The Components of Dental Hard Tissues and Developmental Dental Defects

#### **Chapter 1**

## Organic Matrix of Enamel and Dentin and Developmental Defects

*Eui-Seok Lee, Puneet Wadhwa, Min-Keun Kim, Heng Bo Jiang, In-Woong Um and Yu-Mi Kim*

#### **Abstract**

The anatomical crown of the tooth is covered by enamel and root is covered by cementum. The dentin forms the major part of the tooth. The dentin structure is very similar to that of the bone both physically and chemically which is why many scientists have wondered about using its properties for developing a novel bone graft material. In contrast with hard and brittle enamel dentin is viscoelastic. The organic structure of dentin which is about 35% is composed of mainly type *I* collagen embedded in mucopolysaccharides ground substance. Approximately half of the non-collagenous composition consists of hyperphosphorylated proteins. The acidic glycoproteins, Gla-proteins, serum proteins, proteoglycans etc. composes the remaining part. The dentin matrix consists of many similar proteins as that of bone like dentin phosphoprotein, dentin sialoprotein etc.. The matrix also consists of many growth factors. Any external disturbance like an infection, trauma, calcium or phosphorous metabolic changes can lead to defective amelogenesis. Mutational changes can lead to defect in dentin. An early diagnosis can result in a satisfactory treatment plan contributing to functional and esthetical compensation.

**Keywords:** Enamel matrix, Dentin matrix, Tooth proteins, Growth factors, Tooth developmental defects

#### **1. Introduction**

Enamel and dentin constitute different concentrations of organic, water and mineral contents. This accounts for their specific physical-mechanical properties and their integration allow the tooth to be functionally stable in adverse oral conditions [1]. Dentin tissue underlines the enamel and constitutes the bulk of the tooth. The inorganic to organic ratio is different in various tissues, these variations affect the properties of these tissues. The enamel is tougher and most highly resistant to force in comparison to other hard tissue in the body owing to its high inorganic content. On the other hand the dentin with high organic content serves as a resilient layer under enamel and cementum [2]. Enamel shows higher mineralization than cementum as there is more carbon 49% (wt) in cementum than enamel 3% (wt). Enamel being the hardest tissue and dentin being softer whereas X-ray diffraction (XRD) shows cementum has poorest crystallinity. Following decalcification process for separation of organic and inorganic content the organic components of the dentin are retained thereby maintaining the dentin shape. However due to 90% mineral content of the enamel it is lost after decalcification.

### **2. Enamel**

Tooth enamel possess remarkable structural and mechanical properties making it an unique tissue. Tooth enamel is a complex mineralized tissue comprising of long and parallel apatite crystals configured into decussating enamel rods [3, 4]. The enamel consists of 96% inorganic and 4% organic and water content and is the most mineralized tissue. The organic content of enamel is less than that of dentin. The organic content consist of some unique proteins present only in enamel and lipids [5]. The enamel is formed only once before the eruption of the tooth. Following eruption the tooth organ permanently loses the ability to form new enamel [3].

Being highly mineralized enamel could be expected to be brittle and have low fracture resistance. However, the experimental studies proved that the fracture toughness of enamel is equivalent to or even better than some tough ceramics [6, 7].

#### **2.1 Enamel proteins**

During the development of enamel, ameloblasts secrete enamel matrix protein. Proteins are large complex molecules that are required for the structure, function and regulating body's tissues and organs. Enamel matrix proteins bind to the hydroxyapatite structuring the enamel and modulating crystal growth [8, 9]. Initial developing enamel matrix constitutes 60-70% water, 20-30% proteins and 15-20% of mineral ions. Mineralization process leads to resorption of enamel proteins and water leaving very little amount of organic content in matured enamel [3]. Major components of the enamel matrix protein (EMP) are the amelogenins constituting greater than 90% of all the organic content in the enamel [10, 11]. The other type of protein group is the non – amelogenin including enamelins, tuftelin and sheathlins. Other than these two enzymes, matrix metalloproteinase (MMP)-20 and enamel matrix serine proteinase (EMSP)-1 are also present in the EMP (**Figure 1**) [10].

Enamel proteins consist of 1-2% of the total composition. These proteins are located mainly at the enamel rods interface. The proteins play a role in modulation of the stress in enamel and contributes to the elastic and viscoelastic behavior [12]. Any kind of damage or denaturation of the enamel or dentin non-collagenous proteins can decrease the durability of the tooth [12]. Tooth whitening procedures or treatment with potassium hydroxide leads to loss of enamel proteins causing enamel to be more prone to fracture [12, 13]. Radiation therapy for treatment of oral cancers is also known to damage the enamel proteins [12]. In a study the enamel proteins were extracted using potassium hydroxide treatment from the

**Figure 1.** *Types of enamel matrix proteins.*

#### *Organic Matrix of Enamel and Dentin and Developmental Defects DOI: http://dx.doi.org/10.5772/intechopen.99542*

enamel sections of the molar cusps. The results showed a 40% reduction in fracture toughness in comparison with a fully proteinized control. The organic content of the enamel is very small, but it is of importance crack growth toughening. This is because it helps in forming unbroken ligament and fortify its efficacy [14].

The synthesis and secretion of the organic extracellular matrix is controlled by ameloblasts and deposited along the dentino-enamel junction which eventually controls enamel biomineralization [15].

Amelogenins are hydrophobic in nature, they are rich in proline (25%), glutamine (14%), leucine (9%) and histidine (7%) amino acid residues [4, 15]. Amelogenin functions in regulating orientation, shape and length of enamel crystals [16]. Tuftelin is suggested to function at the level of ameloblast differentiation, it may play a role in extracellular matrix secretion. Tuftelin is also expressed in different soft tissues, which suggest it may have multifunctional role [17]. Ameloblastin also known as sheathlin and amelin present in Tomes' processes of the secretory ameloblasts the sheath space between rod and inter-rod enamel suggest that this protein may play a role in biomineralization. Enamelin is also believed to play a role in enamel

#### **Figure 2.**

*Scanning electron micrograph images of engineered enamel. In this study apatite was grown within a decellularized enamel protein matrix, resulting in decussating enamel prisms containing distinct and separated individual enamel crystals. A SEM image overview of the engineered enamel apatite, b depicts parallel bundles of enamel crystals, and c depicts newly formed decussating enamel rods [3]. Figure adapted from Pandya M et al. (2019).*

biomineralization. Enamelin is hydrophilic and an acidic protein rich in glycine, aspartic acid and serine [4]. The enamel proteins with unique properties requires specific proteases for their removal during enamel maturation whose spatiotemporal expression is impeccably regulated. This requirement is met by serine protease kallikrein-4 and MMP20 [18]. Enamel proteases processes secreted amelogenins, ameloblastin and enamelin in the matrix and eventually degrades and remove them from the mineralizing matrix when maturation of amelogenesis occurs. The sulfated enamel proteins are present in very small amount in the enamel matrix [15].

#### **2.2 Applications of enamel matrix proteins**

Enamel matrix derivative (EMD) is approved by FDA to be used as a material for periodontal regeneration since 1997 [19]. EMD is commercially obtained by heat treated lyophilized proteins that are isolated from porcine enamel at specific stage of development [20]. Emdogain, a mixture of enamel matrix proteins mainly composed of amelogenin is used for repair of hard and soft periodontal tissues [11, 21–23]. Emdogain has shown similar results to guided tissue regeneration with added advantage of easy to use with minimal complications [23].

Owing to its unique properties like toughness and relative fracture resistance researchers are focusing on developing an enamel-like biomaterial. Enamel biomimetics hold a great promise as structural components in a wide range of fields for biomedical and engineering applications. Some examples are like tooth repair, restoring a orthopedic defect site, functional insulator components, brakes and exhaust pollutant filters [3, 24]. Enamel proteins and calcium phosphate growth solutions seems to be a convincing formulation for biologically synthesizing tooth enamel. Based on the established role of enamel proteins, using an EMP researchers were successfully grew elongated and parallel apatite crystals within decussating enamel prisms (**Figure 2**) [3]. The research until now using biochemical approaches can only mimic limited features of apatite and calcium phosphate crystal growth.

#### **3. Dentin**

The dentin consists of 65% inorganic and 35% organic and water content. The presence of more organic content in dentin than enamel makes it very similar to that of bone. The organic part of dentin is composed of collagenous fibrils embedded in ground substance of mucopolysacchrides [5]. Type I collagen is the principal type of collagen in dentin. It contributes about 90% of the organic content, the remaining 10% contains several proteins and proteoglycans, acidic glycoproteins referred to as non-collagenous proteins [25, 26]. Also type I collagen is abundantly present organic constituent of the bone extracellular matrix [27]. The collagen fibrils form a scaffold network and are densely mineralized. The dentin consists of little amounts of type V and III collagen. The odontoblasts synthesize and secretes the non-collagenous proteins as well collagen fibrils [28].

Dentin constitutes tubules ranging in size of micrometer and surrounded by highly mineralized peritubular dentin, embedded in a matrix rich in collagen called intertubular dentin. Lamina limitans a sheet-like structure divide the peritubular and the intertubular dentin and primarily composed of proteoglycans protein cores. The proteoglycans contribute to mechanical behavior of dentin. They link the collagen fibrils securing the collagenous network together [12]. Peritubular dentin is primarily made of glycosaminoglycans and lacks collagen fibrils [29]. Intertubular matrix chiefly constitutes type I collagen fibrils with non-collagenous proteins and proteoglycans which forms a three-dimensional organic network buttressed by apatite mineral crystallites [30].

*Organic Matrix of Enamel and Dentin and Developmental Defects DOI: http://dx.doi.org/10.5772/intechopen.99542*

The adhesive systems used for dentin bonding rely on formation of a hybrid layer. This hybrid layer is formed by demineralized collagen fibrils reinforced by resin matrix. As the resin monomers are unable to infiltrate the mineralized tissues, so adhesive bonding systems are used which has an acid, primer and an adhesive. The acid helps in removing mineral crystals and exposing the collagen. The primer which is a hydrophilic solution permits the infiltration of resin monomer into the demineralized dentin. Finally, the adhesive consisting of a mixture of monomers penetrates the treated surface thereby forming mechanical adhesion with dentin. Removing the unbound water from hybrid layer and suppressing the endogenous enzymatic activity have helped in increasing biocompatibility by inhibiting degradation of the hybrid layer [31].

#### **3.1 Dentin proteins**

The dentin matrix and bone proteins are similar. Type I collagen designs an effective and instructional template for guiding deposition of calcium phosphate polymorphs and subsequently transforming into crystalline hydroxyapatite crystals. The highly complex process of hydroxyapatite nucleation and collagen mineralization is also controlled by non-collagenous proteins. The amount of these non-collagenous proteins in dentin and bone is small, but they play an indispensable role in bone formation and remodeling. Some examples of non-collagenous proteins found in both are osteocalcin, osteopontin and bone sialoprotein. The dentin matrix proteins are of interest because of their calcium binding property in the extracellular matrix which leads to calcification of tissue [32]. Many studies have shown similarities between dentin and bone. Apart from type I collagen being the leading extracellular matrix element, other common proteins and proteoglycans are osteonectin/SPARC, osteocalcin, osteopontin, bone sialoprotein, decorin and biglycan [33].

Dentin proteoglycans plays a key role in mineralization of the dentin and bone, so they perform structural, metabolic, and functional role. The proteoglycans are classified as small leucine-rich proteoglycans (SLRP) and the large aggregating proteoglycans. The SLRP are further divided into 5 classes: decorin; biglycan; fibromodulin; lumican and osteoadherin. Among the large aggregating proteoglycan is only versican has been described well in dentin [25].

Osteocalcin and osteonectin are classified under secretory calcium-binding phosphoprotein a category of non-collagenous proteins. Osteocalcin is a vitamin K-dependent gamma-carboxylated protein. It is a small calcium binding protein consisting of three glutamic acid residues. It is found in dentin in small amounts as compared to the bone [25]. Osteonectin binds collagen, hydroxyapatite and growth factors. It is known to regulate proliferation of cells, prompts angiogenesis and formulation of matrix metalloproteinases [34]. Another subset of the secretory calcium binding phosphoprotein is the Small Integrin-Binding ligand, N-linked Glycoprotein (SIBLING) family. It includes osteopontin, bone sialoprotein, dentin matrix protein 1, dentin sialophosphoprotein, and matrix extracellular phosphoglycoprotein [35].

Dentin phosphoprotein (DPP) and dentin sialoprotein (DSP) were earlier thought to be unique to dentin [5, 33]. Later some immunohistochemical studies established that DSP is also present in the alveolar bone, cellular cementum, osteocytes, cementocytes and their matrices [36]. DPP is rich in aspartic acid and phosphoserine and bind calcium in considerable amounts. DSP is a glycoprotein rich in aspartic acid, serine, glutamic acid, and glycine. Both DPP and DSP are synthesized by odontoblasts and pre-ameloblast cell types. In contrast the bone matrix proteins are not exclusively made by the osteoblasts. This makes dentin unusual based on these dentin specific proteins [33]. DSP has been shown to play a role in prompting differentiation of dental pulp cells in odontoblast-like cells [36].

#### **3.2 Dentin growth factors**

Growth factors are natural activation signals or substances able to stimulate cellular proliferation, wound healing, and sometimes cellular differentiation. Generally, a growth factor is secreted protein or a steroid hormone [37, 38]. They are necessary for regulating various cellular processes that take part in tissue regeneration procedure [39, 40].

Growth factors are generally acting as signaling molecules between the cells, like cytokines and hormones binding to specific receptors on the target cells surfaces. Examples of growth factors in dentin are TGF- *β* group, BMP group, Insulin growth factor-1, hepatocyte growth factor, VEGF, Adrenomedullin, FGF-2, platelet-derived growth factor, growth/differentiation factor etc. a summary of these growth factors is given in **Table 1**.

We can group these growth factors by their actions as: Angiogenisis (FGF-2, PDGF, VEGF, NGF); Differentiation (TGF-β, PDGF, FGF-2, BMPs, IGF, NGF); Proliferation (PDGF, FGF-2, IGF, VEGF, TGF-β, SDF-1); Chemotaxis (PDGF, FGF-2, TGF-β, SDF-1) and Neuronal growth (NGF) [41].


#### **Table 1.**

*Growth factors in dentin matrix and their role.*

The growth factors diffusion into the dentinal-pulpal junction is postulated to activate reactionary dentinogenesis and simultaneous reparative dentinogenesis along with pulp tissue inflammatory reaction [42, 43]. The surviving odontoblasts secrete reactionary dentin as a response to environmental stimuli causing metabolic activity increase in the cells. The inductive molecules determining the success of the pulp healing might be released from damaged dentin and adjacent pulp tissue [44]. Dentin-pulp regeneration process can vary as it depends on the causative agent whether trauma or pathological conditions. An inflammatory reaction is caused by these events, which is supposed to be the beginning of tissue regeneration process [39]. Dentin-pulp defensive and reparative mechanisms mimic the embryonic tooth development stage and growth factors derived from dentin may play a key role in regulating these events [42]. The dentinal matrix constitutes angiogenic growth factors and their release after injury can contribute to overall reparative response of the dentinal-pulpal complex [45].

There are multiple growth factors in dentin that also exist in bone like insulinlike growth factor-1 (IGF-1), insulin-like growth factor-2 (IGF-2), transforming growth factor-beta (TGF-β), fibroblast growth factors (FGFs), platelet-derived growth factor (PDGF), parathyroid bone morphogenetic proteins (BMPs), and certain members of the growth differentiation factor (GDF) group of proteins [46–48]. That is why recent studies have shown good results after using dentin as a bone graft and stated that dentin has shown to be clinically safe and has good boneforming capacity [49, 50].

Also known as autogenous tooth biomaterial it is derived from an extracted tooth through demineralization process. It is useful as graft material because of its osteoconductive properties [51]. This biomaterial can be used alone or combined with other materials for example with platelet-rich fibrin [52], bone marrow mesenchymal stem cells [53] or bone morphogenetic protein (BMP-2) [54] for enhanced bone regeneration effects. Recently a dentin derived barrier membrane acting as an osteoinductive collagen membrane showed successful outcome in guided bone regeneration and dental implantation. The membrane was derived from block type autogenous demineralized dentin matrix with advantage of overcoming the mechanical instability of the collagen membrane. It is mostly composed of type I collagen, making it suitable for use in implant procedures [55].

#### **4. Dental defects**

Enamel has 3 essential enamel proteins to build healthy well mineralized enamel which is secreted from ameloblasts "amelogenin, ameloblastin and enamelin" with the help of two enzymes, MMP20 and kallikrein-4 (Klk4) to form the enamel properly and sequent proteolysis of enamel protein [56]. In the event of alteration in the process of protein removal, enamel and dental defects will emerge like for example, amelogenesis imperfecta (AI), Chalky/Molar Hypomolarization (MH), Dentinogenesis Imperfecta (DI) or fluorosis [57]. **Figure 3** depicts the protein content in healthy and diseased tooth.

#### **4.1 Amelogenesis imperfecta (AI)**

Amelogenesis imperfecta is a rare, inherited enamel development disorder where mutations in the amelogenin gene results in malformation of the enamel layer. It is subdivided to 4 main types hypoplastic (type I), hypomaturation (type II), hypocalcified (type III), hypomaturation/hypoplasia/taurodontism (type IV).

#### **Figure 3.**

*Protein content is compared between healthy and diseased tooth enamel. Different proteins are presented in (rows) as analyzed different tooth conditions (columns). Healthy teeth is presented as reference in light gray, chalky/molar Hypomolarization (MH): Enamel affected by molar hypomineralization, fluorosis and Amelogenesis imperfecta (AI): Hypocalcified and hypomaturation amelogenesis imperfecta enamel; range of percent by weight (wt %) of protein abundance in comparison to healthy enamel show in 4 colors: Healthy range of 0.1–1 wt % (light gray); 2–3 times increase (light teal); 3–30 times increase (dark teal); 0–30 times increase (gray-teal gradient) [57]. Figure adapted from Gil-Bona a et al. (2020).*

Clinical and radiographical features and enamel thickness, of different subtypes are dependent on mode of inheritance and gene mutation. AI occurs due to mutations in several genes, including enamelin, amelogenin, MMP20, Klk4 and FAM83H [58–61]. The mutations can lead to hypoplastic, hypomature, or hypocalcified form of the enamel [62]. AI can be easily seen clinically and radiographically as teeth appears in abnormal color like (yellow, brown, or gray). Soft enamel, due to hypo calcification enamel surface are more susceptible to caries, tooth attrition, teeth hypersensitivity, calculus formation, and gingivitis/periodontitis [63].

Type I hypoplastic AI has reduced thickness of enamel and shows pitting and grooves. In radiographs enamel shows normal contrasts from dentine. Type II hypomaturation AI has enamel of normal thickness but appearance is mottled. It is less severe than hypocalcified type. Radiographically it exhibits similar radiodensity as dentine. Type III hypocalcified AI have defect in enamel calcification. The enamel thickness is normal but is weak in structure and appearance is opaque and chalky. In radiographs enamel is less radio-opaque in comparison to dentin. Type IV hypomaturation/hypoplasia/taurodontism AI exhibits mixed hypomaturation and hypoplasia appearance. In taurodontism enlargement of the body and pulp chamber is observed. The pulp chamber floor and furcation moves apically down the root [58].

A proper diagnosis identifying the different phenotypes is essential to determine molecular etiology. The treatment plan aims at early diagnosis, managing the pain and restoring the defects with regular follow ups [58]. Mild variations can be treated adequately with facial veneers, whereas in severe cases full coverage is mandatory. For young patients milled acetal resin overlays can be used until fully erupted [64].

#### **4.2 Chalky/molar hypomineralrisation (MH)**

It is discolored white patches in one or more molars, porous dental enamel leads to hypersensitivity and risk of caries. Chalky enamel opacities contained unusually high amounts of protein, including serum albumin and other derivatives of blood and saliva [65]. Moderate and severe cases with opacities having a chalky texture exhibit failure of enamel surface soon after the eruption of tooth, it provides a hygiene-resistant nidus for dental plaque accumulation. The porous chalky enamel is invaded by accelerated decay which arises the need for restoration, extraction, or

#### *Organic Matrix of Enamel and Dentin and Developmental Defects DOI: http://dx.doi.org/10.5772/intechopen.99542*

orthodontic treatment. It is observed that MH affects the 2-year molars or 6-year molars, a better understanding of its etiology is necessary [66]. Earlier systemic disturbance of enamel-forming cells (ameloblasts) during the hardening (maturation) stage of enamel formation was thought to be the cause [67]. A different pathomechanism indicating localized exposure of enamel to serum albumin was recently identified [68]. In a recent study the dose–response relationship between albumin and the enamel chalkiness was established. This supports the new pathomechanism also termed as "mineralization poisoning" [66].

MH is a complex problem requiring combinational treatment modalities. The treatment aim may be preventive or symptom control. Various treatment modalities can be adhesive and sealant restoration, composite restoration, glass ionomer restoration, preformed metal crown, microabrasion, bleach or orthodontic extraction [69].

#### **4.3 Fluorosis**

Dental fluorosis is a very common developmental disturbance that is caused by repeated exposures to high concentrations of fluoride during tooth or enamel formation. This leads to disturbance in enamel formation as the fluoride decreases calcium concentration in the matrix. This interferes with protease activity and delays or inhibit enamel matrix protein degradation. An abnormal apatite crystals growth occurs which leads to physical tooth surface changes [70]. It differs from white striations to stained pitting of the enamel depending on case severity [71]. The use of topical fluoride dentifrices in young children may increase the risk of dental fluorosis. In case of concern for fluorosis, in children under 6 years of age toothpaste with fluoride concentration less than 1000 parts per million should be used [70].

Treatment of the case depends on the severity and the esthetics concerns. Mild cases can be treated by bleaching if the tooth. For moderate cases enamel microabrasion with acids can be done. Composite fillings, veneers and crowns can be used for treating cases with severe forms of the disease [72].

The best solution for this condition is to control the fluoride intake for prevention of dental fluorosis [71].

#### **4.4 Dentinogenesis imperfecta (DI)**

DI is also an inherited condition also called "dentin dysplasia" with discolored teeth but most often blue-gray or yellow-brown which leads to wear, breakage, and loss of teeth. This damage can include teeth fractures or small holes (pitting) in the enamel. The enamel may have hypoplastic or hypocalcified defect in nearly one-third of patients and has tendency to crack away from defective dentin. It is a localized mesodermal dysplasia which affects both primary and permanent dentition. It is inherited in simple autosomal dominant mode exhibiting high penetrance and low mutation rate [73].

DI has 3 types: Type I: occurs in people who have osteogenesis imperfecta so, it appears to have other health concern (mutation in COL1A1/A2 gene). Type II: the most common type occurs in people without another inherited disorder (mutation in DSPP). Radiographically it shows complete obliteration of the pulp cavity by dentin. Type II and type III, are actually similar conditions but in different forms but DI type III shows enlarged pulp cavities [63].

In histological findings although enamel is normal in structure it tends to crack. Scalloping is absent in dentino-enamel junction. Mostly mantle dentin structure is normal. However dentinal tubules of the circumferential dentin are found to

be coarse and branched. The tubules are reduced in quantity. An atubular area is present in the dentin with reduction in mineralization and decreased number of odontoblasts. Another common finding is pulpal inclusions and much interglobular dentin [73].

Treatment differs from case to case depend on its severity and presenting pain, also the patient age. Mostly treatments are targeted at maintaining oral hygiene and esthetics. Early diagnosis and treatment can prevent deterioration of teeth and occlusion. In severe cases two treatment stages for primary teeth under general anesthesia is recommended. At the age of 18-20 months the stage 1 treatment involves composite restorations covering for incisors and preformed crowns for first primary molars. At the age of 28-30 months stage 2 aims at protecting second primary molars and canines. For moderate cases one-stage treatment for primary teeth at 30 months of age is optimal. In severe cases composite restoration may not be helpful. A long term follow-up is necessary to adjust treatment according to change in dentition and occlusion [73].

#### **5. Conclusion**

The enamel and dentin organic content varies in amount and its constituents. The enamel proteins help in imparting the elastic and visco-elastic properties to the enamel. The clinical significance of the non-collagenous proteins may be in relation with dentinal growth factor release by calcium hydroxide or mineral trioxide aggregate. The dentin organic matrix constitutes similarity with that of bone, makes it a desirable bone graft material. Demineralized dentin autogenous bone grafts have already been used for dental implant surgeries and provides an easy to prepare and use bone graft material. Any imbalance in the organic content can manifest as developmental disease of the tooth.

#### **Conflict of interest**

The authors declare no conflict of interest.

*Organic Matrix of Enamel and Dentin and Developmental Defects DOI: http://dx.doi.org/10.5772/intechopen.99542*

#### **Author details**

Eui-Seok Lee1†, Puneet Wadhwa1†, Min-Keun Kim2 , Heng Bo Jiang3 , In-Woong Um4 \* and Yu-Mi Kim4

1 Department of Oral and Maxillofacial Surgery, Graduate School of Clinical Dentistry, Korea University, Seoul, Korea

2 Department of Oral and Maxillofacial Surgery, College of Dentistry, Gangneung-Wonju National University, Gangneung, Republic of Korea

3 Stomatological Materials Laboratory, School of Stomatology, Shandong First Medical University and Shandong Academy of Medical Science, Tai'an, China

4 R&D Institute, Korea Tooth Bank, Seoul, Republic of Korea

\*Address all correspondence to: h-bmp@hanmail.net

† Both authors contributed equally.

© 2021 The Author(s). Licensee IntechOpen. 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.

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#### **Chapter 2**

## Fluoride and Other Trace Elements in Dental Hard Tissue

*Y.B. Aswini, Vikrant Mohanty and Kavita Rijhwani*

#### **Abstract**

Fluorides and other trace elements are a part of various biological and chemical responses in the human body. They collaboratively work with all proteins, enzymes, and co-enzymes to carry out the different functions and in redox reactions. The dietary substances may not have an adequate amount of these essential trace elements, resulting in the development of dental soft and hard tissue disorders associated with their deficiencies. To tackle this, dietary supplements will be needed. So, the current chapter has thoroughly addressed the importance of trace elements in dental hard tissues. This has also discussed the effect of fluoride and other trace elements on dental hard tissues, as there is limited literature available in this area. This will provide an overall understanding of how trace elements are an essential part and their importance in oral diseases control and prevention.

**Keywords:** trace elements, fluoride, dental structure, mechanism of action, distribution

#### **1. Introduction**

Carbon, hydrogen, and nitrogen elements make up about 96 percent of all living things. In the living system, nearly half of all recognized elements are present in detectable concentrations. The physiological activities of 23 elements are identified in humans and other mammals, 11 of which are categorized as trace elements (TEs) [1]. Vanadium, chromium, manganese (Mn), iron (Fe), cobalt, copper (Cu), zinc (Zn), and molybdenum are transition elements, while selenium (Se), fluorine, and iodine are non-metal elements [1, 2]. TEs, unlike sodium, calcium, magnesium, potassium, and chlorine, which are macronutrients that must be consumed in large quantities, are micronutrients that must be consumed in small amounts. (usually lower than 100 mg/day). Major and Minor TEs are both essential for human health. Due to natural or man-made causes, a lack or excess of these elements may have serious clinical implications [2].

A tooth's structure includes hard tissue (enamel, dentine, and cement) as well as soft tissue (pulp and periodontal ligaments). A tooth has a multicellular structure that can collaborate with the maxillofacial region functionally [2, 3].

Trace elements (TEs) are essential for human health. Toxic effects are caused by a lack of or an overabundance of TEs. TEs have a huge impact on both human and dental health. It is involved in the functions of essential biological polyphosphate compounds such as ATP, DNA, and RNA. In the tooth structure, TEs are found in various concentrations. Teeth are affected by changes in the density of certain TEs. Caries susceptibility is increased when the density of

certain TEs is altered. Others function as a barrier to the development of caries. Zinc (Zn), phosphorus (P), and magnesium (Mg) are common TEs that have a significant impact on dental health. The use of tissue samplings such as blood, semen, teeth, nails, and hair to measure TE values in order to define and correct these effects has a significant impact. Teeth are widely regarded as a reliable indicator of TEs. As a result, TEs have a big impact on the development of healthy teeth [4].

#### **2. Trace elements in dental hard tissues**

The hard tissue that protects the tooth's surface is known as enamel. This layer's job is to protect the dentine-pulp complex. Enamel is the body's toughest and most resistant tissue. It's made up of 95–97% inorganic material (calcium hydroxyapatite crystals) and 1–2% organic material (proteins like amylogenic, enameline, ameloblastin, and tuftelin, to name a few), and 2–4% water [5]. TEs make up a small percentage of the 97 percent inorganic content and consists of Phosphorus (P-17%), calcium (Ca-36.5%), fluoride (F-0.016%), 3.0% carbon dioxide, 0.2% Na, 0.3% potassium (K), 0.016% Fluoride, 0.1% sulfur (S), 0.01% copper (Cu), 0.016% Zn, 0.003% silicon (Si); and low amounts of silver (Ag), strontium (Sr), barium (Ba), chromium (Cr), manganese (Mn), Vanadium (V). TE is deposited in human tooth enamel by the environment before and after the tooth's mineralization and maturation [6].

After Enamel, the next layer to the tooth is Dentin consists of an inorganic matrix 70% in weight (40–45% in volume) Organic matrix 20% by weight (30% in volume), and water 10% by weight (20–25% in volume). The organic portion consists of proteins like osteonectin, osteopontin, osteoclastin-like dentin Gla protein, dentin phosphorene, dentin matrix protein, and dentin sialoprotein and type I collagen fiber [6, 7]. The inorganic material consists of hydroxyapatite crystals and TEs (40 in number) which include Zn, Sr., Fe, Al, B, Ba, Pb having up to 1000 ppm concentration and Ni, Li, Ag, As, Se, Nb, Hg having 100 ppb concentration. An analysis of the relation with age of 10 trace elements in dentine found that boron (B), manganese (Mn), cobalt (Co), copper (Cu), zinc (Zn), rubidium (Rb), strontium (Sr), molybdenum (Mo), cadmium (Cd), and lead (Pb) and suggested that human dentine is an appropriate substance for relating sex and age [8].

#### **3. Cementum**

Cementum is a type of connective tissue that connects the periodontal ligament to the root surface and covers the root surface's outermost layer of calcite matrix [9]. Cement is a vascularized, mineralized tissue and has higher regeneration potential. It connects the dentin to the periodontal ligament and aids in the repair and regeneration of periodontal tissue after injury [10]. Cement's inorganic portion is identical to that of bone, dentin, and enamel.

The essential mineral part of cementum consists of calcium hydroxyapatite with amorphous calcium phosphate (Ca10 (PO4) 6 (OH) 2) and has a lower crystallinity than other calcifying tissues [11]. This lower crystallinity causes the cementum, to be easily decalcified and increases the tendency to absorb nearby ions like fluoride. That's why a higher concentration of fluoride is found in cementum ad compared to other parts of the tooth. In comparison to other calcifying tissues, the cement of adult mature teeth has higher fluoride content. The amount of magnesium in the cement is about half that of the dentin. In the deep layers of the cement, Mg levels gradually rise [9, 10].

### **4. Dental pulp**

Dental pulp consists of Odontoblastfibroblast (collagen and elastic fibers forming cells), blood vessels, nerves, and lymphatic vessels that make up the tooth pulp that develops from the dental papilla [11]. The cells which are responsible for the formation of pre-dentin, dentin, and reparative dentin are Odontoblast [11]. When the pulp's health is threatened the pulp cells especially fibroblasts produce inflammatory mediators such as IL-8, IL-6, and vascular endothelial growth factors that are responsible for producing symptoms of pulp infection. The tooth pulp is responsible for a variety of biological functions, including nutrition, sensitivity, building, and defense. The health of the pulp is largely influenced by changes in blood pressure and arterial flow in the apical area. When tooth pulp is affected by stimulus or irritants like mechanical, chemical, thermal, or microbial agents causing vascular inflammatory responses like local tissue reactions and lymphatasis(affecting lymphatic drainage of pulp area) [12–14].

Dental caries is a microbiological infectious disease that causes the degradation of calcified tissues and the destruction of the organic part of the tooth leads to cavitation. The bacteria (from mutans Streptococci and Lactobacillus species), a susceptible tooth surface (host), and a nutrient (diet) to provide bacterial growth are all needed for the formation of dental caries. From enamel, caries progress to dentin and causes inflammation of the pulp [15, 16].

In a systematic review analysis of various studies assessing the role of trace elements in oral health, it was found that there are some trace elements that cause dental caries progression whereas certain trace elements may decrease the risk of developing dental caries [4].

The effects of fluoride and various trace elements on dental hard tissues are as follows:

#### 1.**Fluoride as trace element**

Of the existing anticaries agents, fluoride is the most powerful and well-tested. Understanding the mechanism of fluoride's action in the prevention of dental caries is critical for developing the best fluoride delivery systems for optimal caries reduction. Although the exact and full mechanism of action of fluoride cannot be determined at this time, there is enough evidence to suggest that fluoride has a number of subtle effects on the calcium-phosphate system as well as the dental plaque metabolism. Fluorides can affect calcium-phosphate interactions in tooth enamel during the mineralization stage (before the tooth emerges) and, also, post eruptively by surface interactions with enamel, as well as during a carious attack [17, 18].

#### • **Mineral phase of enamel - a review**

Ca2+, PO43-, OH-, and carbonate are the key chemical components of tooth enamel (CO32−). These components are found in the form of microcrystals in enamel and dentin, and their spatial structure resembles that of the pure ternary mineral hydroxyapatite, Ca10(PO4)6(OH)2. Carbonate is a component of enamel's relatively large apatite crystals. Furthermore, teeth's mineral phase contains a variety of trace elements, the most significant of which is fluoride. Some of the elements are adsorbed on the surface of hydroxyapatite crystals, while others with the right size and charge will fill voids or replace calcium or phosphate in the crystal interior. As a result, it's obvious that enamel bioapatite is not pure apatite, but rather includes CO32-, Na+, Mg2+, F-, Sr2+, CI-, and other ions. Enamel apatite deviates from the stoichiometry of pure apatite in terms of Ca/P ratios due to a large number

of substitutions in the crystal lattice. Enamel crystals also have a lot of flaws and are low in calcium and hydroxyl ions. The solubility of enamel tends to increase as voids and deviations from stoichiometry increase [19].

Fluoride incorporation within the apatite lattice has significant consequences. The formation of fluorapatite is caused by the replacement of hydroxyl groups by smaller fluoride ions, which causes a decrease in the dimension of the unit cell and has many effects on the physical and chemical properties of the crystals. Surface enamel (first 10 um) obtained from people living in fluoridated areas may contain 3000–4000 ppm of fluoride, whereas pure fluorapatite has a fluoride concentration of 38,000 ppm. It is clear that drinking fluoridated water causes just a small amount of fluoride ions to be substituted for hydroxyl ions, around 10%. Even this minor substitution appears to play a role in the strong cariostatic impact. The acquisition of fluoride by enamel is considered before exploring the mechanisms of fluoride action [19–22].

#### • **Acquisition of fluoride in enamel**

Fluoride enters dental enamel by two mechanisms: (1) systemically, through absorption of fluorides in water, drinks, foods, or fluoride supplements, and (2) topically, through oral fluids such as saliva, urine, plaque fluid, and topical fluoride solutions bathing enamel. Topical fluoride acquisition is limited to the enamel surface, mostly the first 10- to 30-pm layer, and is often limited to etched surfaces and incipient lesions.

#### • **Systemic acquisition of fluoride**

During the mineralization process, fluorides are introduced pre-eruptively into enamel from tissue fluid. The fluoride level acquired is determined by the fluoride concentration in the plasma, which is a feature of the fluoride consumed in water, food, or supplements. The fluoride concentration is relatively high during the early stages of enamel development, but it gradually decreases as the tooth matures and acquires more minerals [23].

During the pre-eruptively maturation period, when enamel undergoes rapid and more full mineralization, the majority of fluoride is incorporated into the sound surface of the enamel.

Since primary teeth have a shorter time of enamel maturation than permanent teeth, they absorb less fluoride. The slight variations in fluoride concentration between permanent teeth can also be explained by differences in tooth maturation time. In both fluoride and non-fluoride regions, a gradient concentration occurs with a declining concentration towards the dento-enamel junction in unerupted and erupted teeth [23].

While the majority of fluoride is acquired during the pre-eruptive growth of teeth, it is important to note that a large portion of the mineral component of enamel (about 10% in bovine enamel) is acquired during post-eruptive maturation [24].

Furthermore, the optimum value for enamel crystallinity is reached several years after the eruption. A significant amount of fluoride is introduced into surface enamel during this process of mineral deposition. Fluoride is less likely to disperse as teeth age and become more mineralized, so deposition is more limited to the surface. This causes a more pronounced fluoride concentration gradient, with lower concentrations towards the interior of enamel, though this is later decreased by abrasion on exposed areas of the tooth. The concentration of fluoride in populations that consumed water that was optimally fluoridated (1 ppm) during the development of the dentition is higher, Fluoride concentrations in total enamel of permanent teeth range *Fluoride and Other Trace Elements in Dental Hard Tissue DOI: http://dx.doi.org/10.5772/intechopen.102043*

from 200 to 300 ppm, with levels as high as 3000 ppm in the first 10 micrometer. The comparable fluoride concentration in non-fluoridated areas is about 150 ppm in whole enamel and under 2000 ppm in surface enamel. In the outer few micrometers of enamel, the gradient is very steep. These levels are lower in primary teeth, with fluoridated and non-fluoridated communities having 900 and 650 ppm in surface enamel, respectively [17, 25]. Fluoride concentration is the highest in surface enamel and decreases towards the inner parts. Fluoride concentrations in enamel vary from one surface to another on the same tooth. Fluoride concentrations in newly erupted tooth surface enamel are higher near the incisal edge than near the cervical margin [26]. However, after the eruption, subsequent wear and attrition of the enamel destroy the fluoride-rich outer enamel of the incisal edge at a faster rate than it is obtained, allowing it to fall below the cervical enamel.

Topical obtainment of fluoride is often acquired post-eruptively from the oral atmosphere in the enamel surface, but the accumulation is mostly limited to the surface. Foods, water, fluoride-containing beverages, toothpastes, mouth rinses, prophylactic pastes, topical solutions, and gels are all sources of fluoride.

#### • **Mechanisms of Cariostatic Action**

a.**Fluoride's Effect on Enamel Solubility**- It is widely accepted that caries are caused by bacterial acids demineralizing the mineral phase of the tooth. As a result, the solubility of tooth minerals may have an impact on the caries process. A potential mechanism by which fluoride decreases caries is by influencing the solubility of dental enamel, according to these claims. It is relatively easy to show that trace amounts of fluoride (−1 ppm) in an acid buffer solution significantly reduce enamel solubility, and that enamel readily acquires reduced solubility properties when exposed to a fluoride solution.

At pH 4.5, Ten Cate and Duijsters [27] found that 2 ppm F in a solution containing 2.2 mM Ca and P effectively prevented enamel demineralization. Proof that the slight rise of fluoride in enamel caused by drinking fluoridated water causes significant solubility differences is less conclusive.

Isaac et al. and Jenkins [28, 29] Solubility tests of intact enamel obtained from teeth of individuals living in fluoridated and non-fluoridated areas show a trend towards less solubility in the fluoridated classes. Moreno et al. [30] used apatites with well-defined levels of fluoride ranging from 0 to 3.4 percent to come to the conclusion that fluoride concentrations of 4000–8000 ppm were required to produce a significant decrease in enamel solubility. Fluoride concentrations in the molecular layers of surface enamel in fluoridated zones can be higher than those detected by the normal imprecise methods of collecting outer enamel. Explaining how a restricted substitution of fluoride ions for hydroxyl ions in enamel apatite can affect enamel solubility requires another consideration. Low levels of fluoride in the solution can react with the outer surfaces of dissolving hydroxyapatite crystals, forming a shell with fluorapatite solubility properties, according to Brown et al. [22].

The presence of small amounts of fluoride during a carious attack may therefore have a major impact on the properties of enamel crystals. This may explain why fluoride-containing products (dentifrices and mouth-rinses) are highly effective cariostatic agents when used on a regular or weekly basis for long periods of time. As previously stated, substitutions and defects cause enamel apatite to deviate from the stoichiometry of pure hydroxyapatite. Fluoride stabilizes the crystal structure

of enamel, while carbonate and sodium increase its solubility and reactivity. Also, Nikiforuk et al. [31] found some evidence that the presence of fluoride during enamel production results in lower carbonate content. The dissolved enamel crystals preferentially lose carbonate during an incipient carious assault. Crystals containing less carbonate are thought to have lower reactivity and solubility, making them more resistant to caries. Fortunately, as the plaque's pH rises, recrystallization occurs, resulting in the formation of larger, more resistant crystals. The sum of these results is that fluoride has a slight but important effect on enamel solubility, even at the relatively low concentrations found in enamel.


components and fluoride are now recognized as effective natural protection mechanism that allows enamel to respond to cariogenic challenges. In vitro, adding 0.05 mM fluoride to calcium phosphate solutions used to remineralize partially demineralized enamel increases the rate of remineralization by 4- to 8-fold [36]. In comparison to natural plaque, which has high fluoride levels, etched enamel remineralization results in higher fluoride levels in the enamel. This is referred to as enamel's adaptative response to the acidic environment in a specific area [37]. The minerals that form during remineralization are less soluble than those that form in the same solution but do not contain fluorides.

An important reservoir of fluoride is surface enamel from which fluoride is released during the demineralization phase of a carious attack. Fluoride ions are also released from plaque when the pH falls which may contribute to remineralization. The process of remineralization can function at the earliest stage of caries formation, i.e. when the first acid attack occurs.

As the pH starts to grow after the acid attack, fluoride in the microenvironment will trigger enamel dissolution to stop sooner. If the pH increases, fresh, bigger, less soluble crystals form, containing more fluoride, such as fluoridated hydroxyapatite, and less carbonate like fluoridated hydroxyapatite. The enamel is partially remineralized as a result of the procedure. Following exposure to fluoride, saliva, or plaque fluid, the amount of new minerals at the site may increase even more. When fluoride is applied at a later stage of caries growth, such as when a white spot is apparent, fluoride penetrates the surface layer and is absorbed preferentially by the porous sponge like the body of the lesion. This also decreases the solubility of the lesion, making it more vulnerable to acid attacks in the future. On radiographs prepared from thin parts taken through the lesion, successive fluoride exposures and caries attacks often result in a laminated appearance [38]. According to in vitro remineralization tests, the entire body of the white spot lesion does not need to be remineralized to become covered. If only the surface zone of a lesion is remineralized, the lesion can be stopped. When lesions are subjected to re-mineralizing solutions containing relatively high amounts of fluoride or calcium, this is easily accomplished [34]. As a result, the appearance of natural caries white spots in the mouth does not always imply that the region is actually under attack by caries. It may actually signify a region that has been attacked but is now partly remineralized and arrested as a result. Because of the absorption of organic stains, long-standing arrested lesions often appear as brown spots [35].

Because of the buffering effect of saliva and plaque, as well as the high concentrations of calcium and phosphate present, the caries process is complex, with periods of demineralization when plaque pH are minimal, alternating with periods of remineralization as pH rises. If the process is to be pushed in the direction of remineralization, the presence of trace amounts of fluorides released from enamel or normally present in plaque fluid is important [39]. This is a key mechanism by which fluoride decreases the incidence of caries.

c.**Effect of fluoride and tooth morphology** - Fluoride intake can affect the size and morphology of teeth in humans and laboratory animals. Most studies show that if fluoride is present during tooth development, diameters and cusp depths are smaller [40]. Such morphological modifications would help to reduce caries vulnerability by making teeth more self-cleaning, but it's unclear if the effects of optimal fluoride intake are substantial enough to be clinically significant.

Other trace elements (strontium and molybdenum) have similar effects in rats, raising questions about the fluoride effect's specificity. According to Aasenden and Peebles [18], molars. Molars in subjects who consumed fluoridated water or nutrients had shallower fissures and less carious lesions than molars in a non-fluoride control sample, according to Aasenden and Peebles [18], corroborating other clinical impressions. Deep fissures collect more plaque and are more difficult to clean than shallow fissures. The improved morphology of the occlusal surface may be partly to blame for the lower level of occlusal caries observed in fluoridated areas, despite the fact that it is the least affected.

#### **5. Distribution of trace elements other than fluoride in dental hard tissue and its mechanism of action**

As per the various literature, it has been found that various trace elements have different roles in causing and preventing dental caries like Selenium, Cadmium, Magnesium, Platinum, Lead and Silicon are caries promoting elements whereas other than Fluoride, Phosphorus, Molybdenum Vanadium, Strontium and Lithium are cariostatic elements.

The effects of trace elements on oral dental tissues are as follows-.

#### **5.1 Vanadium (V)**

The vanadium is found with industrial resources such as oil refineries and power plants. The majority of food compounds contain lesser concentrations whereas Seafood has a higher concentration of Vanadium and daily uptake from all source's ranges from 0.01–0.02 mg [41].

Various studies have been done to assess the role of Vanadium in the development of prevention of dental caries. It's found to be caries protective in animal studies and studies on rats but on the contrary studies on monkeys when they drank water with Vanadium content tend to have more carious lesions in their mouth. So exact role in the prevention and development of caries is still not clear [4].

#### **5.2 Strontium (SR)**

Strontium is universally present in the environment. Though it is non-essential but still present in all living beings. This element bears a resemblance to Calcium as it has a tendency to be taken by bones and skeleton. Depending upon the amount received, it can have beneficial and harmful effects on humans [42].

Strontium is considered to be caries protective as per the literature. The strontium makes the enamel more stable and stronger as compared to pure calcium content. It also found that remineralized process in enamel with strontium in solution easier and faster as compared to without strontium solution and because of this the tooth enamel stable and more resistant to caries and acid attack [43].

The epidemiological studies suggest that high strontium content is associated with decreased carious lesions or good enamel. The strontium content decrease with age and is found to be more young as compared to older people.

#### **5.3 Lithium (Li)**

Lithium has an inverse relation with the development of dental caries. Various studies reported with reduced incidence of caries in presence of lithium in humans [4]. Mostly the lithium exposure occurs with drinking water and if in excess can have an

effect on different tissues or organs in animals like affects the thyroid function and also causes histopathological changes in salivary glands [44]. It has medicinal use in various psychiatric disorders like bipolar disorders [45].

#### **5.4 Copper (Cu)**

Copper is a component of a variety of metalloenzymes that act as oxidases to reduce molecular oxygen. Adult men and women should consume 900 g of fiber per day. Copper intake from food is approximately 1.0 to 1.6 mg/day for adult men and women in the United States. Adults have a Tolerable Upper Intake Level (UL) of 10,000 g/day (10 mg/day), a value based on protection from liver damage as the critical adverse effect. Greater amounts of copper are found in seafood, green leafy vegetables, animal products, pulses, and grains [46].

Oral Health and Diseases: What Role Does It Play- Hypochromic anemia, neutropenia, hypopigmentation of hair and skin, irregular bone structure with skeletal fragility and osteoporosis, joint pain, reduced immunity, vascular aberrations, and kinky hair are all signs of copper deficiency [47].


#### **5.5 Selenium (Se)**

Selenium salts are essential for a variety of cellular functions in the human body, but too much of them is toxic [53]. It is present in the liver, kidneys, seafood, poultry, grains, grain oils, milk, fruits, and vegetables, and a maximum intake of 70 micrograms is recommended [54]. It is required for the formation of anti-oxidants enzymes in the body.

Selenium is a non-metallic substance that occurs naturally and is absorbed by the body through food or inhalation. Intake of selenium was linked to an increase in dental caries. It has been stated that selenium settles in the enamel's micro-crystal structure at the start of decay, making it more susceptible to dissolution [54].

Furthermore, a reduction in selenium levels in the body has been linked to oxidative stress. According to a new study, patients who developed oral mucositis as a result of high-dose chemotherapy significantly shortened the duration and severity of the condition and also has cytoprotective impact and antiulcer activity on subsequent reinforcement [55].

#### **5.6 Manganese (MN)**

The amount of manganese in food varies greatly. Peanuts and grains have the highest concentrations, while milk products, meat, poultry, fish, and sea products have the lowest. Manganese can also be present in coffee and tea, which account for 10% of daily intake. On average, an adult's body contains 15 mg of manganese, which is often found in nucleic acid. The regular requirement is between 2 and 5 milligrams. Manganese is a component of metalloenzymes and acts as an enzyme activator. Manganese concentrations range from 0.3 to 2.9 ug manganese/g in all mammalian tissues. Tissues with a lot of mitochondria and pigments (like the retina and dark skin) have a lot of manganese concentrations in them.

Manganese is a TE that can be ingested by food, air, or water and incorporated into the enamel. Furthermore, Mn has the ability to change Ca′s position at HAP. Mn can be used in synthetic HAP without degrading the crystal area size, according to several studies [56].

Manganese concentrations are normally higher in bones, livers, pancreas, and kidneys than in other tissues. The bones are the most valuable manganese shop. Manganese is one of 49 elements found in enamel hydroxyapatite crystals, and it is normally present in very small amounts. Manganese concentrations in enamel range from 0.08 to 20 ppm, or 0.08–20 mg/kg, and in dentine from 0.6 to 1000 ppm. The concentration of Mn is higher in permanent dentition compared to primary dentition [57].

Manganese is being increasingly linked to the occurrence of tooth decay. According to one study, the incidence of dental caries in males increased in areas with higher manganese content. As a result, it is stressed that manganese promotes caries [4].

#### **5.7 Zinc (ZN)**

Zinc is found in the human body in amounts ranging from 2 to 4 grams. The prostate, eyeballs, brain, muscles, bones, kidney, and liver all store zinc. It is the only metal used in all enzyme groups and is the second most common transition metal in species after iron. The concentration of Zn in plasma (10%) remains constant even when intake is higher and in plasma 60% is tightly bound to albumin and the rest to transferrin (40%) [58, 59].

#### *Fluoride and Other Trace Elements in Dental Hard Tissue DOI: http://dx.doi.org/10.5772/intechopen.102043*

The RDA of Zinc is 15–20 mg. The pancreas and intestines excrete approximately 2–5 mg per day. Pregnancy, loss of liquid, oral contraceptive use, blood loss, and acute infection all having lower plasma zinc levels.

Zinc is needed for cell reproduction, differentiation, and metabolic functions. Zinc also aids normal development during pregnancy, infancy, and adolescence [60, 61]. Zinc is present primarily in animal products such as beef, milk, and fish. Phytonutrients are poor in zinc bio adjustment [58].

Oral Health and Diseases: What role does it play?


#### **5.8 Cadmium (Cd)**

Cadmium accumulates in the liver and bones as soon as it reaches the body and is released slowly (cadmium reference). It causes a major environmental issue as a result of being received by plants and entering the food chain, or as a result of being washed from the soil and hitting the water environment. Furthermore, chelating agents accelerate the downward carriage of cadmium from the soil, which can contribute to contamination of drinking and irrigation waters as it reaches underground water bodies [68, 69].

Exposure to cadmium has been linked to a number of health problems, including kidney failure and skeletal problems, and heart diseases [70]. It can be released from dentures and materials containing metal alloys in the mouth (rigidly bound with metallothioneins) and can accumulate in teeth and other oral tissues.

Cadmium has been linked to an increase in the occurrence of tooth decay. However, it is said that cadmium settlement in teeth after growth is ineffective in preventing caries. According to some animal studies, there is a clear connection

between the formation of dental caries and cadmium intake during the dental growth period [4]. The power of increased exposure to and diffusion of this toxic material on the general and oral health of vulnerable populations such as children is fetching increasingly significant [4].

#### **5.9 Lead (Pb)**

Lead may be consumed by tainted food and beverages as a result of industrial activity [51]. Lead enters the food chain through vegetables grown in polluted soil, for example. Lead can be transferred from polluted soil to plants and grass, potentially resulting in toxic metal accumulation in vegetating ruminants, especially cattle. Lead accumulation causes toxic effects in animals, as well as toxic effects in people who drink toxic metal-contaminated meat and milk [71].

It is a radioactive metal that is harmful to the human body. At the HAP of teeth, lead has the potential to translocate with Ca + 2 and resulting in decreasing the size of hydroxyapatite crystals [72].

In the atmosphere or diet, lead is passed to body hard tissues such as teeth and might be having an effect on increasing dental caries. Furthermore, it has been discovered that lead promotes the development of enamel hypoplasia. As per the literature, it shows have a probable connection between increasing lead levels in saliva and the formation of dental caries in children with early tooth decay. As a result, lead is critical in the formation of new caries lesions [4, 72, 73].

#### **5.10 Iron (Fe)**

Iron (Fe) is abundant in nature and a biologically important part of all living organisms, unlike other TE. Regardless of geological abundance, when oxygen comes into contact with iron, it forms hardly soluble oxides. As a result, it is poorly absorbed by species [74].

Iron is found in liver, beef, poultry products, and fish, as well as cereals, green leafy vegetables, pulses, nuts, oilseeds, and dried fruits. Iron, as an important nutrient, is primarily absorbed by green vegetables. Enamel has been found to have low iron concentrations [75]. RDA ranges from 4 to 5 gm and is essential to maintain a healthy body.

#### **6. Detection of trace elements and assessment of nutritional status**

This was done as follows:


*Fluoride and Other Trace Elements in Dental Hard Tissue DOI: http://dx.doi.org/10.5772/intechopen.102043*


#### **7. Sources of trace elements**

The location of trace elements on dental hard tissue like enamel and dentin may differ and also within the structure. The Cu, Pb, Co, Al, I, Sr., Se, Ni, and Mn more on enamel whereas Fe and F more on dentin and cementum.

Also, within the enamel, the outer surface has more Iron, Lead, and Manganese than inside layers suggesting that mostly these come from the external environment and get deposited on tooth enamel after an eruption or during calcification.

Trace elements can reach the human body through a variety of routes, including food, water, and air. Dental materials and fluids (such as saliva, dental prosthesis, and dental porcelain) are discussed below as potential sources of trace elements in tooth enamel [81].


in tooth enamel were found to be closely associated. This finding suggests that dental porcelain may be another potential source of these elements in tooth enamel but need to confirm with future studies.

#### **8. Conclusion**

Though trace elements are only needed in trace amounts, their optimal presence is critical for the body's normal physiological functioning and for upholding the body's biodynamics. Excess and deficiency both contribute to the onset, development, and promotion of different disease processes. As a result, having a thorough understanding of these trace elements is critical for disease prevention and optimum health.

Nutritional and clinical diagnosis of trace element defects is one of the most daunting activities. Deficient intake of an important trace element can cause significant biological functions within tissues to be harmed, and restoring physiological levels of that element can restore or prevent that function from being harmed. The amount of main trace metals circulating in the blood and deposited in cells is controlled and regulated by an intricate mechanism in the human body. When the body fails to function properly or there are inappropriate levels in dietary sources, excessive levels of these trace elements may develop. A diet rich in antioxidants and essential minerals is essential for a healthy mind and body, according to numerous lines of proof. In recent years, preventive medicine has gotten more coverage than anything else, as the adage goes, "prevention is better than cure." Oral and general health are inextricably linked, and the oral cavity can effectively reflect systemic health. Oral diseases such as oral leukoplakia, oral submucous fibrosis, oral cancer, and others have been treated with a mixture of micronutrients and trace elements because their combined effect is more effective than a single application. As a result, general and oral healthcare professionals must be familiar with the clinical aspects of trace elements.

#### **Author details**

Y.B. Aswini\*, Vikrant Mohanty and Kavita Rijhwani Department of Public Health Dentistry, Maulana Azad Institute of Dental Sciences, New Delhi

\*Address all correspondence to: phdaswini@gmail.com

© 2022 The Author(s). Licensee IntechOpen. 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.

*Fluoride and Other Trace Elements in Dental Hard Tissue DOI: http://dx.doi.org/10.5772/intechopen.102043*

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#### **Chapter 3**

## Developmental Dental Defects and Tooth Wear: Pathological Processes Relationship

*Francesco Grande and Santo Catapano*

#### **Abstract**

Many conditions or pathologies can modify teeth surfaces and cause several functional and esthetic problems. Congenital dental defects and tooth wear are two of the most important reasons of dental tissue changes. Nowadays, the prevalence of tooth wear is increasing because of a high incidence of non-physiological tooth wear especially in young people. However, distinguishing dental defects originated from tooth wear or developmental dental defects is crucial to plan the most suitable treatment. Then the aim of this work is to present the different pathological conditions caused by these two etiological factors as well as the underlying biochemical mechanisms and incorrect habits related.

**Keywords:** tooth wear, amelogenesis imperfecta, dentinogenesis imperfecta, attrition, abrasion, erosion, abfraction

#### **1. Introduction**

Many conditions or pathologies can modify teeth surfaces and cause several functional and esthetic problems to the dental patient. They could be divided in:


Congenital dental defects include pathologies as amelogenesis imperfecta, dentinogenesis imperfecta and molar-incisor hypomineralization.

On the other side, dental caries, occlusal trauma and tooth wear are recognized as the most important reasons of dental tissue changes, concerning acquired dental defects. However, tooth wear has always been underrated and less considered than dental caries and trauma [1, 2]. Also congenital dental defects are little considered because of the lower prevalence in the population then dental caries although there is a clear association between some types of developmental defects and dental caries in primary dentition [3].

Regarding tooth wear, today the common opinion of dental clinicians is that the prevalence of tooth wear is increasing, because of a high incidence of nonphysiological tooth wear and this is confirmed by important surveys [4, 5]. Also the prevalence of extensive wear is thought to increase, especially erosive tooth wear at young age [6].

Regarding congenital dental defects, the comprehension of genetic and environmental influences on enamel and dentine development are considered crucial for preventive actions and treatment planning of these conditions [7].

With the increased life expectancy and augmented frequency of oral hygiene procedures, problems related with tooth wear and congenital teeth defects are likely to place greater demands upon dental clinicians.

Then, in order to face that, it is important to understand the pathological mechanisms underlying developmental dental defects and dental wear and what biochemical processes and incorrect habits are involved in these conditions.

#### **2. Congenital dental defects**

Congenital dental defects are due to inherited or spontaneous genetic or epigenetic mutations that influence specialized cellular and biochemical pathways involved in dental hard tissue formation [8]. Local or systemic defects depend on where affected genes are expressed [9, 10].

However, these conditions are also caused by environmental factors such as drugs, infections, nutritional deficiencies, medical conditions or trauma [7]. Clinical importance of these defects is related to the risk of tooth decay, especially in respect of biofilm retention [11]. In addition, problems in restorative treatment because of the effectiveness of the materials and cements used for patient rehabilitation could be present.

#### **2.1 Developmental enamel defects**

Developmental enamel defects are mostly due to mutations in genes that code for enamel proteins. Generalized systemic conditions may also be present and could involve neuroectodermal mesenchyme tissues, that share common embryologic origins with enamel and dentin [12]. Otherwise, they could be induced by some pre-, peri- and postnatal factors.

Clinically, enamel abnormalities due to gene mutations are grouped under the name of amelogenesis imperfecta (AI) [7] and can be clinically divided into qualitative and quantitative defects. Qualitative defects differ from quantitative ones because they are characterized by the presence of normal amounts of enamel that is deficiently mineralized while quantitative defects are referred to enamel quantity.

Hypoplasia is a quantitative reduction of enamel formation due to disruption in ameloblast production. It can affect both the primary and permanent teeth [13]. The etiology of hypoplasia is related to insults occurring during the earliest stages of enamel development (matrix formation) [14]. It causes pits, grooves, thin or missing enamel, dental surface breaks and deficiencies.

Hypomineralization is a qualitative defect due to insults occurring in the calcification process. The resulting reduced mineralization could be recognized as soft enamel. When an altered translucency or opacity affects the entire tooth, or a localized area we can also talk of hypomaturation [12]. In case of hypomaturation and/or hypomineralization, enamel could fracture easily under loading [15] and this could result in severe tooth wear.

In the field of hypomineralization defects, a peculiar type of chronological enamel hypomineralization is the molar-incisor hypomineralization (MIH). It determines well demarcated opaque areas on the surface of permanent molars and incisors that could be colored from white to yellow or brownish, depending on the severity of the pathology [16]. In these cases, teeth often show enamel disintegration at the occlusal surfaces, post eruptive tooth structure loss and high

#### *Developmental Dental Defects and Tooth Wear: Pathological Processes Relationship DOI: http://dx.doi.org/10.5772/intechopen.99420*

caries susceptibility. Tooth sensitivity could also be present because of the porous prismatic enamel morphology [17]. This condition may predispose to tooth wear due to attrition between teeth and it can be aggravated in presence of other factors as abrasion and erosion. The severity of the clinical status may require extensive treatment [18–20].

Systemic factors affecting enamel development may also be distinguished in pre-, peri- and postnatal conditions in relation to the timing of the event [18] and could be caused by metabolic disturbances, drugs consumption, local infections, trauma and radiation [21, 22].

Amelogenesis defects may predispose to tooth sensitivity, plaque accumulation and increased caries risk, and in severe cases even space loss and malocclusion [23]. Also tooth wear can be associated to developmental enamel defects [7]. Infact, tooth wear could be a detrimental consequence of attrition between teeth in case of amelogenesis imperfecta and this may also cause the alteration of the normal occlusal pattern. Qualitative enamel defects may decrease the resistance of teeth both to erosion and abrasion because of the weak resistance to acid attacks and friction with foreign bodies. Furthermore, the augmented risk of dental caries and the porosity of enamel structure can enhance the process of tooth breakdown due to occlusal loading. Anterior open bite and increased calculus formation are commonly encountered in association to amelogenesis imperfecta [15] and could worsen the oral condition. Also tooth wear can be associated to developmental enamel defects.

#### **2.2 Developmental dentin defects**

Developmental dentin defects principally origin from mutations in genes coding for the proteins involved in type 1 collagen or in the extracellular matrix as well as in the mineralization processes. Defects may involve only dentine or both dentine and skeleton, if altered proteins are specific to dentine or expressed both in bone and dentine. These two types of clinical phenotype classified inherited dentine defects in the Shield's classification system [24].

Dentinogenesis imperfecta is the most common type of developmental disorder of dentine, affecting both primary and permanent teeth. It is sometimes associated with osteogenesis imperfecta [25]. When dentine and osseous defects are associated, there is a genetic fragile bone condition together with a reduced support of dentine that could show an opalescent brown discoloration. Lacking teeth support leads to easily fractures of the overlying enamel fractures as well as rapid wear and attrition of the teeth. Progressive pulp obliteration usually begins soon after eruption of the teeth and wear could arrive to the gingival level [7]. Dentine dysplasia is less common and shows normal appearing crowns with normal or short roots and pulp reduced in size. Occasionally, other abnormalities such as dental discolorations, bulbous crowns and pulp obliterations may be encountered [26].

Dentin developmental defects are highly expressed in familiar hypophosphatemia, also known as 'vitamin D-resistant rickets', an X-linked dominant inheritance condition [27]. This condition is associated with reduced resorption of phosphate in the renal tubules and characteristic rachitic bone deformities [28]. Spontaneous dental abscesses in children with no history of caries or trauma showing teeth involved in familial hypophosphatemia may occur [29]. Poorly mineralized dentine, and tubular defects extended closed to the dentino-enamel junction could predispose the pulp to exposures and infection as soon as the enamel is removed (superficial caries or attrition) [28, 30].

Because of the X-linked condition, boys are affected by the most severe dental involvement and girls the least. A wide range of spectrum manifestations has been described [26].

#### **3. Tooth wear mechanisms**

Tooth wear is defined as the progressive loss dental hard tissues from the surfaces of the teeth, caused by relative motion (friction) at the surface [1]. This type of wear includes attrition and abrasion, but also dental erosion and abfraction are nowadays included in this condition.

Tooth wear due to masticatory function is regarded as a natural phenomenon and a certain degree of tooth wear is considered unavoidable during age [31]. If the degree of destruction or the rate of loss becomes excessive, overcoming the physiological mechanisms of compensation (e.g. formation of secondary dentin), problems arise with the necessity of treatment [32]. It may cause functional and esthetic problems, dental sensitivity [1], or it could prejudice the survival of the teeth [2]. Wear could be critically pathological when it leads to poor masticatory function with concomitant reduction in quality of life and possible deterioration of systemic health [33].

The presence of developmental dental defects of enamel or dentine origin could enhance the process of tooth wear. In fact, decreased resistance in teeth with enamel and dentin abnormalities is a fact and the etiological mechanical and chemical processes of attrition, abrasion, erosion and abfraction may critically reduce the survival rate of teeth with developmental dental defects.

Then, understanding and recognizing the disruptive processes of tooth wear and if it hides possible developmental dental defects is necessary to prevent and treat several dental pathologies as worn dentition.

#### **3.1 Attrition**

Attritional is defined as the loss of tooth tissue due to friction between opposing teeth and is thus related to dental occlusion. The progressive tooth substance loss (TSL) is considered by Berry and Poole [31] a normal aging process, in which formation of secondary dentine, muscle adaptation, alveolar growth and attrition are all part of a compensation mechanism. In this view, attrition, as a normal process of changing dental morphology, should not be regarded as excessive. However, the loss of tooth tissue usually affects the dental occlusion, and it is still controversial the fact of ignoring a changing occlusion in the management of dental problems such as 'extensive' attrition or temporomandibular disorders. For these reasons and because of different assessment criteria, the exact prevalence of attrition is unclear [1, 2].

The literature on attrition does not provide clear evidence for the efficacy of particular occlusal designs in the management of attrition [34, 35]. Some crosssectional studies [36, 37] indicate that anterior (spatial) relationships and attrition were related. As expected, anterior guidance, which is partially determined by vertical overbite and horizontal overjet, seems to reduce the risk for posterior attrition, but increases the risk for anterior attrition. Canine protection, that ensures anterior guidance, may reduce the posterior tooth substance loss but only one study tried to demonstrate it [37]. Absent posterior support did not necessarily lead to increased attrition of the remaining teeth, whereas a reduced number of teeth may lead to increased wear of the remaining teeth [38].

In dentinogenesis imperfecta, attrition is deleterious. As reported in literature, the reduced support of dentine due to genetic condition leads to easily fractures of the overlying enamel and to a progressively rapid tooth wear caused by attrition [7].

For this reason, attrition is very common in dentinogenesis imperfecta and have to be considered as one of the most important factors of tooth wear.

Attrition in patients with amelogenesis imperfecta may result in widespread exposed dentin both in primary and in permanent teeth. Deficiencies in enamel attachment to dentin and defective enamel structure take part in the process of

#### *Developmental Dental Defects and Tooth Wear: Pathological Processes Relationship DOI: http://dx.doi.org/10.5772/intechopen.99420*

tooth wear, that could be faster and result in dentoalveolar abnormalities because of the continuous eruption of teeth [39].

In Molar-incisor hypomineralization (MIH), tooth substance loss could be enhanced due to attrition mechanisms [40]. MIH complicated with tooth substance loss may not only compromise the esthetics and function but also endanger the pulp and longevity of the affected teeth. Tooth substance loss might be complicated by eruption of the teeth with its dentoalveolar processes which obliterate the space for any restorations [41].

Attention in these patients should also be placed when a prosthetic restoration is performed on the antagonist tooth because of the possible increased wear. The material choice is fundamental regarding mechanical properties, hardness and patient occlusion scheme, and the prosthetic restoration of the antagonist with the same material could be considered.

Attrition may be accelerated by "demastication", intended as a tooth wear process occurring during mastication of food influenced by the abrasiveness of the individual food particles [42, 43]. High levels of inorganic compounds and salts were found in snuff by Dahl et al. [44] while silica abrasive particles were also discovered in tobacco chewing by Bowles et al. [45].

Despite the possible augmented tooth substance loss because of the food particles abrasiveness, a restorative rehabilitation of the patient with developmental dental defects is important also for reestablish an appropriate food intake. In fact, the tooth wear and pain disturbances evoked by some types of food may altered patient's alimentary habits, avoiding the consumption of some important nutrients [46, 47].

Some parafunctional habits (bruxism and clenching) may contribute to attrition [1, 48]. One study concluded that excessive forceful grinding during ongoing sleep bruxism events may cause canine attrition (**Figure 1**) [49]. While the prevalence of bruxism is unclear, studies report between 5–96% of the population may be affected [1]. Its prevalence on population with developmental dental defects is not reported in literature but considering the weakness of the tooth tissues in these patients, it could be responsible of a severely worn dentition in young age [50]. Night bruxism and clenching are detrimental and a thorough dental and muscular examination has to be carried out to identify signs of bruxism and clenching in order to avoid major dental destruction. A misdiagnosis may involve future complex oral rehabilitations in order to treat patients with developmental dental defects and severe worn dentition [50].

#### **3.2 Dental abrasion**

Dental abrasion is defined as the loss of tooth substance due to friction with food and foreign body (e.g. toothbrush) and may obliterate attrition wear patterns

**Figure 1.** *A case of teeth attrition caused by bruxism.*

caused by friction of opposing teeth [51]. Some types of dental abrasion may be related to habit or occupation [1, 2, 52]. Notching of incisal edges may be caused by pipe smoking, nut and seed cracking, nail biting, and hairpin biting [51, 53].

The etiology may also be deduced from the location and pattern of abrasion [52, 54]. The most common cause of dental abrasion can be found at the cervical areas and is related to toothbrushing. The technique applied, the time and frequency, the bristle design, and also the dentifrice used during toothbrushing can strongly influence this pattern [1, 48, 52]. A zealous, vigorous and repeated toothbrushing as well the use of toothbrush with not rounded tips of the bristles and abrasive dentifrice, could lead to an important dental abrasion.

In literature studies, premolars were more frequently affected with lesions varying from wedge-shaped and dish-shaped to flattened irregular and concave, with several depth and size (**Figures 2** and **3**) [55]. Data analysis revealed that vigorous toothbrushing is the major etiologic factor [56–60].

In patients with developmental dental defects, it is important to place a strong emphasis on an adequate oral home-care regimen. Education of the patient and parent guardian on an adequate tooth brushing technique and recommended oral

**Figure 2.** *Mild abrasion in canine and premolar teeth.*

**Figure 3.** *Severe abrasion and abfraction lesions of the first and fourth quadrant teeth.*

#### *Developmental Dental Defects and Tooth Wear: Pathological Processes Relationship DOI: http://dx.doi.org/10.5772/intechopen.99420*

hygiene habits is required. Pitted enamel surfaces and roughness of teeth especially in amelogenesis imperfecta may predispose plaque accumulation and augmented susceptibility to dental caries. Oral hygiene could be poor in some patients, often because of tooth hypersensitivity and the presence of an anterior open bite associated with mouth breathing [61]. Patients have to be informed regarding their situation and instruct to maintain correct oral hygiene habitudes.

Motivation to home oral hygiene instructions is important not only for the health of hard dental tissues but also for the soft gingival tissues. Restorative procedures are usually performed in patients suffering of enamel and dentine defects. Then, teeth surfaces may retain more plaque and gingival hyperplasia can be expressed near restorations.

Dental abrasion is principally associated with horizontal brushing technique [56], but also with brush stiffness [62, 63], dentifrice abrasiveness [57, 58] and age [64, 65]. It was observed that hard bristles caused the least amount of tooth abrasion while soft bristles caused the most amount of abrasion, because of the major retention of toothpaste offered by smaller diameter filaments and denser tufts [66, 67].

Although studies show a strong association of cervical abrasions to toothbrushing, some authors affirm that dental erosion plays a great role in this tooth wear [1, 48, 63]. Experiments show that an interval of 1-hour should be considered before toothbrushing after an acid attack, in order to allow a period of remineralization necessary for improving the resistance of eroded enamel against brushing abrasion [68, 69]. Seong et al. [70] observed that enamel repair commences within 2 hours following an acidic attack and is completed 4–24 hours later. Then it could be concluded that the enamel repair process is relatively slow, exposing to high risk of tooth wear mediated by erosion/abrasion. In this context, patients with developmental dental defects and especially with enamel hypomineralization should have particular attention to avoid toothbrushing after eating acid foods and drinks. In this context, two mechanisms could accelerate tooth wear: the increased demineralization after an acid attack due to the enamel matrix hypomineralization and the reduced rate of remineralization caused by the alteration of the enamel matrix [14].

Obviously, the amount of saliva produced by each patient is one of the most important protective factors to avoid erosion of tooth structure. An appropriate evaluation of salivary rate production should be performed in this sense.

Dental hypersensitivity related to cervical abrasion and exposure of dentin to the oral environment may be possible and generally more frequent than in other populations [71].

#### **3.3 Dental erosion**

Erosion is known as the dissolution of the surface of an object by means of fluids. Dental erosion is always caused by acid dissolving hard tooth tissues [72] and has been defined as the irreversible loss of dental hard tissue caused by a chemical process not involving bacteria (**Figure 4**) [43].

A general trend of increasing tooth wear by acid erosion in particular, amongst the young people, was highlighted by several authors [73–75]. In particular, young women (15–25 years old) are often affected by psychosomatic eating disorders [76].

These phenomena often clinically overlap with other clinical pathologies such as abrasion and attrition (**Figure 5**). This could lead to a difficult differentiation, especially at the initial stages. However, as the degree of erosion increases, a more suitable differential diagnosis can be performed. It is very important to establish if dental erosion underlines any developmental dental defect that may contribute to the pathologic condition observed. And it is already fundamental to understand what type of developmental defects may affect the dentition similarly or in addition

**Figure 4.** *Occlusal erosion of molar teeth.*

**Figure 5.** *Increased tooth wear of mandibular teeth cause by a combination of attrition and erosion.*

to acid erosion. Sometimes, it could be difficult to distinguish if teeth with missing enamel and dental surface breaks are affected by hypoplasia, that is a quantitative reduction of enamel formation or by acids consumption. Erosion mediated by acids may also be undistinguished from enamel hypomaturation, when diffused opacities are observed. Then, the area of the opacities or structure deficiencies must be carefully observed and all the mouth have to be analyzed to understand if those defects are localized in only a part of the mouth or widespread. A correct anamnesis of the patient must also be performed regarding diet habits, gastrointestinal pathologies or drugs assumption. Dietary analysis and advice regarding erosion and sugars are fundamental to reduce further problems in teeth affected by amelogenesis imperfecta [77]. Conversely, children with AI and DI will often avoid ice cream and fridge-cold products because of the hypersensitivity and this constitute a protective factor. However, a lot of other cariogenic or acidic products may be responsible for erosion processes.

In the advanced state, the erosion can extend into dentin. The level of painful hypersensitivities as well as the esthetic or functional limitations are generally related to the extension of the erosion, although sometimes an individual component for dentin hypersensitivity may exacerbate this phenomenon. Also in this case, poorly mineralized dentine, and tubular defects in dentinogenesis imperfecta may express as extensive tooth wear, similarly to advanced case of erosion with similar hypersensitivity.

*Developmental Dental Defects and Tooth Wear: Pathological Processes Relationship DOI: http://dx.doi.org/10.5772/intechopen.99420*

From an etiologic point of view, erosive defects can be distinguished in endogenous and exogenous. The consumption of acidic food and drugs, as well as occupational acid exposure such as wine tasters and professional swimmers, are considered extrinsic exposures [78]. Instead, intrinsic erosion is intended when gastric fluids come into contact with the oral cavity, especially in patients suffering of gastrointestinal reflux disease, eating disorders, and/or alcohol abuse [79].

Usually, a palatal and occlusal localization of the erosion defects is due to an intrinsic erosion, while an extrinsic erosion affects the labial surfaces of the anterior teeth [80]. Both types of erosion produce deleterious effects on dental elements, with a pattern of destruction dependent on the erosivity of the erosion-causing solution (pH, buffer capacity, and mineral concentration), and also on the frequency and type of acid exposure. However, as gastric fluid is evaluated as 1 in the pH scale and is provided with a high amount of free acid, its erosive potential is higher than that of extrinsic acids [81]. Moreover, patients with eating disorders often show xerostomia because of the lower salivary flow rate caused by the general dehydration or by the antidepressant drugs, which could further increase the risk of developing erosive lesions.

#### **3.4 Abfraction**

Abfraction or Non Carious Cervical Lesions (NCCL) have been used to describe wedge shaped cervical lesions as a wear defect [82]. It is recognized as the loss of cervical tooth tissues induced by mechanical loading which led to enamel and dentin flexure and failure [83]. Some biomechanical analyses show that the most important area of stress concentration is located at the cervical areas of the teeth in response to overloading, that leads to initiation of a cervical lesion [84, 85].

Another study, using FEM, suggested that oblique loading on the tooth stretches the enamel surface near the cemento-enamel junction causing plastic deformation at the cervical area [86]. It was seen that lateral forces produce compressive stresses on the side toward which the tooth bends and the tensile stresses are on the other side. These stresses create microfractures at the cervical region which propagate perpendicularly to the long axis of the tooth, leading to a localized defect around the CEJ [87]. The tensile forces could disrupt the hydroxyapatite (HA) crystals of the enamel structure, allowing saliva and other small molecules to penetrate between the prisms and prevent re-establishment of the interprismatic bonds on release of the stress (**Figure 6**). Ultimately, when the enamel breaks away at the cervical margin and exposes the dentin, the process continues in this way and may accelerate because of the structure of the dentin [82].

Cervical lesions depend on type and severity of the etiologic factor, and not all these lesions require restorations. They appear primarily at the cervical region of the dentition and are typically wedge-shaped, with sharp internal and external line angles [55].

Treatment planning of non carious cervical lesions is based on the reduction of stress concentration in order to strengthen the tooth, the prevention of dentin hypersensitivity with major pulp protection and the modification of oral hygiene habits, improving also the esthetics [82]. Composites and glass ionomer restorations can be adopted if lesions are not too much extended. On the other hand, metal crowns can be used where the masticatory load is higher. In order to treat hypersensitivity, dentin bonding agents, fluoride varnishes and other desensitizing agents may be useful. Gnatologic devices also can be fabricated to protect teeth during night, however changing of dietary and oral habits is mandatory [88, 89].

**Figure 6.** *Abfraction lesions associated with moderate tooth wear.*

#### **4. Diagnosis and management of patients with developmental dental defects and tooth wear**

Tooth wear is multifactorial in origin [51]. The major factors responsible for tooth wear should be identified starting from a correct and thorough anamnesis of the patient in order to establish a predictable treatment plan. Several signs may result useful in the differential diagnosis process and the appearance of worn tooth surfaces resulting from the various types of wear differ. In order to make a correct diagnosis of the etiology of tooth wear it is fundamental not only to observe the wear pattern but also to investigate if any erosive or abrasive factor is present in the anamnesis. However, if a clear etiological factor is not find, the observed tooth wear may be due to the mechanical type. However, identification and recognition of developmental dental defects is of extreme importance (**Table 1**) [23, 94]. In fact, early diagnosis and preventive care are essential for the successful treatment of developmental dental defects. Children with a family history of amelogenesis or dentinogenesis imperfecta, or medical syndromes commonly associated with them such as prematurity of birth or hypophosphatemia should be assessed for developmental dental defects as soon as the teeth erupt. Defects in primary teeth may possibly indicate a risk also for permanent dentition [7].

For children with developmental dental defects, a preventive program should be instituted immediately after diagnosis. Neutral sodium fluoride gels or varnishes professional applications every 3/6 months, in addition with calcium and phosphate rich agents (casein phosphopeptide-amorphous calcium phosphate, CPP-ACP) are recommended to reduce caries risk and developmental opacities in teeth with enamel hypoplasia [95]. Because of the structural weakness of the teeth with developmental dental defects, other important recommendations are the same as erosive protection advices such as reduced consumption of acidic food, diet and soft drinks, control of eventual psychosomatic disorders, because of the possibility of frequent vomiting [90]. It is also important to consider that the risk of erosive lesions is increased when acid or soft drinks are assumed by children from a feeding bottle at bed- or nap-time, because of the lower salivary flow rate during sleep [96]. Furthermore, several drinking habits (sips drinking, use of a straw in direct contact with teeth, and intensive rinsing) cause a prolonged pH drop in the oral

*Developmental Dental Defects and Tooth Wear: Pathological Processes Relationship DOI: http://dx.doi.org/10.5772/intechopen.99420*


#### **Table 1.**

*Summary table of the etiology, clinical signs and preventive and therapeutic options of developmental dental defects and tooth wear conditions. Clinicians must consider possible associations between these two pathological entities.*

cavity compared to a short consumption [97]. Then, patients should restrict the consumption of acidic food and drinks only to main meals. Acidic beverages should be consumed cool and as fast as possible in order to reduce their erosivity. Some foods as yogurts that have high concentrations of calcium and phosphate, result non-erosive despite their low pH [91].

When tooth wear is already present, the treatment planning in children with extensive enamel defects due to may involve complex restorations, orthodontics, exodontia and prosthodontics [77].

Normally, without any developmental dental defects, the treatment planning depends on the severity of tooth wear. The amount of tooth wear necessary for intervention is not clear from the scientific literature, even if with the Smith and Knight index [98], the threshold to start restorative treatment is set once dentine was involved. A recent paper summarizes when it is recommended a restorative treatment [99]. Another paper indicates several techniques and treatment strategies for tooth wear, clearly distinguishing between pathological and physiological tooth wear; it is also highlighted that dentist has to detect the speed and severity of tooth wear process in order to decide when intervening [100]. However, difficulties in detecting a pathological dental loss at early stages differently from physiological loss, is challenging for the dentist. A complicating factor is also that tooth wear may be cyclical and can be inactive in the majority of the patients, despite obvious wear facets in their dentitions [101].

However, in developmental dental defects, because the structural weakness of the hard tissues leads to its readily deterioration under masticatory stresses

and both amelogenesis and dentinogenesis imperfecta are associated with rapid toothwear and crown fractures, protection from toothwear is recommended soon after eruption [102]. Ideally, restorative stabilization of the dentition should be completed before excessive wear and loss of vertical dimension occur [103]. Guidelines for the treatment of developmental dental anomalies have been established by AAPD (American Academy of Pediatric Dentistry) [104]. For developmental enamel defects, treatment should begin as soon as possible according to patient compliance in office dental care. Early identification and preventive interventions are critical for infants and children with enamel defects due to amelogenesis imperfecta in order to avoid the negative social and functional consequences of the disorder. The appearance, quality, and amount of affected enamel and dentin will dictate the type of restorations necessary to achieve esthetic, masticatory, and functional health. Depending on the severity of enamel defects and tooth wear, treatment can range from bleaching and/or microabrasion [92] to composite resin, porcelain veneers [105] or full coverage restorations with crowns placement [39].

Treatment of dentinogenesis imperfecta frequently includes preventing severe attrition associated with enamel loss and rapid wear of the poorly mineralized dentin, rehabilitating dentitions that have undergone severe wear, optimizing esthetics, and preventing caries and periodontal disease [104].

Stainless steel crowns are a highly durable restoration choice for the prophylactic coverage of teeth affect by developmental dental defects. In teeth with dentine defects, they reduce the risk of pulp exposure and infection, especially in some types of dentine defects (hypophosphatemia) [28]. Fluoride applications and desensitizing agents may also diminish tooth sensitivity [106]. In teeth affected by enamel hypoplasia both primary and permanent molars show a reduction in tooth sensitivity and in cusp fractures after prosthetic rehabilitation with stainless teel crowns. This also helps to maintain space and crown height, important also for orthodontic issues. The crowns are best inserted using a conservative technique, originally proposed by Seow, that involves a minimal removal of tooth structure in order to protect teeth with large pulps and dentin defects [28, 107]. In adulthood, the stainless steel crowns may be replaced with gold or porcelain crowns to provide long term protection of the teeth.

It should also be considered that marginal leakage around restorations and recurrent caries with eventual pulp involvement may be determined from the enamel deterioration [108, 109]. Materials as resin modified glass-ionomer cements and polyacid modified composites should be used for restoring teeth affected by enamel defects in order to take advantage of the optimal bonding of these material with both dentine and enamel [110]. However, despite their esthetic value, composite resins have low adhesion to poorly mineralized enamel. Then, it is important to consider the amount of tooth wear in order to proceed with conservative or prosthetic rehabilitation.

In cases with significant loss of vertical dimension because of tooth wear, the reestablishment of a more normal vertical dimension is crucial for a correct function, mastication and esthetics. Cases showing severe loss of coronal tooth structure and vertical dimension have to be considered candidates for overdenture therapy. Overlay dentures placed on teeth that are covered with fluoride-releasing glass ionomer cement have also been used with success [111].

#### **Conflict of interest**

The authors declare no conflict of interest.

*Developmental Dental Defects and Tooth Wear: Pathological Processes Relationship DOI: http://dx.doi.org/10.5772/intechopen.99420*

#### **Author details**

Francesco Grande\* and Santo Catapano Dental School, Dental Clinic, University of Ferrara, Ferrara, Italy

\*Address all correspondence to: francesco.grande90@gmail.com

© 2021 The Author(s). Licensee IntechOpen. 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.

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### Section 2
