair in 1884. He developed the surgical technique of repair using a geometric cutting procedure, the flap exchange, which in principle is in practice up to now. Thus, he founded basics of oriented surgical procedures that were described later by clinicians in the twentieth century [7].

## **2. Incidence of cleft lip and palate**

Incidence of cleft lip and palate had been the subjects of many studies. There are significant differences in the incidence of cleft lip and palate, with the highest rates in Asian populations and Native Americans, intermediate rates in Caucasians, and lowest rates in African American. According to the European registration of congenital and twins (EUROCAT), incidence rates of cleft lip and palate for various regions in Europe between the year 1980 and 1988 were 1.45–1.57/1000 living birth [8]. Unilateral cleft lip and palate (UCLP) occurred in 40% of all cleft groups with male/female ratio (2:1) and was more common on the left side [9]. On the other hand, isolated cleft palate occurs more in females and is usually associated with syndromes [10].

## **3. Classification of cleft lip and palate**

Different systems were introduced to classify cleft lip and palate.

#### **3.1. Veau classification (1931)**

Veau (1931) classified oral clefts based on the anatomy of the oral cavity into four groups:

**1.** Cleft of soft palate.

**Figure 1.** Surgical instruments for cleft surgery (Heister's surgical textbook, 1731).

mon findings among unilateral cleft lip and palate patients [5].

of the cleft or lack of continuity of tissues [6].

notch in the lip to a complete fissure extending into the roof of the mouth and nose. Due to their disturbing appearance in many cases, these deformities have attracted much attention in terms of treatment and research. The large impact of the cleft lip and palate on appearance and function renders them a major public health problem worldwide [2]. Data from human and animal studies have suggested that the etiology of cleft lip and palate results from gene-environment interaction where genes have a major influence. Current research is emphasizing on detection of location and nature of mutations in genes associated with cleft

In comparison with unaffected children, individuals with unilateral cleft lip and palate (UCLP) present with striking asymmetries of the soft tissues as well as the nasomaxillary and lower facial structures. The facial profile is significantly affected by the cleft anomaly; the profile is generally concave due to the maxillary retrognathia. Several studies had reported that unilateral cleft lip and palate children have increased nose width, reduced mouth width, nose asymmetry, increased nose width/mouth width ratio, reduced upper lip length [3], and reduced lip elasticity [4]. For the dentoalveolar relationships, crossbite and open bite are com-

Bishara et al. suggested that differences in dentoalveolar morphology between cleft and noncleft subjects could be related to many factors. These include the morphogenetic pattern of the cleft anomaly, long-term management, and adaptive changes due to the mechanical presence

lip and palate.

100 Insights into Various Aspects of Oral Health

**2.** Cleft of soft and hard palate from incisive foramen up to the secondary palate.


#### **3.2. Classification by International Confederation for Plastic and Reconstructive Surgery (1966)**

International Confederation for Plastic and Reconstructive Surgery had classified oral cleft into three groups:


#### **3.3. Kernahan and Stark classification (1958)**

This classification is based on embryology and classifies oral clefts into two main groups:


Kernahan and Stark classification was widely accepted because it is simple and embryologically sound [11].

#### **3.4. Kernahan stripped "Y" classification**

This classification is represented as a stripped "Y" with numbered blocks. Different numbers represent a specific affected area in the cleft deformity (**Figure 2**).


The shaded boxes represent the site of cleft deformity.

#### **3.5. Iowa classification**

**3.** Complete unilateral cleft from the uvula to incisive foramen, going on one side through the

**4.** Complete bilateral cleft from the incisive foramen to the alveolus, the premaxilla remains

**3.2. Classification by International Confederation for Plastic and Reconstructive Surgery** 

International Confederation for Plastic and Reconstructive Surgery had classified oral cleft

**2.** Clefts of anterior and posterior palate, where the alveolus and the hard palate are

This classification is based on embryology and classifies oral clefts into two main groups:

**2.** Cleft of secondary palate: extends from soft and hard palate up to incisive foramen. Both groups could be complete or incomplete, unilateral or bilateral (Kernahan and Stark,

Kernahan and Stark classification was widely accepted because it is simple and embryologi-

This classification is represented as a stripped "Y" with numbered blocks. Different numbers

**1.** Clefts of anterior primary palate, where the lip and alveolus are affected.

**3.** Clefts of the posterior palate, where the hard and soft palate are affected.

**1.** Cleft of primary palate: extends from alveolus up to the incisive foramen.

represent a specific affected area in the cleft deformity (**Figure 2**).



The shaded boxes represent the site of cleft deformity.

alveolus at the side of the future lateral incisor tooth.

suspended from the nasal septum.

102 Insights into Various Aspects of Oral Health

**3.3. Kernahan and Stark classification (1958)**

**3.4. Kernahan stripped "Y" classification**




**(1966)**

into three groups:

affected.

1958).

cally sound [11].

Iowa classification had classified cleft lip and palate into five groups (**Figure 3**). This descriptive classification was a variation of Veau classification and is more commonly used.


**Figure 3.** Iowa classification of cleft lip and palate.

## **4. Embryology background**

Knowledge of the normal embryological development of the lip and palate is essential for understanding and management of cleft lip and palate. The face is formed by the fusion of a number of embryonic processes that form around the primitive oral cavity (stomodeum). By the 4th week of intrauterine life, five branchial arches develop at the site of future neck. The nasomaxillary complex is formed through the development of the first branchial arch (the mandibular arch). The upper boundary of the stomodeum (primitive oral cavity) originates as a large frontal prominence. The primary mouth is divided from the foregut by the buccopharyngeal membrane. The dorsal end of developing mandibular arch gives off a bud called maxillary process with the formation of the nasal pit. One medial and two lateral nasal processes are formed as the frontonasal process gets divided [12] (**Figure 4**).

#### **4.1. Development of the primary palate (upper lip and premaxilla)**

The maxillary process undergoes rapid growth between the 5th and the 6th weeks of intrauterine life. By the 7th week, the maxillary, the medial, and lateral nasal processes are integrated to form the intermaxillary segment with its labial component forming the philtrum of the upper lip while its triangular palatal component forming the maxillary incisors and extend backwards to the incisive foramen. As a result, the upper lip and the maxilla are formed. Cleft lip may develop due to inadequate proliferation of the maxillary and medial nasal processes.

#### **4.2. Development of the secondary palate**

The rest of the palatal shelves forms hard and soft palates, which are formed from secondary palate. By the 6th week of the intrauterine life, palatal shelves are formed from the medial surface of the maxillary process. These will grow medially and downwards, lateral to the tongue being elevated in the 7th week, and more marked in the anterior region and leading to growth of the mandible.

**Figure 4.** Facial embryo at day 45.

The tongue plays a vital role in the initial prevention of the palatal shelves union. Thus, the shelves grow vertically down. By the 8th week of intrauterine life, palatal shelves approximate touching each other. As a result, the related epithelium degenerates and mesenchyme from both shelves join in the midline. Final closure by fusion is completed by the 10th week and usually occurs a little bit later in males than females. Failure of fusion of the maxillary shelves with each other and with the frontonasal processes results in cleft palate.

## **5. Etiology of cleft lip and palate**

Recent studies have shown that the etiology of cleft lip and palate is multifactorial. The underlying genetic factors are enhanced by environmental factors [13].

#### **5.1. Genetic factors**

**4. Embryology background**

104 Insights into Various Aspects of Oral Health

**4.2. Development of the secondary palate**

of the mandible.

**Figure 4.** Facial embryo at day 45.

Knowledge of the normal embryological development of the lip and palate is essential for understanding and management of cleft lip and palate. The face is formed by the fusion of a number of embryonic processes that form around the primitive oral cavity (stomodeum). By the 4th week of intrauterine life, five branchial arches develop at the site of future neck. The nasomaxillary complex is formed through the development of the first branchial arch (the mandibular arch). The upper boundary of the stomodeum (primitive oral cavity) originates as a large frontal prominence. The primary mouth is divided from the foregut by the buccopharyngeal membrane. The dorsal end of developing mandibular arch gives off a bud called maxillary process with the formation of the nasal pit. One medial and two lateral nasal pro-

The maxillary process undergoes rapid growth between the 5th and the 6th weeks of intrauterine life. By the 7th week, the maxillary, the medial, and lateral nasal processes are integrated to form the intermaxillary segment with its labial component forming the philtrum of the upper lip while its triangular palatal component forming the maxillary incisors and extend backwards to the incisive foramen. As a result, the upper lip and the maxilla are formed. Cleft lip may develop due to inadequate proliferation of the maxillary and medial nasal processes.

The rest of the palatal shelves forms hard and soft palates, which are formed from secondary palate. By the 6th week of the intrauterine life, palatal shelves are formed from the medial surface of the maxillary process. These will grow medially and downwards, lateral to the tongue being elevated in the 7th week, and more marked in the anterior region and leading to growth

cesses are formed as the frontonasal process gets divided [12] (**Figure 4**).

**4.1. Development of the primary palate (upper lip and premaxilla)**

The genetic factors for the etiology of nonsyndromic cleft lip with or without cleft palate and for nonsyndromic cleft palate only were first indicated in the population studies of Fogh-Anderson. Animal studies of cleft deformity were directed toward the importance of the secondary palate formation. These studies have pointed out the importance of extracellular matrix proteins and soluble factors in normal palate formation. Transforming growth factor-α (TGF-α), epidermal growth factor, fibroblast growth factor, and TGF-β3 are of clinical significance in this process. Moreover, transforming growth factor-α (TGF-α) has been suggested as a target gene in the etiology of nonsyndromic cleft deformity. In animal studies, high levels of TGFA were detected in the epithelial tissue of the medial edge of the palatal shelves at the time of shelf fusion. The biologic support for the role of TGFA gene in cleft etiology was addressed due to the reported association of TGFA alleles with human cleft lip and palate [14].

Glu mutation of the PVRL 1 gene proved to be a genetic factor for nonsyndromic clefts of the primary and the secondary palates, but simultaneous occurrence of PVRL1 and CLPTM 1 gene mutations in cleft patients does not correlate with the type of cleft (left, right, bilateral) or the gender of the patients [15, 16].

#### **5.2. Environmental factors**

A positive association between maternal cigarette smoking and cleft lip and palate has been observed in number of studies [17]. A case-control study of the association between cleft lip and palate and maternal exposure to tobacco smoke during the first trimester of pregnancy in United Kingdom proved that there is a statistically significant positive association between active smoking during pregnancy and the risk of developing cleft lip and palate [18]. B group vitamin deficiency (including folic acid) during pregnancy has been shown to be a teratogen in the etiology of cleft lip and palate formation in humans [19].

Krost and Schubert evaluated the seasonal influence on the occurrence of cleft lip and palate and proved a significant maximum risk in spring and minimum in winter for the conception date. They claimed that there are seasonal factors implicated in the etiology of cleft lip and palate. These include deficiency of vitamins and fluctuations in mother's diet, intensive UV light exposure, the use of fertilizers and pesticides in agriculture, and infectious disease cycles [20].

## **6. Cleft management**

Management of children with cleft lip and palate should go through a multidisciplinary team who will provide the optimal treatment (Bill, 2006). The managing team should provide comprehensive diagnosis, planning, and treatment. The cleft team usually includes orthodontist, maxillofacial surgeon, plastic surgeon, prosthodontist, speech therapist, audiologist (ENT specialist), psychologist, and pediatrician [21]. Goals of treatment of the child with a cleft lip and palate should include the repairing the birth defect (lip, palate, and nose), achieving normal speech, language, hearing, functional occlusion, and good dental health. It should also optimize the psychosocial and developmental outcomes [22]. However, protocols for the management of CLP patients vary from center to center. According to the Eurocleft project between 1996 and 2000, there were 194 different surgical approaches followed for treatment of unilateral cleft alone [23]. Management is discussed according to specific time periods as shown below.

#### **6.1. Pre-natal diagnosis**

Ultrasound examination may detect clefts of the lip and alveolus unlike cleft palate, which is difficult to diagnose through routine screening (**Figure 5**). Additional examinations and tests can confirm the presence of deformity. These include cephalic presentation of the child, low body mass index of the mother, and examination preferably around the 20th gestational week [24]. Moreover, information about family history should be addressed so that provisions for postnatal measures in adequately equipped hospitals can be made in with improvement in ultrasound technology.

In case of cleft identification, genetic counseling the family including amniocentesis should be performed. For this purpose, a complete pregnancy progress and family history should be addressed. Exposure to any teratogenic factors, the presence of family members with cleft or other birth defects, developmental problems, and genetic syndromes are all important parameter to explore during counseling. In cases where clefts are diagnosed prenatally, the cleft team will be involved in the management so that the family can learn about the nature of the deformity and its care and treatment strategies. Psychological and emotional support of the family is very essential procedure at this time due to the very negative effect once the diagnosis was confirmed.

#### **6.2. Birth time**

The most immediate problem caused by orofacial clefting is likely to be difficulty with feeding. The anatomical characteristics of cleft lip and palate greatly hinder infants' ability to feed. Poor intraoral suction may produce choking, emission of milk through the nose, and

These include deficiency of vitamins and fluctuations in mother's diet, intensive UV light exposure, the use of fertilizers and pesticides in agriculture, and infectious disease cycles [20].

Management of children with cleft lip and palate should go through a multidisciplinary team who will provide the optimal treatment (Bill, 2006). The managing team should provide comprehensive diagnosis, planning, and treatment. The cleft team usually includes orthodontist, maxillofacial surgeon, plastic surgeon, prosthodontist, speech therapist, audiologist (ENT specialist), psychologist, and pediatrician [21]. Goals of treatment of the child with a cleft lip and palate should include the repairing the birth defect (lip, palate, and nose), achieving normal speech, language, hearing, functional occlusion, and good dental health. It should also optimize the psychosocial and developmental outcomes [22]. However, protocols for the management of CLP patients vary from center to center. According to the Eurocleft project between 1996 and 2000, there were 194 different surgical approaches followed for treatment of unilateral cleft alone [23]. Management is discussed according to specific time periods as

Ultrasound examination may detect clefts of the lip and alveolus unlike cleft palate, which is difficult to diagnose through routine screening (**Figure 5**). Additional examinations and tests can confirm the presence of deformity. These include cephalic presentation of the child, low body mass index of the mother, and examination preferably around the 20th gestational week [24]. Moreover, information about family history should be addressed so that provisions for postnatal measures in adequately equipped hospitals can be made in with improvement in

In case of cleft identification, genetic counseling the family including amniocentesis should be performed. For this purpose, a complete pregnancy progress and family history should be addressed. Exposure to any teratogenic factors, the presence of family members with cleft or other birth defects, developmental problems, and genetic syndromes are all important parameter to explore during counseling. In cases where clefts are diagnosed prenatally, the cleft team will be involved in the management so that the family can learn about the nature of the deformity and its care and treatment strategies. Psychological and emotional support of the family is very essential procedure at this time due to the very negative effect once the

The most immediate problem caused by orofacial clefting is likely to be difficulty with feeding. The anatomical characteristics of cleft lip and palate greatly hinder infants' ability to feed. Poor intraoral suction may produce choking, emission of milk through the nose, and

**6. Cleft management**

106 Insights into Various Aspects of Oral Health

shown below.

**6.1. Pre-natal diagnosis**

ultrasound technology.

diagnosis was confirmed.

**6.2. Birth time**

**Figure 5.** Three-dimensional neonatal view—various cleft deformities.

excessive air intake. The feeding process can also be extremely stressful for the parents of such infants who often struggle to find effective feeding method [25]. Early referral to the infant-feeding specialist or nurses associated with cleft teams can facilitate to solve this problem. Those children need special teat and bottles that allow milk to be delivered to the back of throat where it can be swallowed (**Figure 6**). In addition, we may use special dental plates (palatal prosthesis) to seal the cleft side. Such prosthesis could be effective in increasing the volume of fluid intake, decreasing time of feeding, and promoting adequate growth and gain in infants with cleft lip and palate [26]. Some babies may not have the energy to suck from a teat, and here a cup and spoon method may be helpful (**Figure 7**).

Presurgical orthopedics and nasoalveolar molding have become part of the treatment protocol in many cleft centers to improve the treatment outcome. Presurgical orthopedics approximates the maxillary alveolar segments and results in reduction of the tension on the repaired lip. The Latham appliance is an active presurgical orthopedic device used for cleft defects (**Figure 8**). Its long-term effects are debated. The basic idea behind appliance is to decrease the anatomical dilemma in cleft deformity so that better surgical outcome can be obtained. The device has proved its success in expanding and aligning the maxillary segments; retruding protruded premaxilla; aligning bilateral alveolar ridges; reducing tension on surgical closures; and reducing rates of fistula development. However, its long-term effect on maxillary development or occlusion has not been proven [27].

On the other hand, presurgical nasoalveolar molding (PNAM) can reduce soft tissues and cartilaginous cleft deformity to facilitate surgical soft tissue repair with minimum tension

**Figure 6.** Special feeding bottle for cleft patients.

**Figure 7.** Spoon feeding for cleft patients.

to minimize scar formation [28]. It stimulates and redirects growth of the alveolar segments, which will lead to ideal arch formation. Moreover, it aids in normal speech development through better positioning of the tongue. Other benefits include improvement of appearance

**Figure 8.** Pre-surgical orthopedic plate—Latham appliance.

psychosocial wellbeing, better feeding, and bone contour [29]. PNAM appliance consists of a removable alveolar molding plate made of orthodontic acrylic from a dental cast of the infant's maxilla. The nasal stent is bent at the end of a 0.032-inch stainless steel wire that is embedded into the anterior portion of the alveolar molding plate (**Figure 9**). The nasal stent

**Figure 9.** Active alveolar molding appliance.

to minimize scar formation [28]. It stimulates and redirects growth of the alveolar segments, which will lead to ideal arch formation. Moreover, it aids in normal speech development through better positioning of the tongue. Other benefits include improvement of appearance

**Figure 6.** Special feeding bottle for cleft patients.

108 Insights into Various Aspects of Oral Health

**Figure 7.** Spoon feeding for cleft patients.

and the intraoral molding plate are adjusted weekly or biweekly to gradually correct the nasal and alveolar deformities, giving rise to the name nasoalveolar molding. PNAM can be applied to the entire range of cleft deformities including complete clefts without an intact nasal floor [30].

#### **6.3. Lip repair**

There is a wide variation in the timing and techniques of primary lip repair depending upon the preference and protocol of the surgeon and cleft team involved. These include LeMesurier—1949, Tennison—1952, Randall—1959, Pfeifer—1970, Millard—1976, Del cheilorhinoplasty technique (Delaire—1978), "alar-leapfrog" technique (Pigott—1985) and many others. In broad terms, lip repair is performed at 3 months of age and palate repair at 12 months of age (Millard technique). Other schools perform surgery earlier (soft palate repair at 3 months of age and lip and hard palate repair at 6 months of age) as in the case of Malek protocol [31]. Cleft surgery has a major target in dissecting and approximating the muscles of the lip and alar base in their correct anatomical position. Debates continue to point out the suitable dissection procedure (subperipostal dissection or supraperiosteal dissection) [32].

Neonatal repair is still being evaluated. Some schools suggest doing the surgery as early as possible. According to them, the early surgery improves the facial appearance and reduces parent's apprehension. Moreover, earlier surgeries would help in the development of normal articulation [33]. On the other hand, some schools oppose earlier surgical intervention as this will restrict future growth leading to maxillary collapse and occlusal crossbites. Moreover, delayed surgery means that surgeons will have more tissues to deal with giving better outcome.

#### **6.4. Palate repair**

Cleft palate repair is a challenging procedure to learn because of the delicate tissue handling required and the small confines of the infant oral cavity. Hard and soft palate repair is performed at the age range of 9–18 months. The idea behind this relatively early intervention is giving priority to development of normal articulation, which can be extremely difficult to eradicate after the age of 5 years [34]. Different surgical protocols are followed to repair the palate; these include: Von Langbeck repair, vomer flap repair, and Z-plasty repair. In general, scar retraction due to exposed bone in palatoplasty is the leading cause of constricted maxilla. Modern techniques have focused on minimizing the effects of scarring by reducing the exposure of the bone area.

It is self-evident that a physical defect that affects the structures of the mouth and face has the potential to influence articulatory development [35]. Cleft palate often causes problems with speech and hearing. It has been primarily considered as a disorder of the vocal tract. Parents are encouraged to stimulate and converse with infants normally expecting the development of good speech. Speech and language therapist should carry out early assessment with special expertise in clefts. Assessment at 18 months gives a good indication and is repeated, for example, at 3 years. In most cases, the majority of children following cleft palate repair have normal intelligibility. On the other hand, many babies with cleft lip and palate have recurrent otitis media and develop glue ear. A possible etiology for this is that palatal muscles (levator palati and tensor palati) are involved in cleft deformity leading to eustachian tube dysfunction. Cleft subjects need extensive screening in ENT department [36].

#### **6.5. Primary dentition (2–6 years)**

and the intraoral molding plate are adjusted weekly or biweekly to gradually correct the nasal and alveolar deformities, giving rise to the name nasoalveolar molding. PNAM can be applied to the entire range of cleft deformities including complete clefts without an intact

There is a wide variation in the timing and techniques of primary lip repair depending upon the preference and protocol of the surgeon and cleft team involved. These include LeMesurier—1949, Tennison—1952, Randall—1959, Pfeifer—1970, Millard—1976, Del cheilorhinoplasty technique (Delaire—1978), "alar-leapfrog" technique (Pigott—1985) and many others. In broad terms, lip repair is performed at 3 months of age and palate repair at 12 months of age (Millard technique). Other schools perform surgery earlier (soft palate repair at 3 months of age and lip and hard palate repair at 6 months of age) as in the case of Malek protocol [31]. Cleft surgery has a major target in dissecting and approximating the muscles of the lip and alar base in their correct anatomical position. Debates continue to point out the suitable dissection procedure (subperipostal dissection or supraperiosteal dissection) [32].

Neonatal repair is still being evaluated. Some schools suggest doing the surgery as early as possible. According to them, the early surgery improves the facial appearance and reduces parent's apprehension. Moreover, earlier surgeries would help in the development of normal articulation [33]. On the other hand, some schools oppose earlier surgical intervention as this will restrict future growth leading to maxillary collapse and occlusal crossbites. Moreover, delayed surgery means that surgeons will have more tissues to deal with giving better outcome.

Cleft palate repair is a challenging procedure to learn because of the delicate tissue handling required and the small confines of the infant oral cavity. Hard and soft palate repair is performed at the age range of 9–18 months. The idea behind this relatively early intervention is giving priority to development of normal articulation, which can be extremely difficult to eradicate after the age of 5 years [34]. Different surgical protocols are followed to repair the palate; these include: Von Langbeck repair, vomer flap repair, and Z-plasty repair. In general, scar retraction due to exposed bone in palatoplasty is the leading cause of constricted maxilla. Modern techniques have focused on minimizing the effects of scarring by reducing the expo-

It is self-evident that a physical defect that affects the structures of the mouth and face has the potential to influence articulatory development [35]. Cleft palate often causes problems with speech and hearing. It has been primarily considered as a disorder of the vocal tract. Parents are encouraged to stimulate and converse with infants normally expecting the development of good speech. Speech and language therapist should carry out early assessment with special expertise in clefts. Assessment at 18 months gives a good indication and is repeated, for example, at 3 years. In most cases, the majority of children following cleft palate repair have normal intelligibility. On the other hand, many babies with cleft lip and palate have recurrent

nasal floor [30].

110 Insights into Various Aspects of Oral Health

**6.3. Lip repair**

**6.4. Palate repair**

sure of the bone area.

Velopharyngeal insufficiency (VPI) is a common finding in cleft patients. VPI is the incomplete closure of the velopharyngeal sphincter resulting in hypernasal resonance, which can compromise speech intelligibility. Most sounds are divided to be oral (produced in the oral cavity) and nasal (m & n only). Speech nasality happens when the oral cavity is not completely sealed from the nasal cavity. As a result, air escapes through the nose. Even after palate repair, cleft patients can still sound nasal due to the inability of the soft palate to seal and separate these two cavities. The reason for that is weakness in muscles of the soft palate. Moreover, the soft palate is short, which hinders its contact with pharyngeal wall [37]. Speech assessment might be commenced as early as 18 months of age taking into consideration the needs of the patient [38]. Assessment of speech must continue through childhood along with cleft team to detect any developing problems that may arise with growth. ENT surgeon will be involved throughout all monitoring phase. Lip revision and closure of any residual palatal fistula before schooling might be considered to support speech development [39].

Orthodontic treatment in this stage is limited to the correction of certain posterior crossbite and anterior crossbite of mild-to-moderate degree. Posterior crossbites are of both skeletal and dental origin. A crossbite of a dental origin and accompanied with occlusal shift can be managed by selective grinding; anterior crossbite of mild-to-moderate degree can be managed by the use of elastic protraction forces delivered through a facial mask [40]. However, if this crossbite is related to severe maxillary hypoplasia, the patient is best managed with surgical procedures that are done at later stages. During this age, it is important to develop good dental care habits, instituting fluoride supplements in nonfluoridated areas [41].

#### **6.6. Mixed dentition (6–12 years)**

The negative effects of surgical repair become clear during this phase including maxillary collapse and arch discrepancies. Moreover, defects in alveolar bone, tooth number, formation, and position can be detected. Surgeons start to consider alveolar bone graft to correct the maxillary defects at this stage (**Figure 10**). Grafting is best performed with autogenously cancellous bone. Alveolar bone grafting will provide maxillary-alveolar ridge continuity for tooth eruption and alignment. It also provides nasal base support and provides bone through which the permanent canines and laterals can erupt into the dental arch. In bilateral cases, alveolar bone grafting stabilizes the premaxillary segment with bone support [42]. Alveolar bone grafting is performed using a gingival flap of mucoperiosteum, turned back "book" flaps and cancellous bone harvested from the iliac crest. The covering flap of gingival mucoperiosteum is used to cover the graft in the alveolus, nostril floor, and anterior maxilla. The ideal age for bone grafting is 9–11 years to give chance for the lateral incisor or the canine to erupt through the graft and stabilize it. Supernumerary teeth in the surgical site should be extracted 8–12 weeks before surgery. This will allow the surgeon to have intact

**Figure 10.** Alveolar bone graft.

gingival tissues for proper coverage of the alveolar bone graft. At the time of complete eruption of permanent dentition (approximately 12 or 13 years of age), orthodontic treatment is commenced.

The timing of bone grafting will be decided on the basis of the dental development of individual patients [43]. In patients with well-formed lateral incisors that are in the line of the dental arch, bone grafting can be done quite early, around 7 or 8 years. However, most patients with complete unilateral cleft lip and palate have a missing, ectopic, or deformed lateral incisor, so it is preferable that bone grafting is postponed until they are 10 or 11 years of age (**Figure 11**). This allows the root development of the cleft-side canine to progress more and may help in better canine eruption [44].

An interceptive orthodontic treatment is undertaken in the mixed dentition to reposition the dentition adjacent to the cleft preparing the cleft side for the secondary alveolar bone graft,

**Figure 11.** CBCT of alveolar bone graft in UCLP patient (A: before and B: after).

but such procedure must be postponed until the development of the incisor roots to avoid any resorptive effect on teeth. If maxillary segments and dentition on either side of the cleft are well aligned, it is not necessary to do presurgical orthodontics [45]. Thus, orthodontic treatment is not generally commenced until age 9 or 10 years when, if necessary, the maxillary segments are expanded to correct the transverse relationship using palatal expansion appliances, these include upper removable appliance, quad helix (**Figure 12**), rapid maxillary expansion, bonded "fan" appliance (**Figure 13**), and others [46, 47].

#### **6.7. Permanent dentition**

gingival tissues for proper coverage of the alveolar bone graft. At the time of complete eruption of permanent dentition (approximately 12 or 13 years of age), orthodontic treatment is

The timing of bone grafting will be decided on the basis of the dental development of individual patients [43]. In patients with well-formed lateral incisors that are in the line of the dental arch, bone grafting can be done quite early, around 7 or 8 years. However, most patients with complete unilateral cleft lip and palate have a missing, ectopic, or deformed lateral incisor, so it is preferable that bone grafting is postponed until they are 10 or 11 years of age (**Figure 11**). This allows the root development of the cleft-side canine to progress more and may help in

An interceptive orthodontic treatment is undertaken in the mixed dentition to reposition the dentition adjacent to the cleft preparing the cleft side for the secondary alveolar bone graft,

**Figure 11.** CBCT of alveolar bone graft in UCLP patient (A: before and B: after).

commenced.

**Figure 10.** Alveolar bone graft.

112 Insights into Various Aspects of Oral Health

better canine eruption [44].

Definitive orthodontic treatment must be commenced at this time. The goals of treatment are similar to those for noncleft patients, but certain conditions must be taken into consideration during the treatment planning. These include maintenance of the integrity of the dentition and supporting structures especially for teeth adjacent to the cleft side, correction of impacted and transposed teeth, and management of congenitally missing teeth [48].

If the cleft side lateral incisor is missing, management will be based on either replacing the missing tooth with prosthesis or closing the space. In those patients with missing lateral incisor in whom the maxillary canine has migrated mesially and is erupting into the grafted alveolar ridge, replacement of the missing lateral incisor by the canine and movement of all posterior teeth forward will be the treatment of choice. In cases where the alveolar bone graft is not ideal, bone morphology can be improved by moving the canine forward into graft side [49].

Extractions may be required to create space for arch alignment with the second premolars being first choice in the maxilla. This is related to formation of scar tissue during the course of primary palatal repair, which pulls the premolars palatally. However, relapse is common after orthodontic correction. Invariably, fixed appliances are required to achieve a satisfactory degree of precision in tooth alignment with sound values of tip and torque movements [50]. Once the permanent dentition has been established, planning for orthognathic surgery must take place in a tempt to correct mid-face retrusion. Factors such as maxillary retrognathia, the magnitude and effect of any future growth, and patient wishes should be taken into consideration. Surgical correction is indicated only when growth is complete. Surgical revision of the nose (rhinoplasty) will be the last surgical step. This is because movement of the underlying bone will affect the contour of the nose [51].

Hypodontia, microdontia, and conical crowns are common findings in cleft lip and palate (**Figure 14**). In broad terms, treatment strategies reflect the pattern of tooth absence, the amount of residual spacing, existing malocclusions, and patient's attitude [52, 53]. The congenital missing of teeth may result in minimal spacing; still, it may not be an esthetic concern to patients and can be accepted. Space closure and modification of the canine to resemble a lateral incisor is a common treatment option where maxillary lateral incisors are missing. However, where several teeth are congenitally absent, the orthodontic redistribution of space to allow restoration with prostheses is frequently the treatment of choice. The esthetic and functional outcomes of such an approach should be confirmed with a trial diagnostic set-up.

**Figure 12.** Quad helix expansion in UCLP.

Replacement of missing teeth with prosthesis includes removable partial dentures, conventional and adhesive bridges, and implant supported prostheses. Clearly, both the timing and manner of their application must reflect the needs and limitations imposed by a young, growing individual [54].

#### **6.8. Orthognathic surgery**

The midfacial hypoplasia or maxillary constriction is a common secondary deformity in cleft deformity involving primary palate. This hypoplasia and constriction are related to growth impairment and scar formation in hard palate during the palate repair. Despite of orthodontic treatment, up to 25% of patients with cleft lip and palate needs surgical interventions to achieve balanced and harmonious facial appearance.

Cleft Lip and Palate Management from Birth to Adulthood: An Overview http://dx.doi.org/10.5772/intechopen.68448 115

**Figure 13.** Bonded "fan" expansion appliance.

**Figure 14.** Hypodontia in cleft lip and palate.

Replacement of missing teeth with prosthesis includes removable partial dentures, conventional and adhesive bridges, and implant supported prostheses. Clearly, both the timing and manner of their application must reflect the needs and limitations imposed by a young, grow-

The midfacial hypoplasia or maxillary constriction is a common secondary deformity in cleft deformity involving primary palate. This hypoplasia and constriction are related to growth impairment and scar formation in hard palate during the palate repair. Despite of orthodontic treatment, up to 25% of patients with cleft lip and palate needs surgical interventions to

ing individual [54].

**6.8. Orthognathic surgery**

**Figure 12.** Quad helix expansion in UCLP.

114 Insights into Various Aspects of Oral Health

achieve balanced and harmonious facial appearance.

At approximately the age of 17–18, a final assessment of facial pattern is carried out clinically. Detailed cephalometric assessment and growth analyses are carried out to plan for orthognathic surgery. No orthognathic surgery is carried out until growth is complete. Surgeons perform the corrective surgery in the maxillary bone or both jaws according to the severity of the underlying skeletal discrepancy. The advantage of this surgical-orthodontic approach is that the clinicians can provide the patient with occlusal relations close to ideal and markedly improved function and esthetics.

#### **6.9. Psychological effects**

Children with craniofacial anomalies are at greater risk of developing behavioral, emotional, or social competence problems [55]. Some children with oral clefts have decreased social competence as shown by fewer friends and poor social interaction. Slifer et al. have found that 30–50% of children with cleft lip and/or palate between the ages of 6 and 16 are rated by their parents to be 1.0 or more standard deviations below the mean compared to noncleft peers on measures of social adjustment and competence (sharing their friends in social activities, degree, and quality of social interaction). Unfortunately, this tendency continued through adolescence and into adulthood [56].

All the above features will have psychological effects on cleft patients as well as their families; these effects become more significant when patients get younger. Two stages where those children have a real challenge to deal with; are when they go to school (5–6) years i.e. the difficulty of being different. The second when they start to look after their appearance, i.e. the pre-puberty and adolescence time. Children with visible clefts are often very self-conscious about their appearance, speech, and schooling.

#### **6.10. Learning disorders and behavioral problems**

Children with cleft lip and palate are at an increased risk for learning disorders. There is a consensus that language skills of cleft palate patients tend to be delayed even if the cleft was a small one [57]. Broder et al. have examined the prevalence of learning disability, level of school achievement, and prevalence of grade retention by type of cleft and gender at two craniofacial centers. The results showed that 46% of subjects with cleft had learning disability and 47% had deficient educational progress. Moreover, 27% had repeated a grade in the school. The results also showed that males with only cleft palate and females with cleft lip and palate were at higher risk among all cleft subjects [58].

## **Acknowledgments**

To my wife Huda Zurigat whose never-failing sympathy and encouragement, without your support, this chapter would not have been finished on time.

## **Author details**

Maen Hussni Zreaqat<sup>1</sup> \*, Rozita Hassan<sup>1</sup> and Abdulfattah Hanoun<sup>2</sup>


## **References**

**6.9. Psychological effects**

116 Insights into Various Aspects of Oral Health

adolescence and into adulthood [56].

about their appearance, speech, and schooling.

**6.10. Learning disorders and behavioral problems**

palate were at higher risk among all cleft subjects [58].

support, this chapter would not have been finished on time.

\*, Rozita Hassan<sup>1</sup>

2 Orthodontic Department, Universiti Sains Malaysia, Penang, Malaysia

\*Address all correspondence to: maenzreqat@yahoo.com

1 Universiti Sanins Malaysia, Kota Bharu, Malaysia

**Acknowledgments**

**Author details**

Maen Hussni Zreaqat<sup>1</sup>

Children with craniofacial anomalies are at greater risk of developing behavioral, emotional, or social competence problems [55]. Some children with oral clefts have decreased social competence as shown by fewer friends and poor social interaction. Slifer et al. have found that 30–50% of children with cleft lip and/or palate between the ages of 6 and 16 are rated by their parents to be 1.0 or more standard deviations below the mean compared to noncleft peers on measures of social adjustment and competence (sharing their friends in social activities, degree, and quality of social interaction). Unfortunately, this tendency continued through

All the above features will have psychological effects on cleft patients as well as their families; these effects become more significant when patients get younger. Two stages where those children have a real challenge to deal with; are when they go to school (5–6) years i.e. the difficulty of being different. The second when they start to look after their appearance, i.e. the pre-puberty and adolescence time. Children with visible clefts are often very self-conscious

Children with cleft lip and palate are at an increased risk for learning disorders. There is a consensus that language skills of cleft palate patients tend to be delayed even if the cleft was a small one [57]. Broder et al. have examined the prevalence of learning disability, level of school achievement, and prevalence of grade retention by type of cleft and gender at two craniofacial centers. The results showed that 46% of subjects with cleft had learning disability and 47% had deficient educational progress. Moreover, 27% had repeated a grade in the school. The results also showed that males with only cleft palate and females with cleft lip and

To my wife Huda Zurigat whose never-failing sympathy and encouragement, without your

and Abdulfattah Hanoun<sup>2</sup>


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120 Insights into Various Aspects of Oral Health

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**Provisional chapter**

## **Treatment of Class II Malocclusion (Hypodivergent Face) with MEAW Therapy Face) with MEAW Therapy**

**Treatment of Class II Malocclusion (Hypodivergent** 

DOI: 10.5772/intechopen.69331

Paulo Augusto de Sousa Beltrão Paulo Augusto de Sousa Beltrão Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69331

#### **Abstract**

Patients with class II deep bite malocclusion and hypodivergent skeletal typology represent complex and prolonged cases of treatment due to their muscular characteristics. The etiology of the class II deep bite is multifactorial: environmental and/or genetic factors represent an important part in the establishment of class II deep bite. However, there is a close connection between three class II factors and the adaptation of mandible and occlusal function. These factors are lack of vertical dimension, inclination of the upper occlusal plane, lack of occlusal support, and pressure of TMJ. According to Tanaka and Sato, there is a relationship between the inclination of the maxillary posterior occlusal plane and the mandibular position, consistent with the etiology of different dento-skeletal structures. The occlusal plane is more tilted in patients with class II and more flat in patients with class III than in individuals with class I occlusions. **Patients and methods**: Two male teenagers were treated with MEAW therapy, and both treatments lasted 24 months. **Results**: The MEAW therapy appropriately corrected the class II deep bite over a period of 24 months, achieving a good occlusal, functional, and esthetic result. **Conclusions**: The MEAW therapy proved to be effective in the treatment of class II deep bite malocclusion, in growing patients.

**Keywords:** class II deep bite, steep occlusal plane, hypodivergent, MEAW

## **1. Introduction**

During the process development of skeletal class II, there are three important factors (insufficient height of bite, strong inclination of the occlusal plane, lack of occlusal support), which are closely related with the adaptation of the mandible and the occlusal function [1–3].

The maxillary dentition of patients with class II malocclusion has low vertical dimension in the posterior area, and the upper posterior occlusal plane is steep. The occlusal interferences

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

in the molar area prevent the mandible to adapt to a forward position, instead the mandible adapts posteriorly, aggravating the distoclusion. Actually, 70% of the class II malocclusion does not imply the protrusion of the maxilla but is known to be caused by retrusion of the mandible (McNamara [4]).

Morphological characteristics of the class II deep overbite are the following: the mandible is small and retruded, insufficient vertical dimension and occlusal support, steepening of the occlusal plane in the upper posterior area, occlusal interferences in the molar area, and labial tipping of the upper anterior teeth. The skeletal characteristics of class II deep bite malocclusion are closely related to the lack of vertical dimension and the steepness of the occlusal plane. Some authors proved that the vertical disproportion was in many cases at the origin of anterior-posterior dysplasias.

Therefore, a treatment approach based on the control of the occlusal plane and vertical dimension is essential to the success of the treatment. The treatment objectives for class II deep bite are the following: to increase the vertical dimension, to rebuild and flatten the upper posterior occlusal plane, to coordinate upper and lower dental arch width, to move the mandible forward, to improve overbite (deep bite), to obtain normal intercuspidation, and to improve the profile.

The treatment of low-angle class II malocclusions must prevent occlusal interferences and extrude the upper molars to increase their vertical height and flatten the occlusal plane. As a result, the mandible readapts to the physiological position, and occlusal function is attained. The steps of the class II deep overbite malocclusion are leveling, elimination of occlusal interferences, establishing mandibular position, reconstruction of the occlusal plane, and achieving a physiological occlusion.

## **2. The multiloop edgewise arch wire (MEAW)**

In 1967, Young H. Kim created the multiloop edgewise arch wire (MEAW) to treat open bite malocclusions, which he achieved with great efficiency. Subsequently, Prof. Sadao Sato (Kanagawa Dental College, Japan) [5] developed the MEAW philosophy of treatment and applied it to all types of malocclusions. MEAW can be constructed with stainless steel 0.016 × 0.022 (bracket 0.018 inch slot) or 0.017 × 0.025 ss (bracket 0.022 inch slot).

The arches have ideal dental arch shape with five loops on each side of the arch. The loops between the teeth act as a force breaker and allow smooth and continuous forces to be distributed through the teeth, as well as individual control of vertical, horizontal, and torque forces on the teeth. The use of MEAW arches with activation must be done together with the use of intraoral elastics (appropriate to the malocclusion), in order to obtain a successful reconstruction of the posterior occlusal plane (**Figure 1**).

**Figure 1.** Upper and lower multiloop edgewise arch wire (MEAWs).

## **3. Cephalometric analysis**

#### **3.1. Analysis of Kim**

in the molar area prevent the mandible to adapt to a forward position, instead the mandible adapts posteriorly, aggravating the distoclusion. Actually, 70% of the class II malocclusion does not imply the protrusion of the maxilla but is known to be caused by retrusion of the

Morphological characteristics of the class II deep overbite are the following: the mandible is small and retruded, insufficient vertical dimension and occlusal support, steepening of the occlusal plane in the upper posterior area, occlusal interferences in the molar area, and labial tipping of the upper anterior teeth. The skeletal characteristics of class II deep bite malocclusion are closely related to the lack of vertical dimension and the steepness of the occlusal plane. Some authors proved that the vertical disproportion was in many cases at the origin of

Therefore, a treatment approach based on the control of the occlusal plane and vertical dimension is essential to the success of the treatment. The treatment objectives for class II deep bite are the following: to increase the vertical dimension, to rebuild and flatten the upper posterior occlusal plane, to coordinate upper and lower dental arch width, to move the mandible forward, to improve overbite (deep bite), to obtain normal intercuspidation, and to improve

The treatment of low-angle class II malocclusions must prevent occlusal interferences and extrude the upper molars to increase their vertical height and flatten the occlusal plane. As a result, the mandible readapts to the physiological position, and occlusal function is attained. The steps of the class II deep overbite malocclusion are leveling, elimination of occlusal interferences, establishing mandibular position, reconstruction of the occlusal plane, and achiev-

In 1967, Young H. Kim created the multiloop edgewise arch wire (MEAW) to treat open bite malocclusions, which he achieved with great efficiency. Subsequently, Prof. Sadao Sato (Kanagawa Dental College, Japan) [5] developed the MEAW philosophy of treatment and applied it to all types of malocclusions. MEAW can be constructed with stainless steel 0.016 ×

The arches have ideal dental arch shape with five loops on each side of the arch. The loops between the teeth act as a force breaker and allow smooth and continuous forces to be distributed through the teeth, as well as individual control of vertical, horizontal, and torque forces on the teeth. The use of MEAW arches with activation must be done together with the use of intraoral elastics (appropriate to the malocclusion), in order to obtain a successful reconstruc-

mandible (McNamara [4]).

124 Insights into Various Aspects of Oral Health

anterior-posterior dysplasias.

ing a physiological occlusion.

**2. The multiloop edgewise arch wire (MEAW)**

tion of the posterior occlusal plane (**Figure 1**).

0.022 (bracket 0.018 inch slot) or 0.017 × 0.025 ss (bracket 0.022 inch slot).

the profile.

Kim [6, 7] developed his cephalometric analysis in order to identify the types of vertical and anterior-posterior growth and their connection with the inclination of the occlusal plane:


#### **3.2. Overbite depth indicator (ODI)**

The ODI is the sum of two angles: the A–B plane with the mandibular plane (MP) and the palatal plane with the Frankfort horizontal (FH) plane. The angle is negative when the palatal plane inclines superiorly in relation to the FH plane and is read as a positive angle when the palatal plane inclines inferiorly in relation to the FH plane.

There is a norm of 74.5 degrees with a standard deviation of 6.07. A value lower than 74.5 (±6.07 degrees) shows a skeletal open bite tendency. A highest value of 74.5 (±6.07 degrees) shows a deep bite skeletal pattern tendency. In these patients with skeletal deep bite tendency, tooth extractions should be avoided, in order not to lose occlusal support, because loss of occlusal support increases the risk of relapse (**Figure 2**).

#### **3.3. Anteroposterior dysplasia indicator (APDI)**

The APDI consists of three angles: the angle of the facial plane (Frankfurt horizontal (FH)/ facial plane (FP)), added or decreased to the angle Downs, and added or decreased to the angle of the palatine plane in relation to the plane HF. The APDI can also be calculated by the value of the angle formed by the palatine plane (PP) (line linking points A and B).

APDI = (FH-FP) + (AB-FP) + (FH-PP). The average APDI value is 81.4°. A value higher than 81.4° shows a trend skeletal class III; on the contrary a smaller value shows the tendency for skeletal class II and molar class II relationship. APDI unlike ODI (which is slight altered by the treatment) shows the potential of the treatment of the clinical case, because the APDI can be significantly changed by growth and treatment. Kim (Kim and Vietas, 1978) [5] considered

**Figure 2.** Kim cephalometric analysis.

that at the end of the treatment the APDI should be close to the norm (81.4°) in order to have a clinical case with stability and the risk of relapse decreased.

#### **3.4. Combination factor (CF)**

tooth extractions should be avoided, in order not to lose occlusal support, because loss of

The APDI consists of three angles: the angle of the facial plane (Frankfurt horizontal (FH)/ facial plane (FP)), added or decreased to the angle Downs, and added or decreased to the angle of the palatine plane in relation to the plane HF. The APDI can also be calculated by the

APDI = (FH-FP) + (AB-FP) + (FH-PP). The average APDI value is 81.4°. A value higher than 81.4° shows a trend skeletal class III; on the contrary a smaller value shows the tendency for skeletal class II and molar class II relationship. APDI unlike ODI (which is slight altered by the treatment) shows the potential of the treatment of the clinical case, because the APDI can be significantly changed by growth and treatment. Kim (Kim and Vietas, 1978) [5] considered

value of the angle formed by the palatine plane (PP) (line linking points A and B).

occlusal support increases the risk of relapse (**Figure 2**).

**3.3. Anteroposterior dysplasia indicator (APDI)**

126 Insights into Various Aspects of Oral Health

**Figure 2.** Kim cephalometric analysis.

The combination factor (CF) [8] is a combination of ODI and APDI.

A value of CF above 155° shows a trend for a skeletal pattern of low angle. A value of CF below 155° exhibits the trend for high angle, and the necessity for tooth extraction is increased.

The CF provides guidance if the clinical case should be treated with or without extractions.

## **4. The importance of cranial base and the development scheme of skeletal class II deep bite malocclusion**

The base of the skull is formed by the ethmoid, sphenoid, and occipital bones, joined by spheno-occipital and sphenoethmoidal synchondrosis. The sutures fuse with age, sphenoethmoidal at 7–8 years and spheno-occipital at 18–20 years, but allow small movements. Hooper in 1986 referred to spheno-occipital synchondrosis as the most important at the base of the skull where the flexion/extension movements occurred. The various malocclusions show different cranial base angles. Thus, in class I occlusions, the angle of the base of the skull (Na-S-Ar) approaches to 124.2°, in class II the angle is more obtuse approaching to 130°, and in class III, the base of the skull presents flexion, being the angle approximately 120°. The movement of flexion/extension occurred in the spheno-occipital suture is transmitted by the Vomer to maxillary. According to the movement occurred in the spheno-occipital suture, also the direction of growth of the maxillary will be different. When sphenoid flexion occurs, the maxillary growth is more vertical, growing more in height and less in length, resulting in posterior dental discrepancy; this is what happens in class III skeletal frame. On the contrary, when extension at the base of the skull occurs, the force transmitted by the Vomer to maxillary will push it protrusively, and maxillary will grow more in length and less in height. This protrusive rotation of maxillary is responsible for the inclination of the incisors and spaces between them (typical in class II/1 malocclusion).

The results of a poor maxillary vertical dimension are:


When the posterior occlusal plane (POP) is steep, the mandible adapts posteriorly with molar distoclusion; on the contrary, when the POP is flat, the mandible adapts in an anterior position producing molar mesioclusion. In 1975, Petrovic [9] reported on the cybernetic theory of Petrovic, who stated that the maxillary anterior-inferior growth was responsible for the anterior functional adaptation of the mandible followed by secondary growth of the condyles.

## **5. Low-angle class II deep bite malocclusion characteristics**

McNamara and Moyers et al. have suggested that the fundamental problems in class II malocclusion are due not to maxillary prognathism but rather to mandibular retrognathism.

The characteristics of the class II deep bite malocclusion are the following: the mandible is small and retruded, the posterior maxillary occlusal plane is steep, presence of posterior occlusal interferences, upper incisors normally labially inclined with spaces between them, labial incompetence, low vertical dimension, lack of occlusal support, molar teeth slightly erupted (infraeruption), deep overbite, low gonial angle (GOA), and small lower facial height (LFH) [10].

The APDI is less than 74.5°, and the overbite depth indicator (ODI) is quite high (1980s and 1990s). The angle of the cranial base is extended.

The skeletal characteristics of class II malocclusion are closely related to vertical occlusion deficiencies.

## **6. Treatment of class II low-angle malocclusion based on the control of occlusal plane**

In the 1970s, several studies (Petrovic, Carlson, McNamara, and Woodside) showed the ability to change the growth pattern of the mandible according to its function. McNamara, Graber, Harvold, and Bass (1970) evidenced that the amount of changes in mandibular growth due to cell increase in the condyles was in conformity with the modifications of the occlusal function. Fushima et al. (1989) measured vertical height of molar and premolar teeth in patients with mandibular asymmetry. They verified that the vertical dimension of the posterior teeth of the displaced side was smaller than the contralateral dental height (nonshifted side).

The MEAW philosophy created by Dr. Young Kim and developed by Prof. Sadao Sato considers that the treatment of class II low-angle malocclusion should eliminate occlusal interferences, increase the vertical dimension (extruding the maxillary molars), and reconstruct the occlusal plane. Once the vertical dimension increases, the mandible moves anteriorly to a functional position [11–13].

The mandibular dentition, especially the premolars, is extruded to increase the vertical dimension and flatten the occlusal plane, creating conditions for the mandible to move to a forward position, more physiologically, and improving the occlusal function.

The forward adaptation of the mandible followed by adaptive remodeling of the TMJ is necessary for the success and stability of the treatment.

The objectives of class II deep bite treatment are:


**5. Low-angle class II deep bite malocclusion characteristics**

1990s). The angle of the cranial base is extended.

deficiencies.

**occlusal plane**

128 Insights into Various Aspects of Oral Health

functional position [11–13].

McNamara and Moyers et al. have suggested that the fundamental problems in class II malocclusion are due not to maxillary prognathism but rather to mandibular retrognathism.

The characteristics of the class II deep bite malocclusion are the following: the mandible is small and retruded, the posterior maxillary occlusal plane is steep, presence of posterior occlusal interferences, upper incisors normally labially inclined with spaces between them, labial incompetence, low vertical dimension, lack of occlusal support, molar teeth slightly erupted (infraeruption), deep overbite, low gonial angle (GOA), and small lower facial height (LFH) [10].

The APDI is less than 74.5°, and the overbite depth indicator (ODI) is quite high (1980s and

The skeletal characteristics of class II malocclusion are closely related to vertical occlusion

**6. Treatment of class II low-angle malocclusion based on the control of** 

In the 1970s, several studies (Petrovic, Carlson, McNamara, and Woodside) showed the ability to change the growth pattern of the mandible according to its function. McNamara, Graber, Harvold, and Bass (1970) evidenced that the amount of changes in mandibular growth due to cell increase in the condyles was in conformity with the modifications of the occlusal function. Fushima et al. (1989) measured vertical height of molar and premolar teeth in patients with mandibular asymmetry. They verified that the vertical dimension of the posterior teeth of the

The MEAW philosophy created by Dr. Young Kim and developed by Prof. Sadao Sato considers that the treatment of class II low-angle malocclusion should eliminate occlusal interferences, increase the vertical dimension (extruding the maxillary molars), and reconstruct the occlusal plane. Once the vertical dimension increases, the mandible moves anteriorly to a

The mandibular dentition, especially the premolars, is extruded to increase the vertical dimension and flatten the occlusal plane, creating conditions for the mandible to move to a forward

The forward adaptation of the mandible followed by adaptive remodeling of the TMJ is neces-

displaced side was smaller than the contralateral dental height (nonshifted side).

position, more physiologically, and improving the occlusal function.

• Rebuilding and flattening of the upper posterior occlusal plane

sary for the success and stability of the treatment.

The objectives of class II deep bite treatment are:

• Increase of the vertical dimension

• Obtaining correct occlusion and improving the profile

Sequence of class II deep bite treatment:

(1) Alignment and leveling, (2) correction of occlusal interferences, (3) attaining a physiological mandibular position, (4) rebuilding the occlusal plane, and (5) attaining a physiological occlusion (**Figure 3**).

**Figure 3.** Sequence of low-angle class II deep bite treatment.

## **7. Case report 1**

A male patient 14 years and 10 months old, with skeletal class II and dental class II/1 on a hypodivergent face pattern (FMA 17°), deep bite (8 mm), overjet (5 mm), steep posterior occlusal plane producing interferences in the posterior area, insufficient occlusal support on the posterior area, crossbite on the right side, crown fracture of 11, posterior discrepancy, and crowding on the anterior maxillary area. The patient began the treatment at the age of 14 years and 10 months old, and the treatment lasted 24 months. The type of appliance was an edgewise multi-bracket 0.022 × 0.028 slot, 0° torque, 0° angulation, and MEAWs arch wires along with short class II elastics.

The treatment objectives for this patient with class II deep bite were increasing the vertical dimension, elimination of the posterior interferences, reconstruction of posterior occlusal plane (flatten), coordination between both arches, production of anterior adaptation of the mandible, and secondarily induction condylar remodeling. The patient and their parents refused the extraction of 38 and 48 to eliminate the posterior mandibular discrepancy and were advised to the consequences of such refusal.

Sequence of treatment:


**Step 1**: Leveling (alignment), onset with 0.016″ ss arch wires.

**Step 2:** Elimination of occlusal interferences—0.017 × 0.025 multiloop edgewise arch wires were inserted in both arches, through the use of small class II (3/16 inch, 6 ounces) elastics bilaterally.

**Step 3:** Achieving a functional mandibular position: step-down bends (premolars) in the upper arch and step-up bends (premolars) in the lower arch were done to bite rising (to apply small class II, 3/16 inch, 6 ounces of elastics). When this phase is finished, the molar relationship is class I.

**Steps 4 and 5:** Rebuilding the posterior occlusal plane (flatten the posterior occlusal plane) and establishing a physiological occlusion.

The retention period was done with maxillary Hawley plate for nighttime use (12 months) and bonded lingual wire from 33 to 43.

The posttreatment results demonstrate an improved smile, profile, and facial balance.

The intraoral photos show a normal class I relationship, a correct overbite, and overjet. The cephalometric analysis shows a reduction of ANB angle of 4°, mandibular advancement (point B has advanced 3°), an AO-BO reduction of 3 mm, and a better profile. The APDI increased 7° (from 66 to 73°) showing an improvement of the skeletal class II malocclusion (**Figures 4**–**11**, **Tables 1** and **2**).

**Figure 4.** Pretreatment extraoral (A–C) and intraoral (D–H) photographs.

Treatment of Class II Malocclusion (Hypodivergent Face) with MEAW Therapy http://dx.doi.org/10.5772/intechopen.69331 131

**Figure 5.** Pretreatment records (A–C).

**Step 2:** Elimination of occlusal interferences—0.017 × 0.025 multiloop edgewise arch wires were inserted in both arches, through the use of small class II (3/16 inch, 6 ounces) elastics

**Step 3:** Achieving a functional mandibular position: step-down bends (premolars) in the upper arch and step-up bends (premolars) in the lower arch were done to bite rising (to apply small class II, 3/16 inch, 6 ounces of elastics). When this phase is finished, the molar relation-

**Steps 4 and 5:** Rebuilding the posterior occlusal plane (flatten the posterior occlusal plane)

The retention period was done with maxillary Hawley plate for nighttime use (12 months)

The intraoral photos show a normal class I relationship, a correct overbite, and overjet. The cephalometric analysis shows a reduction of ANB angle of 4°, mandibular advancement (point B has advanced 3°), an AO-BO reduction of 3 mm, and a better profile. The APDI increased 7° (from 66 to 73°) showing an improvement of the skeletal class II malocclusion (**Figures 4**–**11**,

The posttreatment results demonstrate an improved smile, profile, and facial balance.

bilaterally.

130 Insights into Various Aspects of Oral Health

ship is class I.

**Tables 1** and **2**).

and establishing a physiological occlusion.

**Figure 4.** Pretreatment extraoral (A–C) and intraoral (D–H) photographs.

and bonded lingual wire from 33 to 43.

**Figure 6.** Photos during the treatment (a–m).

**Figure 7.** Posttreatment extraoral (A–C) and intraoral (D–F) photos.

**Figure 8.** Posttreatment records (A–D) and superimpositions between pre- and posttreatment (E–F).

Treatment of Class II Malocclusion (Hypodivergent Face) with MEAW Therapy http://dx.doi.org/10.5772/intechopen.69331 133

**Figure 9.** Postretention extraoral photos (A–C) and intraoral photos (D–F).

**Figure 7.** Posttreatment extraoral (A–C) and intraoral (D–F) photos.

132 Insights into Various Aspects of Oral Health

**Figure 8.** Posttreatment records (A–D) and superimpositions between pre- and posttreatment (E–F).

**Figure 10.** Postretention records (G–H) and postretention superimpositions.

**Figure 11.** Three years after the end of treatment: extraoral photos (A–C) and intraoral photos (D–F).


**Table 1.** Cephalometric analysis (Kim).


**Table 2.** Cephalometric analysis (Tweed-Merrifield) [14, 15].

## **8. Case report 2**

A young male patient 13 years and 10 months old, with small anterior facial height, skeletal class II (FMA = 18°), dental class II/1 with deep bite of 7 mm and an overjet of 10 mm, hypodivergent face scheme, mandibular retrognathism, steep posterior occlusal plane creating interferences in the molar area, and lack of occlusal support.

The z angle of 66° confirms an unbalanced face which is based on a rethrognatic chin, absence of crowding and shape of dental arches is different due to an old habit of thumb sucking.

According to Kim's cephalometric analysis, the patient shows a low-angle skeletal pattern (ODI = 86°), and removal of permanent teeth is not advised, due to the high potential for deep bite relapse. The APDI = 70° shows a class II skeletal pattern, and the combination factor = 156°

indicates a skeletal pattern that has a capacity to accommodate the entire dentition. Onset of treatment with age of 13 years and 10 months, after 2 months a double arch wire (DAW) was placed to extrude maxillary molars and to align and intrude upper incisors [16]. After 5 months, MEAWs were inserted in both dental arches, along with small class II elastics (3/16 inch, 6 ounces).

The duration of the treatment was 24 months. The posttreatment photographs (**Figure 15**) show a better pleasant face, an improved facial profile, a pleasant wide smile, a stable class I molar occlusion, and overbite and overjet corrected.

The mandibular incisors were kept in its pretreatment position. The cephalometric superimposition between pretreatment and posttreatment displays the entire mandibular improvement in height and length. The APDI = 80 at the end of treatment is a guarantee to define this clinical case as stable and with little tendency to relapse (**Figures 12**–**20**, **Tables 3** and **4**).

**Figure 12.** Pretreatment extraoral (A–C) and intraoral (D–F) photos.

**Figure 13.** Pretreatment records (A–C).

**8. Case report 2**

**Table 1.** Cephalometric analysis (Kim).

134 Insights into Various Aspects of Oral Health

A young male patient 13 years and 10 months old, with small anterior facial height, skeletal class II (FMA = 18°), dental class II/1 with deep bite of 7 mm and an overjet of 10 mm, hypodivergent face scheme, mandibular retrognathism, steep posterior occlusal plane creating inter-

**Pretreatment Posttreatment End of retention**

**Range Pretreatment Posttreatment End of retention**

ODI MP/AB 83 69 77 63 76 62 FH/PP −14 −14 −14 APDI HF/FP 90 66 91 73 91 74 FP/AB −10 −4 −3 HF/PP −14 −14 −14 CF ODI + APDI 135 136 136

FMIA 67 ± 3° 73 73 72 FMA 25 ± 3° 17 17 17 IMPA 88 ± 3° 90 90 91 SNA 82 ± 2° 78 78 78 SNB 80 ± 2° 73 77 76 ANB 2 ± 2° 05 01 02 AO-BO 2 mm 4 mm 1 mm 1 mm OP 10–14° 7 5 5 Z 75 ± 5° 83 80 81 PFH 45 mm 45 47 48 AFH 65 mm 66 70 72 INDEX 0.69 0.68 0.67 0.67

The z angle of 66° confirms an unbalanced face which is based on a rethrognatic chin, absence of crowding and shape of dental arches is different due to an old habit of thumb sucking.

According to Kim's cephalometric analysis, the patient shows a low-angle skeletal pattern (ODI = 86°), and removal of permanent teeth is not advised, due to the high potential for deep bite relapse. The APDI = 70° shows a class II skeletal pattern, and the combination factor = 156°

ferences in the molar area, and lack of occlusal support.

**Table 2.** Cephalometric analysis (Tweed-Merrifield) [14, 15].

**Figure 14.** Treatment sequence images. (A–C) In the third month of treatment, a double arch wire (DAW) was placed and remained in mouth 5 months. (D–F) One year of treatment (5 months with MEAWs along with small class II elastics (6 ounces, 3/16 inch)). (G–I) Eighteenth month of treatment. (J–M) Twenty-second months of treatment.

**Figure 15.** End of treatment: extraoral photos (A–C) and intraoral photos (D–F).

Treatment of Class II Malocclusion (Hypodivergent Face) with MEAW Therapy http://dx.doi.org/10.5772/intechopen.69331 137

**Figure 16.** Posttreatment records (A–C).

**Figure 14.** Treatment sequence images. (A–C) In the third month of treatment, a double arch wire (DAW) was placed and remained in mouth 5 months. (D–F) One year of treatment (5 months with MEAWs along with small class II elastics

(6 ounces, 3/16 inch)). (G–I) Eighteenth month of treatment. (J–M) Twenty-second months of treatment.

136 Insights into Various Aspects of Oral Health

**Figure 15.** End of treatment: extraoral photos (A–C) and intraoral photos (D–F).

**Figure 17.** Superimpositions between pre- and posttreatment (D, E).

**Figure 18.** Postretention: extraoral photos (A–C) and intraoral photos (D–H).

**Figure 19.** Postretention records (A–B) and superimpositions between posttreatment and postretention (C–E).

**Figure 20.** Three years after the end of treatment: extraoral photos (A–C) and intraoral photos (D–F).


**Table 3.** Cephalometric analysis (Kim).


**Table 4.** Cephalometric analysis (Tweed-Merrifield).

## **9. Conclusion**

**Figure 19.** Postretention records (A–B) and superimpositions between posttreatment and postretention (C–E).

138 Insights into Various Aspects of Oral Health

**Figure 20.** Three years after the end of treatment: extraoral photos (A–C) and intraoral photos (D–F).

The superimposed tracings confirm in both cases that the mandible shifted forward, the flattening of the posterior occlusal plane, and the vertical dimension increased during active appliance therapy.

The objectives of both treatments were successfully achieved by the use of MEAW therapy. A good functionally occlusion and an esthetic profile had been attained. The records 3 years after the end of treatment show the stability of the treatment and the occlusion.

The MEAW technique proved to be effective in the treatment of class II deep bite malocclusion.

## **Author details**

Paulo Augusto de Sousa Beltrão Address all correspondence to: paulobeltrao@sapo.pt French Board of Orthodontics, Portugal

#### **References**


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**Author details**

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**Innovations in Dental Restorations**

**Provisional chapter**
