**2.2 Oral microbiota on the surface of teeth**

Dental plaque consists of microorganisms producing a complex matrix composed of extracellular products of microorganisms and salivary components. Bacteria isolated from supragingival plaques include mostly Gram-positive, facultatively anaerobic species, particularly streptococci, and members of the genus *Actinomyces.* Bacteria of the genera *Veillonella*, *Haemophilus* and *Bacterioides* are usually isolated from deeper layers.

Formation of the dental plaque can be divided to several stages: formation of pellicle, initial bacterial adhesion, bacterial colonisation and plaque maturation and finally its mineralisation and calcification (**Figures 2** and **3**), i.e., formation of dental calculus (*calculus dentis*) [9].

Some bacteria are able to adhere to the tooth surface and by their factors of virulence and metabolic products are capable of causing dental caries or other bacterial diseases of additional parts of the oral cavity [15]. After disturbance of the balance between the original microbiota and the propagated potentially pathogenic microorganisms, various diseases frequently occur in the oral cavity. Therefore, these microorganisms may exhibit some pathogenicity, but only under certain conditions, and therefore, we refer to them as facultative or opportunistic pathogens [16]. From the surface of teeth, we may isolate *Streptococcus sanguis*, *Streptococcus mutans* and bacteria of the genera *Neisseria*, *Haemophilus*, *Lactobacillus*, *Propionibacterium*, *Actinomyces*, *Leptotrichia*, *Fusobacterium*, *Veillonella*, *Bacteroides* and *Bacterionema*, described in **Table 1**.

**283**

**Figure 3.**

**Table 1.**

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

*Deposit of dental calculus on the lingual area of teeth in the mandible.*

*Actinomyces viscosus Propionibacterium* spp. *Lactobacillus* spp. *Actinomyces israelii Actinomyces naeslundii Nocardia* spp. *Rothia dentocariosa Peptostreptococcus Actinomyces israelii Veillonella* spp. *Fusobacterium* spp. *Leptotrichia* spp. *Prevotella oralis Actinomyces odontolyticus*

**2.3 Oral microbiota of the tongue**

*Oral microbiota on the surface of teeth.*

Teeth surface *Prevotella buccalis*

**2.4 Oral microbiota of the saliva**

resembles that of the tongue (**Tables 2** and **3**).

From the tongue, there was isolated particularly *Streptococcus salivarius,* while *Streptococcus mutans* and *Streptococcus sanguis* appeared in the oral cavity only after eruption of teeth [17]. The tongue may become a reservoir of microorganisms participating in periodontal diseases. Bacteria that occur in the saliva may originate from various parts of the oral cavity and the microbial composition of saliva

**Anaerobic microorganisms Aerobic microorganisms**

*Neisseria* spp. *Protozoa*

*Streptococcus mutans*

*Mycoplasma* spp. *Streptococcus sanguis*

*Aggregatibacter Actinomycetemcomitans*

Free fluoride ions, found in the saliva in concentrations ranging from 0.01 to 0.05 ppm, are an important factor of remineralisation of enamel [18]. Individual proportions of calcium, fluorine and phosphates indicate potential remineralisation effect of the saliva on the dental tissue. Saliva has a positive suppression effect on the development of dental caries. This effect results from the content of unsaturated ions of phosphates, fluorine and calcium while there is a continuous exchange of these ions between the tooth crown and the saliva. At neutral pH, a balance is established between enamel minerals and the saliva. When the action of organic

**Figure 2.** *Deposit of supragingival dental calculus on the vestibular area of teeth in the mandible.*

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

### **Figure 3.**

*Bacterial Biofilms*

**2.2 Oral microbiota on the surface of teeth**

usually isolated from deeper layers.

dental calculus (*calculus dentis*) [9].

*lentum*, *Propionibacterium acnes*, *Catonella* spp., *Johnsonella* spp., *Rothia dentocariosa*, *Actinomyces viscosus*, *Actinomyces odontolyticus*, *Actinomyces naeslundii*, *Capnocytophaga gingivalis*, *Capnocytophaga ochracea*, *Prevotella oralis*, *Prevotella denticola*, *Bacteroides melaninogenicus*, *Fusobacterium nucleatum*, *Eikenella corrodens*, *Wolinella* spp., *Campylobacter sputorum*, *Selenomonas sputigena*, *Treponema* spp., and *Leptotrichia* spp*., Granulicatella* spp. [13]. Of the more noteworthy representatives, one should mention parasitic protozoa *Entamoeba gingivalis* and *Trichomonas tenax* [14].

Dental plaque consists of microorganisms producing a complex matrix composed of extracellular products of microorganisms and salivary components. Bacteria isolated from supragingival plaques include mostly Gram-positive, facultatively anaerobic species, particularly streptococci, and members of the genus *Actinomyces.* Bacteria of the genera *Veillonella*, *Haemophilus* and *Bacterioides* are

Formation of the dental plaque can be divided to several stages: formation of pellicle, initial bacterial adhesion, bacterial colonisation and plaque maturation and finally its mineralisation and calcification (**Figures 2** and **3**), i.e., formation of

Some bacteria are able to adhere to the tooth surface and by their factors of virulence and metabolic products are capable of causing dental caries or other bacterial diseases of additional parts of the oral cavity [15]. After disturbance of the balance between the original microbiota and the propagated potentially pathogenic microorganisms, various diseases frequently occur in the oral cavity. Therefore, these microorganisms may exhibit some pathogenicity, but only under certain conditions, and therefore, we refer to them as facultative or opportunistic pathogens [16]. From the surface of teeth, we may isolate *Streptococcus sanguis*, *Streptococcus mutans* and bacteria of the genera *Neisseria*, *Haemophilus*, *Lactobacillus*, *Propionibacterium*, *Actinomyces*, *Leptotrichia*, *Fusobacterium*, *Veillonella*, *Bacteroides* and *Bacterionema*, described in **Table 1**.

*Deposit of supragingival dental calculus on the vestibular area of teeth in the mandible.*

**282**

**Figure 2.**

*Deposit of dental calculus on the lingual area of teeth in the mandible.*


### **Table 1.**

*Oral microbiota on the surface of teeth.*

### **2.3 Oral microbiota of the tongue**

From the tongue, there was isolated particularly *Streptococcus salivarius,* while *Streptococcus mutans* and *Streptococcus sanguis* appeared in the oral cavity only after eruption of teeth [17]. The tongue may become a reservoir of microorganisms participating in periodontal diseases. Bacteria that occur in the saliva may originate from various parts of the oral cavity and the microbial composition of saliva resembles that of the tongue (**Tables 2** and **3**).

### **2.4 Oral microbiota of the saliva**

Free fluoride ions, found in the saliva in concentrations ranging from 0.01 to 0.05 ppm, are an important factor of remineralisation of enamel [18]. Individual proportions of calcium, fluorine and phosphates indicate potential remineralisation effect of the saliva on the dental tissue. Saliva has a positive suppression effect on the development of dental caries. This effect results from the content of unsaturated ions of phosphates, fluorine and calcium while there is a continuous exchange of these ions between the tooth crown and the saliva. At neutral pH, a balance is established between enamel minerals and the saliva. When the action of organic

acids produced by bacteria disturbs this balance, pH in the oral cavity decreases and demineralisation of tooth surface occurs. Some components of the saliva neutralise the acidic environment and reduce the demineralisation rate and thus prevent the dental caries. This buffering capacity of the saliva is ensured by phosphate, bicarbonate and proteinaceous buffers [19].

Glycoprotein mucin acts as a lubricant of the oral cavity surface, produces a protective barrier against the external environment and, at the same time, facilitates chewing, swallowing and speech. It is one of the agglutination factors of the saliva that causes aggregation of bacteria. It can interact with *Streptococcus sanguis*, *Streptococcus mitis*, *Streptococcus gordonii*, *Aggregatibacter actinomycetemcomitans*, *Pseudomonas aeruginosa* and *Escherichia coli*. Saliva also contains other biologically active compounds, such as hormones, glucose, cholesterol, fatty acids and urea [20].

Microorganisms do not tolerate large variations in the level of pH. The pH in the oral cavity is close to neutral and ranges between 6.75 and 7.25. Saliva exhibits remineralisation abilities but the remineralisation process requires some time [21]. Increased frequency of easily metabolizable saccharides at the presence of plaques increases the risk of development of caries [22]. In this respect, saccharose plays a significant role as it easily diffuses into the plaque and is highly soluble [21]. Saccharides use microorganisms as a source of energy and a building material. Organic acids synthesised by microorganisms during metabolic processing of saccharides cause a decrease in the level of pH and a subsequent loss of minerals from the teeth surface [23].


### **Table 2.**

*Oral microbiota of the tongue.*


#### **Table 3.**

*Oral microbiota of the saliva.*

### **3. Oral cavity diseases**

A variety of diseases involve the oral cavity including dentition problems, maxillary and mandibular disorders and diseases, gingivitis, diseases of the tongue,

**285**

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

**3.1 Focal infection**

palate, internal mucosa and lips [24]. In the oral cavity, there are also salivary glands that fulfil very important functions within the digestive system and these paired glands may be afflicted with various inflammatory and noninflammatory diseases that can cause additional complications in the oral cavity [25]. Due to the diversity of anatomical structures and varied microbiota in the oral cavity, this part of the body can be affected by a great number of diseases such as tumour and benign diseases, inflammatory and noninflammatory and inherent or acquired diseases [22]. They are caused by infectious and noninfectious agents. The infectious agents include viruses, bacteria and fungi, and other may be caused by hormonal changes, systemic

diseases, hypersensitive responses, immunodeficiency states or tumours [11].

Focal infection of dentogenic origin is defined as a secondary or total infection caused by spreading of microorganisms to distant organs, while the primary infection is located in the tissues of apical and marginal periodontium. Oral focus is a focus of the chronic inflammatory process of primary infection localised in the tissues of the oral cavity, which is the source of infection. From the point of view of focal infection, the most serious etiological agents are *Streptococcus viridans*, *Streptococcus mitis*, *Streptococcus milleri* and *Streptococcus sanguis* [26]. As a matter of fact, this involves a numerous group of diseases or states that include also periodontitis or periodontitis marginalis. Focal infection is a focus from which the infection spreads to the entire organism and causes damage to tissues and organs [27]. In the course of several years, the opinion about the source of focal infection in the oral cavity gradually changed. In the past, mostly foci in the area of teeth roots, the so-called dead teeth, were considered the sources of focal infection [28]. Due to insufficient possibilities of treatment of root canals, many teeth were extracted [29]. Currently, this very practice is the subject of increasingly serious discussions within professional circles as a potential massive source of infection of an organism. Endodontics is a branch of dentistry dealing with diagnosis and treatment of pathological conditions of dental pulp and periapical tissues [30]. Endodontic treatment means the treatment of the dental pulp, in the majority of cases its complete removal and perfect filling of root canal using correct techniques and treatment procedures. The role of root filling is to close hermetically the entry to foramen apicale dentis and fill up completely the infection-free tooth canal [31]. Such treatment will prolong functionality and life of inflammation-affected teeth pillars. Imperfect removal of the infected tooth pulp or transfer of infection to the periapical space and incomplete

filling of the root canal turns such tooth into a source of focal infection.

anatomic conditions in this cavity.

*3.2.1 Dental pulp necrosis and gangrene*

**3.2 Sources of focal infection**

There are many foci in the oral cavity that can become potential sources of focal

odontogenic infection. Origin of these foci may be attributed to neglected care of the oral cavity, pathological action of some microorganisms or unfavourable

Dental pulp necrosis may develop after injury or as a result of degenerative processes in the dental pulp, and can be affected as a whole or only its part. The principal cause is a pronounced damage to vascular supply. Colliquative necrosis results in decomposition of the dental pulp tissue. At coagulation necrosis, the infected dental pulp produces fluid rich in proteins. Such condition may occur during preparation close to the dental pulp [22]. Dental pulp gangrene is a secondarily

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

palate, internal mucosa and lips [24]. In the oral cavity, there are also salivary glands that fulfil very important functions within the digestive system and these paired glands may be afflicted with various inflammatory and noninflammatory diseases that can cause additional complications in the oral cavity [25]. Due to the diversity of anatomical structures and varied microbiota in the oral cavity, this part of the body can be affected by a great number of diseases such as tumour and benign diseases, inflammatory and noninflammatory and inherent or acquired diseases [22]. They are caused by infectious and noninfectious agents. The infectious agents include viruses, bacteria and fungi, and other may be caused by hormonal changes, systemic diseases, hypersensitive responses, immunodeficiency states or tumours [11].

### **3.1 Focal infection**

*Bacterial Biofilms*

bonate and proteinaceous buffers [19].

**284**

**Table 3.**

**Table 2.**

*Oral microbiota of the saliva.*

*Oral microbiota of the tongue.*

**3. Oral cavity diseases**

**Microorganisms**

*Bacteroides (Bacteroides melaninogenicus)*

Tongue *Campylobacter (Campylobacter sputorum) Propionibacterium Actinomyces Veillonella*

> *Prevotella (Prevotella oralis) Peptostreptococcus*

> > *Streptococcus salivarius Actinomyces* spp. *Veillonella* spp. *Streptococcus sanguis Streptococcus mitior Lactobacillus* spp. *Streptococcus mutans*

A variety of diseases involve the oral cavity including dentition problems, maxillary and mandibular disorders and diseases, gingivitis, diseases of the tongue,

acids produced by bacteria disturbs this balance, pH in the oral cavity decreases and demineralisation of tooth surface occurs. Some components of the saliva neutralise the acidic environment and reduce the demineralisation rate and thus prevent the dental caries. This buffering capacity of the saliva is ensured by phosphate, bicar-

Glycoprotein mucin acts as a lubricant of the oral cavity surface, produces a protective barrier against the external environment and, at the same time, facilitates chewing, swallowing and speech. It is one of the agglutination factors of the saliva that causes aggregation of bacteria. It can interact with *Streptococcus sanguis*, *Streptococcus mitis*, *Streptococcus gordonii*, *Aggregatibacter actinomycetemcomitans*, *Pseudomonas aeruginosa* and *Escherichia coli*. Saliva also contains other biologically active compounds, such as hormones, glucose, cholesterol, fatty acids and urea [20]. Microorganisms do not tolerate large variations in the level of pH. The pH in the oral cavity is close to neutral and ranges between 6.75 and 7.25. Saliva exhibits remineralisation abilities but the remineralisation process requires some time [21]. Increased frequency of easily metabolizable saccharides at the presence of plaques increases the risk of development of caries [22]. In this respect, saccharose plays a significant role as it easily diffuses into the plaque and is highly soluble [21]. Saccharides use microorganisms as a source of energy and a building material. Organic acids synthesised by microorganisms during metabolic processing of saccharides cause a decrease in the

level of pH and a subsequent loss of minerals from the teeth surface [23].

**Anaerobic microorganisms Aerobic microorganisms**

*Streptococcus mitis Streptococcus salivarius Staphylococcus* spp. *Enterobacteriaceae Streptococcus sanguis Corynebacterium* spp.

*Micrococcus* spp. *Staphylococcus* spp. *Neisseriaceae*

*Candida* and other microscopic fungi

Saliva *Streptococcus milleri*

*Peptococcus*

Focal infection of dentogenic origin is defined as a secondary or total infection caused by spreading of microorganisms to distant organs, while the primary infection is located in the tissues of apical and marginal periodontium. Oral focus is a focus of the chronic inflammatory process of primary infection localised in the tissues of the oral cavity, which is the source of infection. From the point of view of focal infection, the most serious etiological agents are *Streptococcus viridans*, *Streptococcus mitis*, *Streptococcus milleri* and *Streptococcus sanguis* [26]. As a matter of fact, this involves a numerous group of diseases or states that include also periodontitis or periodontitis marginalis. Focal infection is a focus from which the infection spreads to the entire organism and causes damage to tissues and organs [27]. In the course of several years, the opinion about the source of focal infection in the oral cavity gradually changed. In the past, mostly foci in the area of teeth roots, the so-called dead teeth, were considered the sources of focal infection [28]. Due to insufficient possibilities of treatment of root canals, many teeth were extracted [29]. Currently, this very practice is the subject of increasingly serious discussions within professional circles as a potential massive source of infection of an organism. Endodontics is a branch of dentistry dealing with diagnosis and treatment of pathological conditions of dental pulp and periapical tissues [30]. Endodontic treatment means the treatment of the dental pulp, in the majority of cases its complete removal and perfect filling of root canal using correct techniques and treatment procedures.

The role of root filling is to close hermetically the entry to foramen apicale dentis and fill up completely the infection-free tooth canal [31]. Such treatment will prolong functionality and life of inflammation-affected teeth pillars. Imperfect removal of the infected tooth pulp or transfer of infection to the periapical space and incomplete filling of the root canal turns such tooth into a source of focal infection.

There are many foci in the oral cavity that can become potential sources of focal odontogenic infection. Origin of these foci may be attributed to neglected care of the oral cavity, pathological action of some microorganisms or unfavourable anatomic conditions in this cavity.

### **3.2 Sources of focal infection**

### *3.2.1 Dental pulp necrosis and gangrene*

Dental pulp necrosis may develop after injury or as a result of degenerative processes in the dental pulp, and can be affected as a whole or only its part. The principal cause is a pronounced damage to vascular supply. Colliquative necrosis results in decomposition of the dental pulp tissue. At coagulation necrosis, the infected dental pulp produces fluid rich in proteins. Such condition may occur during preparation close to the dental pulp [22]. Dental pulp gangrene is a secondarily altered necrosis that develops after infection of the necrotic pulp and can be of two types, dry or wet. Dry gangrene develops after partial infection of the necrotic pulp and the remnant pulp dries up. Wet gangrene is more frequent—it develops by the action of multiple microbiota from the carious dentin. Necrotic dental pulp tissue has a strong offensive smell due to accumulated gases such as skatole and indole [31].

### *3.2.2 Teeth with chronic dental pulp inflammation*

Chronic-closed dental pulp inflammations, *pulpitis chronica clausa* in Latin, occur frequently in teeth with caries that penetrated into the dental pulp. The consequence is a chronic abscess with clinically mutedental pulp. During preparation, small amount of pus or dark blood is sometimes discharged from the pulp cavity [22]. Chronic-closed dental pulp inflammations are also frequently clinically mute, and in such cases, the dental pulp shows fibrocystic or at atrophic changes.

The affected pulp tissue is prone to calcification or denticles. The residual pulp shows chronic inflammatory infiltration. Such condition may result in partial or complete obliteration of the root canal [28]. Internal granuloma (*pulpitis chronica granulomatosa interna*) is a chronic productive inflammation with typical finding of considerably hyperaemic granular tissue. A characteristic feature of this process is fibroblasts that form capillaries and cells of chronic inflammatory cellularization [32]. Injury is the most frequent cause of this type of chronic inflammation, also chronic traumatization of the tooth may contribute to damage to the dental pulp [33].

### *3.2.3 Teeth with periapical findings*

Inflammations in the periodontium region affect several types of tissues such as parts of the suspension apparatus of teeth, compacta, spongiosis of alveolar bone and root surface cementum. Such changes are collectively referred to as periodontitis [34]. The causes of periapical inflammation may include infections, chemical irritation and acute or chronic trauma. The most frequent cause of the development of periapical focus is necrotic, passively infected tooth pulp in the root canal. This way altered dental pulp contains compound microbiota with predominance of Gram-positive streptococci, but also enterococci, lactobacilli, *Candida* and *Neisseria* species and anaerobic bacteria such as *Fusobacteria* and *Bacteroides* [35]. Infection causes softening of the dentin wall of the root canal and the metabolic products of microorganisms induce inflammatory conditions in the periodontium region (**Figure 4**). The most frequent site of the development is the apex of the tooth root, but the inflammation process is observed also in the areas of lateral ramifications or sub-pulpal tooth canal. The inflammation is acute or primarily chronic, or chronic with acute exacerbation.

### *3.2.4 Periodontal abscesses*

Abscess is a collection of pus in a newly formed cavity. Periodontitis may be associated with development of periodontal abscesses [34]. They are divided into soft tissue and hard tissue abscesses. They manifest themselves by oedemas and pain, the more advanced forms also by the presence of yellowish pus. Retraction of gingiva may result in evacuation of pus. Bone abscess affects bone spongiosa and is manifested by intense strong pain upon tapping a tooth close to the abscess. Sometimes even shivers may occur and pus is not evacuated after retraction of gingiva [36]. Untreated bone abscess may result in sequestration of the affected bone, but this form is very rare [31].

**287**

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

*Periapical finding in tooth No. 34, X-ray - opg 2D image.*

*3.2.5 Periodontal pockets*

**Figure 4.**

*3.2.6 Gingivitis*

Periodontal pockets develop by extension of periodontal fissure, most frequently with approximal localisation. It can be located by one tooth but can affect all teeth in the maxilla and in the mandible. The periodontal pocket mostly contains subgingival dental plaque, subgingival dental calculus, dead microorganisms, leukocytes, proliferating nonspecific granular tissue and inflammatory exudate [37]. Periodontal pockets are classified as true, false, active and nonactive. The false periodontal pockets develop by enlargement of the marginal gingiva without shift of the dento-gingival connection, and the alveolar bone remains intact [11]. The true periodontal pockets are associated with resorption of the alveolar bone. The true periodontal pocket has been described as a space between the gingiva and tooth, coronary delimited by the edge of the marginal gingiva and apically delimited by the base of the periodontal pocket [38]. The difference between the true and false periodontal pockets is diagnosed by X-ray examination [22]. In the active pocket, one may find signs of inflammation, purulent exudations and postprobe haemorrhage. These active periodontal pockets require treatment. The nonactive pockets are free of marked findings. It suffices to carry out

regular monitoring of these quiescent forms of periodontal pockets [34].

are varied and can be divided to local and general [34].

Gingivitis is the most frequent microbial inflammation in the human body induced by microbiota of the dental plaque. It can occur as a constant symptom of periodontitis. According to its course, gingivitis may be classified as acute or chronic. Acute gingivitis is painful, the gingiva is red to red-violet and haemorrhage occurs upon stimulus but also spontaneously. Chronic gingivitis manifests itself by a red-pink colour, haemorrhage upon probing and stimulus-induced pain. The shape of the gingiva is altered and large false pockets are frequently observed. The causes

We recognise several types of acute gingivitis. Gingivae affected by gingivitis acuta simplex are slightly reddened while those affected by gingivitis catarrhalis acuta are hyperaemic and swollen. If this process is limited to one or two papillae, we refer to it as papilitis [37]. Gingivitis vesiculosa is manifested by production of vesicles with a clear content and reddened surrounding of vesicles. Gingivae affected by gingivitis pseudomembranosa are red, swollen, associated with production of pseudomembranes—this is fibrinous purulent inflammation. The most frequent form of gingivitis is ulcerous gingivitis that affects younger people [35]. The causes of this disease are many—weakened organism due to infectious disease, vitamin deficit, stress and drugs. The symptoms include swollen gums and the

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

**Figure 4.** *Periapical finding in tooth No. 34, X-ray - opg 2D image.*

### *3.2.5 Periodontal pockets*

*Bacterial Biofilms*

indole [31].

*3.2.2 Teeth with chronic dental pulp inflammation*

*3.2.3 Teeth with periapical findings*

with acute exacerbation.

*3.2.4 Periodontal abscesses*

bone, but this form is very rare [31].

altered necrosis that develops after infection of the necrotic pulp and can be of two types, dry or wet. Dry gangrene develops after partial infection of the necrotic pulp and the remnant pulp dries up. Wet gangrene is more frequent—it develops by the action of multiple microbiota from the carious dentin. Necrotic dental pulp tissue has a strong offensive smell due to accumulated gases such as skatole and

Chronic-closed dental pulp inflammations, *pulpitis chronica clausa* in Latin, occur frequently in teeth with caries that penetrated into the dental pulp. The consequence is a chronic abscess with clinically mutedental pulp. During preparation, small amount of pus or dark blood is sometimes discharged from the pulp cavity [22]. Chronic-closed dental pulp inflammations are also frequently clinically mute,

The affected pulp tissue is prone to calcification or denticles. The residual pulp shows chronic inflammatory infiltration. Such condition may result in partial or complete obliteration of the root canal [28]. Internal granuloma (*pulpitis chronica granulomatosa interna*) is a chronic productive inflammation with typical finding of considerably hyperaemic granular tissue. A characteristic feature of this process is fibroblasts that form capillaries and cells of chronic inflammatory cellularization [32]. Injury is the most frequent cause of this type of chronic inflammation, also chronic traumatization of the tooth may contribute to damage to the dental pulp [33].

Inflammations in the periodontium region affect several types of tissues such as parts of the suspension apparatus of teeth, compacta, spongiosis of alveolar bone and root surface cementum. Such changes are collectively referred to as periodontitis [34]. The causes of periapical inflammation may include infections, chemical irritation and acute or chronic trauma. The most frequent cause of the development of periapical focus is necrotic, passively infected tooth pulp in the root canal. This way altered dental pulp contains compound microbiota with predominance of Gram-positive streptococci, but also enterococci, lactobacilli, *Candida* and *Neisseria* species and anaerobic bacteria such as *Fusobacteria* and *Bacteroides* [35]. Infection causes softening of the dentin wall of the root canal and the metabolic products of microorganisms induce inflammatory conditions in the periodontium region (**Figure 4**). The most frequent site of the development is the apex of the tooth root, but the inflammation process is observed also in the areas of lateral ramifications or sub-pulpal tooth canal. The inflammation is acute or primarily chronic, or chronic

Abscess is a collection of pus in a newly formed cavity. Periodontitis may be associated with development of periodontal abscesses [34]. They are divided into soft tissue and hard tissue abscesses. They manifest themselves by oedemas and pain, the more advanced forms also by the presence of yellowish pus. Retraction of gingiva may result in evacuation of pus. Bone abscess affects bone spongiosa and is manifested by intense strong pain upon tapping a tooth close to the abscess. Sometimes even shivers may occur and pus is not evacuated after retraction of gingiva [36]. Untreated bone abscess may result in sequestration of the affected

and in such cases, the dental pulp shows fibrocystic or at atrophic changes.

**286**

Periodontal pockets develop by extension of periodontal fissure, most frequently with approximal localisation. It can be located by one tooth but can affect all teeth in the maxilla and in the mandible. The periodontal pocket mostly contains subgingival dental plaque, subgingival dental calculus, dead microorganisms, leukocytes, proliferating nonspecific granular tissue and inflammatory exudate [37]. Periodontal pockets are classified as true, false, active and nonactive. The false periodontal pockets develop by enlargement of the marginal gingiva without shift of the dento-gingival connection, and the alveolar bone remains intact [11]. The true periodontal pockets are associated with resorption of the alveolar bone. The true periodontal pocket has been described as a space between the gingiva and tooth, coronary delimited by the edge of the marginal gingiva and apically delimited by the base of the periodontal pocket [38]. The difference between the true and false periodontal pockets is diagnosed by X-ray examination [22]. In the active pocket, one may find signs of inflammation, purulent exudations and postprobe haemorrhage. These active periodontal pockets require treatment. The nonactive pockets are free of marked findings. It suffices to carry out regular monitoring of these quiescent forms of periodontal pockets [34].

### *3.2.6 Gingivitis*

Gingivitis is the most frequent microbial inflammation in the human body induced by microbiota of the dental plaque. It can occur as a constant symptom of periodontitis. According to its course, gingivitis may be classified as acute or chronic. Acute gingivitis is painful, the gingiva is red to red-violet and haemorrhage occurs upon stimulus but also spontaneously. Chronic gingivitis manifests itself by a red-pink colour, haemorrhage upon probing and stimulus-induced pain. The shape of the gingiva is altered and large false pockets are frequently observed. The causes are varied and can be divided to local and general [34].

We recognise several types of acute gingivitis. Gingivae affected by gingivitis acuta simplex are slightly reddened while those affected by gingivitis catarrhalis acuta are hyperaemic and swollen. If this process is limited to one or two papillae, we refer to it as papilitis [37]. Gingivitis vesiculosa is manifested by production of vesicles with a clear content and reddened surrounding of vesicles. Gingivae affected by gingivitis pseudomembranosa are red, swollen, associated with production of pseudomembranes—this is fibrinous purulent inflammation. The most frequent form of gingivitis is ulcerous gingivitis that affects younger people [35]. The causes of this disease are many—weakened organism due to infectious disease, vitamin deficit, stress and drugs. The symptoms include swollen gums and the

apexes of papillae truncated by necrosis. It is localised mostly in the zone of frontal teeth and molars [22]. Chronic gingivitis is classified as gingivitis cattarrhalis chronica, gingivitis gravidarum, gingivitis pubertalis, gingivitis scurbutica, gingivitis at epilepsies and leukaemia and elephantiasis fibromatosis gingivae [34].

## *3.2.7 Retained radices (radices relictae)*

This condition occurs in patients with neglected hygiene. If the crown portion of the tooth disintegrates due to untreated caries, the roots of teeth are retained in the gums. Failure to ensure timely treatment of root canal may result in infection of the root pulp and thus in potential dental focal infection [36].

### **3.3 Diseases of the lips-cheilitis**

Inflammation of lips extending to or beyond the border of lips can occur as acute or chronic. The factors most frequently involved in cheilitis are external factors. The currently known forms of cheilitis are actinic, angular, allergic, exfoliative, glandular and granulomatous [39].

Actinic cheilitis is referred to as solar cheilosis or solar keratosis of the lips that develops due to excessive exposure to UV radiation. It is localised in the lower lip in men and in the upper one in women. The risk group are fair-skinned (Caucasian) types of people. The clinical symptoms include dryness and scaliness of lips, their greyish colouration, swelling, ulceration, deepened folds and coarse lesions. Histological examination will confirm hyperkeratosis as a consequence of thickening of the epithelial cells and epithelial dysplasia. The potential ways of treatment include cryosurgery, electro-surgery, laser, and 5-fluorouracyl [40, 41].

Angular cheilitis is also referred to as angular cheilosis, commissural cheilitis or angular stomatitis. It is an inflammation of one or eventually of both angles of the mouth. The causes include bacterial (*Staphylococcus aureus*, haemolytic *Streptococcus*) or yeast infections (*Candida albicans*) mechanical damage to lips by denture prosthesis of fixation apparatus. Also, malnutrition involving deficiency of group B vitamins should be considered. Granulomatos cheilitis presents as swelling of the upper and lower lips and, at the same time, as one of the manifestations of orofacial granulomatosis, which is a separate disease, or as a monosymptomatic form of the Melkersson-Rosethal syndrome. Three symptoms are characteristic of this disease—recurrent orofacial swelling, recurrent facial paralysis and fissured tongue. One can also observe chapped, red-brown lips or buccal nerve paralysis. It is induced by allergic response to cinnamon or various benzoates and can represent also early manifestation of Crohn disease, mycobacterial infection or sarcoidosis. Aetiology of the disease is unknown. It has been assumed that sudden inflammation or random aggregation of inflammatory cells may be involved. Diagnosis is very difficult, important are histological results, which may indicate presence of granulomas and the positive findings may imply the Melkersson-Rosethal syndrome. This finding was obtained also in patients with Crohn disease and affected mouth.

### **3.4 Diseases of the tongue**

The most important diseases of the tongue include atrophy of the tongue fur, rhomboid glossitis, geographic tongue, fissured tongue, herpetic geometric glossitis, black hairy tongue, oral leucoplakia and macroglossia [37].

Rhomboid glossitis also known as central papillary atrophy presents as typical loss of tongue papillae along the midline posterior dorsal tongue, caused by oral candidiasis (**Figure 5**).

**289**

**Figure 5.**

from this disease [22].

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

smoking and the use of antimycotics [39].

on antihistaminics and corticosteroids.

The tongue lesion is shiny, frequently symmetrical, well delineated, depapillated. The risk factors include smoking, inadequate oral hygiene, use of unsuitable prosthesis and HIV infection. The treatment is based on the use of corticosteroid inhalators and sprays. It occurs worldwide and affects men, women and children. Diagnosis is based on clinical examination and laboratory confirmation of *Candida* spp. The most effective prevention/treatment, especially in smokers, is giving up

The term geographic tongue, lingua geographica, is used to describe inflammation affecting the dorsal surface of the tongue. Its characteristic feature is depapillation of some parts of the tongue resulting in the alternation of depapillated and

The depapillated areas are smooth and more intensively red coloured, and except this colour differences, the condition mostly causes no other symptoms. However, it may cause burning mouth syndrome after consumption of some foods [34]. The exact aetiology is unknown but association with smoking, stress and genetic association with human leukocyte antigens (HLAs), diabetes or psoriasis has been assumed. Diagnosis is made on the basis of clinical and histological examination. Differential diagnosis must distinguish this condition from oral lichenic planus, erythematous candidiasis and leucoplakia. Effective drug therapy is based

Fissured tongue affects 5–10% of population with higher susceptibility occurring in older individuals. The exact aetiology is unknown but imbalance of the level of salivary electrolytes and haematological abnormalities were observed. This condition affects the dorsal side of the tongue. In the central part, a central fissure (groove) is observed with multiple smaller fissures branching off the central one. Patients with Down, Melkersson-Rosethal and Sjögren syndromes are at risk. Improvement in oral hygiene, particularly the tongue, may result in the recovery

Black hairy tongue is the term used to refer to the hypertrophy of filiform papillae of the tongue that acquire black colour. This disease affects the dorsal part of the

normal-structure areas producing a map-like (geographic) pattern.

*A white coating on the tongue caused by an overgrowth of Candida albicans.*

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

*Bacterial Biofilms*

*3.2.7 Retained radices (radices relictae)*

**3.3 Diseases of the lips-cheilitis**

lar and granulomatous [39].

**3.4 Diseases of the tongue**

candidiasis (**Figure 5**).

apexes of papillae truncated by necrosis. It is localised mostly in the zone of frontal teeth and molars [22]. Chronic gingivitis is classified as gingivitis cattarrhalis chronica, gingivitis gravidarum, gingivitis pubertalis, gingivitis scurbutica, gingivi-

This condition occurs in patients with neglected hygiene. If the crown portion of the tooth disintegrates due to untreated caries, the roots of teeth are retained in the gums. Failure to ensure timely treatment of root canal may result in infection of the

Inflammation of lips extending to or beyond the border of lips can occur as acute or chronic. The factors most frequently involved in cheilitis are external factors. The currently known forms of cheilitis are actinic, angular, allergic, exfoliative, glandu-

Actinic cheilitis is referred to as solar cheilosis or solar keratosis of the lips that develops due to excessive exposure to UV radiation. It is localised in the lower lip in men and in the upper one in women. The risk group are fair-skinned (Caucasian) types of people. The clinical symptoms include dryness and scaliness of lips, their greyish colouration, swelling, ulceration, deepened folds and coarse lesions. Histological examination will confirm hyperkeratosis as a consequence of thickening of the epithelial cells and epithelial dysplasia. The potential ways of treatment

Angular cheilitis is also referred to as angular cheilosis, commissural cheilitis or angular stomatitis. It is an inflammation of one or eventually of both angles of the mouth. The causes include bacterial (*Staphylococcus aureus*, haemolytic *Streptococcus*) or yeast infections (*Candida albicans*) mechanical damage to lips by denture prosthesis of fixation apparatus. Also, malnutrition involving deficiency of group B vitamins should be considered. Granulomatos cheilitis presents as swelling of the upper and lower lips and, at the same time, as one of the manifestations of orofacial granulomatosis, which is a separate disease, or as a monosymptomatic form of the Melkersson-Rosethal syndrome. Three symptoms are characteristic of this disease—recurrent orofacial swelling, recurrent facial paralysis and fissured tongue. One can also observe chapped, red-brown lips or buccal nerve paralysis. It is induced by allergic response to cinnamon or various benzoates and can represent also early manifestation of Crohn disease, mycobacterial infection or sarcoidosis. Aetiology of the disease is unknown. It has been assumed that sudden inflammation or random aggregation of inflammatory cells may be involved. Diagnosis is very difficult, important are histological results, which may indicate presence of granulomas and the positive findings may imply the Melkersson-Rosethal syndrome. This finding was obtained also in patients with Crohn disease and affected mouth.

The most important diseases of the tongue include atrophy of the tongue fur, rhomboid glossitis, geographic tongue, fissured tongue, herpetic geometric glos-

Rhomboid glossitis also known as central papillary atrophy presents as typical loss of tongue papillae along the midline posterior dorsal tongue, caused by oral

sitis, black hairy tongue, oral leucoplakia and macroglossia [37].

include cryosurgery, electro-surgery, laser, and 5-fluorouracyl [40, 41].

tis at epilepsies and leukaemia and elephantiasis fibromatosis gingivae [34].

root pulp and thus in potential dental focal infection [36].

**288**

**Figure 5.** *A white coating on the tongue caused by an overgrowth of Candida albicans.*

The tongue lesion is shiny, frequently symmetrical, well delineated, depapillated. The risk factors include smoking, inadequate oral hygiene, use of unsuitable prosthesis and HIV infection. The treatment is based on the use of corticosteroid inhalators and sprays. It occurs worldwide and affects men, women and children. Diagnosis is based on clinical examination and laboratory confirmation of *Candida* spp. The most effective prevention/treatment, especially in smokers, is giving up smoking and the use of antimycotics [39].

The term geographic tongue, lingua geographica, is used to describe inflammation affecting the dorsal surface of the tongue. Its characteristic feature is depapillation of some parts of the tongue resulting in the alternation of depapillated and normal-structure areas producing a map-like (geographic) pattern.

The depapillated areas are smooth and more intensively red coloured, and except this colour differences, the condition mostly causes no other symptoms. However, it may cause burning mouth syndrome after consumption of some foods [34]. The exact aetiology is unknown but association with smoking, stress and genetic association with human leukocyte antigens (HLAs), diabetes or psoriasis has been assumed. Diagnosis is made on the basis of clinical and histological examination. Differential diagnosis must distinguish this condition from oral lichenic planus, erythematous candidiasis and leucoplakia. Effective drug therapy is based on antihistaminics and corticosteroids.

Fissured tongue affects 5–10% of population with higher susceptibility occurring in older individuals. The exact aetiology is unknown but imbalance of the level of salivary electrolytes and haematological abnormalities were observed. This condition affects the dorsal side of the tongue. In the central part, a central fissure (groove) is observed with multiple smaller fissures branching off the central one. Patients with Down, Melkersson-Rosethal and Sjögren syndromes are at risk. Improvement in oral hygiene, particularly the tongue, may result in the recovery from this disease [22].

Black hairy tongue is the term used to refer to the hypertrophy of filiform papillae of the tongue that acquire black colour. This disease affects the dorsal part of the tongue. There are several causes that induce this disease: keratinization of cells, restoration of the epithelial layer without complete exfoliation of the old layer, change in pH in the oral cavity, use of oxidation agents, smoking, antibiotics, bacterial and yeast infections and radiotherapy. Complication of this disease involves papillae that are markedly elongated and thus can cause tickling sensation, which may result in vomiting. Therapy consists in intensive cleaning of the tongue and administration of antimycotics [42].

### **3.5 Diseases of the salivary glands**

The diseases afflicting salivary glands include xerostomia, siallorhoea, inflammation of salivary glands—sialadenitis, Sjögren syndrome, calculi in salivary glands—sialolithiasis, cysts, sialadenosis and tumours of salivary glands [43].

Xerostomia or dry mouth syndrome is associated with reduced production of saliva, and this condition is also termed hyposalivation. It is caused by carcinomas or unsuitable therapy. An extensive group of diseases are inflammations of the salivary glands—sialadenitis. They are classified as acute bacterial sialadenitis, chronic sialoadenitis, viral sialadenitis, specific sialadenitis and autoimmmune sialadenitis—the Sjögren syndrome [34].

Acute bacterial sialadenitis is most frequently caused by pathogenic bacteria *Streptococcus aureus*, *Streptococcus viridans* and *Streptococcus pneumoniae*. The principal pathways of spreading of this infection are haematogenic and lymphogenic. The risk factors that support the development of infection include decreased production of saliva, cachexia sialolihtiasis and malignancies. Clinical manifestations include purulent and abscess forms.

### **3.6 Dental caries and periodontitis**

Dental caries is the most frequent dental and oral disease. It occurs worldwide [31]. Root caries is caused by *Streptococcus mutans*, *Lactobacillus acidophilus*, *Actinomyces* sp. and *Nocardia* sp. Bacteria first pass through the enamel, then through dentin, and finally, they reach the cementum layer. During clinical examination of dentition, black or dark yellow lesions are observed on teeth [44]. The most important mineral in teeth is hydroxyapatite. Remineralisation of teeth is ensured by prolin and minerals contained in the saliva [45]. Residues of food in the oral cavity, sweet beverages, beverages with high concentration of acids and citrus fruit are sources of bacterial nutrition.

The ability of bacteria *Streptococcus mutans* to form biofilms is important from the clinical point of view, particularly in relation to the development of dental caries. Dental caries has a multispecies aetiology. Mutant streptococci are referred to as a cluster of acidogenic streptococci species inhabiting dental plaques. *Streptococcus mutans* and *Streptococcus sobrinus* are the bacteria most frequently isolated from dental carious lesions. There were published individual case reports involving infectious endocarditis with participation of these bacteria [46]. The development of dental caries starts with dissolution of the mineral portion of tooth manifested by lesions and white sports on teeth, followed by local destruction of the enamel and dentin. If this process is left alone without treatment, inflammation of the dental pulp and periapical tissues follows. Many strategies focused on reduction of the occurrence of dental caries and their specific effect consisting in reduction of counts or acidogenic activity of *Streptococcus mutans* in the dental plaque [47].

In 2011, information about new bacterial species *Scardovia wiggsiae* appeared in professional microbiological and stomatological literature. The authors reported

**291**

**Figure 6.**

*Periodontitis afflicted lower front teeth in the mandible.*

able to multiply.

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

that in addition to *Streptococcus mutans,* this bacterium participates in the development of dental plaques and acute early age dental caries affecting dentition of children [44]. The relevant investigations were carried out by a team of scientists from Forsyth Institute, Cambridge, headed by A. C. R. Tanner, and involved bacterial population in samples of dental plaques and from the depth of cavities in primary dentition of 2–6-year-old children. The results were compared with the findings in the plaques of children without dental caries or white spots indicating demineralisation of enamel [48]. Because dental caries develops with participation of acidotolerant bacteria, the laboratory cultivation was carried out in anaerobic environment on blood agar of pH 5.0. In this way, the authors selected species that may play an important role in cariogenesis. Partial 16S rRNA sequences obtained from 5608 isolates were characterised on the basis of species. Subsequently, the findings of individual bacterial species from children with and without caries were compared. The species most frequently isolated from children with acute dental caries were *Streptococcus mutans*, *Scardovia wiggsiae*, *Veilonella parvula*, *Streptococcus cristatus* and *Actinomyces gerensceriae*. According to Human Oral Microbiome Database, the authors identified 198 taxons and 45 of them were until then characterised as noncultivable. The results showed that both *Streptococcus mutans* and the new bacteria *Scardovia wiggsiae* were isolated from 80% of the children with dental caries, but these bacteria were absent in 80% of children free from dental caries. The microorganism most frequently present in progressing dental caries was *Streptococcus mutans* and the newly discovered species *Scardovia wiggsiae* co-participated in the development of dental caries but was cultivated also independently from the cases of progressing dental caries. Many saccharolytic bacteria participate in reduction of pH, but their growth is selectively restricted at low pH at which the cariogenic acidotolerant species that include also the newly discovered *Scardovia wiggsiae* are

Periodontitis is a serious infection of gingiva that damages soft tissues and degrades the osseous tissue, can cause looseness of teeth or result in their loss (**Figure 6**). It affects approximately 10% of the world population. It is a subject to internal and external factors and the influence of bacteria, particularly the Grampositive ones, referred to sometimes as the "red complex", namely *Treponema* 

*denticola*, *Porphiromonas gingivalis* and *Tanerella forsythia* [39].

*Oral Microbiota from the Stomatology Perspective DOI: http://dx.doi.org/10.5772/intechopen.89362*

*Bacterial Biofilms*

tion of antimycotics [42].

**3.5 Diseases of the salivary glands**

sialadenitis—the Sjögren syndrome [34].

purulent and abscess forms.

**3.6 Dental caries and periodontitis**

fruit are sources of bacterial nutrition.

tongue. There are several causes that induce this disease: keratinization of cells, restoration of the epithelial layer without complete exfoliation of the old layer, change in pH in the oral cavity, use of oxidation agents, smoking, antibiotics, bacterial and yeast infections and radiotherapy. Complication of this disease involves papillae that are markedly elongated and thus can cause tickling sensation, which may result in vomiting. Therapy consists in intensive cleaning of the tongue and administra-

The diseases afflicting salivary glands include xerostomia, siallorhoea, inflammation of salivary glands—sialadenitis, Sjögren syndrome, calculi in salivary glands—sialolithiasis, cysts, sialadenosis and tumours of salivary glands [43]. Xerostomia or dry mouth syndrome is associated with reduced production of saliva, and this condition is also termed hyposalivation. It is caused by carcinomas or unsuitable therapy. An extensive group of diseases are inflammations of the salivary glands—sialadenitis. They are classified as acute bacterial sialadenitis, chronic sialoadenitis, viral sialadenitis, specific sialadenitis and autoimmmune

Acute bacterial sialadenitis is most frequently caused by pathogenic bacteria *Streptococcus aureus*, *Streptococcus viridans* and *Streptococcus pneumoniae*. The principal pathways of spreading of this infection are haematogenic and lymphogenic. The risk factors that support the development of infection include decreased production of saliva, cachexia sialolihtiasis and malignancies. Clinical manifestations include

Dental caries is the most frequent dental and oral disease. It occurs worldwide

The ability of bacteria *Streptococcus mutans* to form biofilms is important from the clinical point of view, particularly in relation to the development of dental caries. Dental caries has a multispecies aetiology. Mutant streptococci are referred

In 2011, information about new bacterial species *Scardovia wiggsiae* appeared in professional microbiological and stomatological literature. The authors reported

[31]. Root caries is caused by *Streptococcus mutans*, *Lactobacillus acidophilus*, *Actinomyces* sp. and *Nocardia* sp. Bacteria first pass through the enamel, then through dentin, and finally, they reach the cementum layer. During clinical examination of dentition, black or dark yellow lesions are observed on teeth [44]. The most important mineral in teeth is hydroxyapatite. Remineralisation of teeth is ensured by prolin and minerals contained in the saliva [45]. Residues of food in the oral cavity, sweet beverages, beverages with high concentration of acids and citrus

to as a cluster of acidogenic streptococci species inhabiting dental plaques. *Streptococcus mutans* and *Streptococcus sobrinus* are the bacteria most frequently isolated from dental carious lesions. There were published individual case reports involving infectious endocarditis with participation of these bacteria [46]. The development of dental caries starts with dissolution of the mineral portion of tooth manifested by lesions and white sports on teeth, followed by local destruction of the enamel and dentin. If this process is left alone without treatment, inflammation of the dental pulp and periapical tissues follows. Many strategies focused on reduction of the occurrence of dental caries and their specific effect consisting in reduction of counts or acidogenic activity of *Streptococcus mutans* in

**290**

the dental plaque [47].

that in addition to *Streptococcus mutans,* this bacterium participates in the development of dental plaques and acute early age dental caries affecting dentition of children [44]. The relevant investigations were carried out by a team of scientists from Forsyth Institute, Cambridge, headed by A. C. R. Tanner, and involved bacterial population in samples of dental plaques and from the depth of cavities in primary dentition of 2–6-year-old children. The results were compared with the findings in the plaques of children without dental caries or white spots indicating demineralisation of enamel [48]. Because dental caries develops with participation of acidotolerant bacteria, the laboratory cultivation was carried out in anaerobic environment on blood agar of pH 5.0. In this way, the authors selected species that may play an important role in cariogenesis. Partial 16S rRNA sequences obtained from 5608 isolates were characterised on the basis of species. Subsequently, the findings of individual bacterial species from children with and without caries were compared. The species most frequently isolated from children with acute dental caries were *Streptococcus mutans*, *Scardovia wiggsiae*, *Veilonella parvula*, *Streptococcus cristatus* and *Actinomyces gerensceriae*. According to Human Oral Microbiome Database, the authors identified 198 taxons and 45 of them were until then characterised as noncultivable. The results showed that both *Streptococcus mutans* and the new bacteria *Scardovia wiggsiae* were isolated from 80% of the children with dental caries, but these bacteria were absent in 80% of children free from dental caries. The microorganism most frequently present in progressing dental caries was *Streptococcus mutans* and the newly discovered species *Scardovia wiggsiae* co-participated in the development of dental caries but was cultivated also independently from the cases of progressing dental caries. Many saccharolytic bacteria participate in reduction of pH, but their growth is selectively restricted at low pH at which the cariogenic acidotolerant species that include also the newly discovered *Scardovia wiggsiae* are able to multiply.

Periodontitis is a serious infection of gingiva that damages soft tissues and degrades the osseous tissue, can cause looseness of teeth or result in their loss (**Figure 6**). It affects approximately 10% of the world population. It is a subject to internal and external factors and the influence of bacteria, particularly the Grampositive ones, referred to sometimes as the "red complex", namely *Treponema denticola*, *Porphiromonas gingivalis* and *Tanerella forsythia* [39].

**Figure 6.** *Periodontitis afflicted lower front teeth in the mandible.*
