**2. Canine dental biofilm**

The oral cavity is a host for a variety of microorganisms including bacteria, viruses, fungi and protozoa that colonize teeth, tongue, oral mucosa, hard palate, caries lesions, periodontal pocket and similarly. The distribution of microorganisms in the oral cavity is not random; most species prefer certain places to others due to the specific local conditions that these sites provide, for example, the anaerobic environment of the gingival sulcus [10, 11]. However, the oral cavity environment is also hostile to microbial life, so only a certain groups of microorganisms entering it are able to colonize it, and survive in this environment. Microorganisms must attach to the surface and form biofilms to remain in oral cavity [12].

Dog oral cavity hides a rich and diverse bacterial community and exceeds the estimates of culture-based studies. Of the cultivable oral microbiota, genera *Actinomyces*, *Streptococcus* and *Granulicatella* are most commonly isolated from saliva. Genera *Porphyromonas*, *Actinomyces* and *Neisseria* are most commonly isolated from plaque [13]. Genera *Porphyromonas*, *Fusobacterium*, *Capnocytophaga*, *Derxia*, *Moraxella*, *Bergeyella*, non-cultivable *Lachnospiraceae*, *Enhydrobacter*, non-classified *Peptostreptococcaceae*, *Xylanibacter*, *Parabacteroides*, *Tannerella*, *Neisseria*, *Treponema* and *Bacteroides* were identified by the pyrosequencing of the 16S rRNA gene [14]. In another oral microbiota study also by pyrosequencing the 16S rRNA gene, the bacterial genera *Actinomyces*, *Porphyromonas*, *Fusobacterium*, *Neisseria*, *Pasteurella*, *Lampropedia*, *Capnocytophaga*, *Frigovirgula*, *Filifactor*, *Conchiformibius*, *Eubacterium*, *Streptococcus*, *Corynebacterium* and *Derxia* have been identified with an abundance >1% [15]. Based on the sequencing of the 16S rRNA gene the presence of other genera in the oral cavity of dogs such as *Abiotrophia*, *Aerococcus*, *Campylobacter*, *Cardiobacterium*, *Clostridium*, *Curtobacterium*, *Dialister*, *Dietzia*, *Dysgonomonas*, *Eikenella*, *Enterococcus*, *Eubacterium*, *Gemella*, *Globicatella*, *Granulicatella*, *Haemophilus*, *Lactobacillus*, *Leptotrichia*, *Leucobacter*, *Micrococcus*, *Micromonas*, *Peptostreptococcus*, *Prevotella*, *Propionibacterium*, *Propionivibrio*, *Rothia*, *Selenomonas*, *Schwartzia*, *Sporocytophaga*, *Wolinella*, *Xanthomonas* and *Xenophilus* was confirmed [16]. Many of them are part of the biofilm formed on teeth surface. In dogs, also in humans, a subgingival biofilm includes colonies of anaerobic, Gram-negative (*Bacteroides* spp., *Capnocytophaga* spp., *Fusobacterium* spp., *Porphyromonas* spp., *Prevotella* spp., *Tannerella* spp. and *Treponema* spp.) as well as Gram-positive bacteria (*Actinomyces* spp., *Corynebacterium* spp., *Eubacterium* spp., *Peptostreptococcus* spp. and *Streptococcus* spp.) [17].

The formation of dental biofilm in the oral cavity is a multi-stage process [18]. It can be divided into four main stages: pellicle formation, initial bacterial adhesion, plaque maturation and finally bacterial dispersion [11]. Initially, a semipermeable layer called pellicle is formed on the tooth surface, which mediates the interaction between tooth, oral fluids and microorganisms [19]. Primary colonizers form biofilm autoaggregation (aggregation between the same species) and coaggregation (aggregation between different species) [20]. In addition, they facilitate the arrival of additional bacteria by providing multiple diverse adhesive sites. They also begin to build a matrix that holds the biofilm together. Some species are incapable of adhering to the surface, but are often able to anchor to a matrix or directly to earlier colonizers [21]. Representatives of the genera *Neisseria*, *Corynebacterium*

**247**

disease spectrum [31].

*Dental Biofilm as Etiological Agent of Canine Periodontal Disease*

and *Stenotrophomonas* are involved as primary colonizers in the formation of canine dental biofilm. The most common species of the genus *Neisseria* are *N. zoodegmatis*, *N. animaloris* and *N. weaveri*. Representatives of the genera *Actinomyces*, *Porphyromonas*, *Moraxella*, *Leucobacter*, and the families *Peptostreptococcaceae* and *Pasteurellaceae* probably play the roles of secondary colonizers. Species *Actinomyces canis* and *Porphyromonas gingivicanis* show high levels of biofilm incorporation. The species which featured most frequently in the role of third community member are *Peptostreptococcaceae* spp., *Porphyromonas gingivicanis* and *Leucobacter* spp. [22]. Bacteria from dental biofilm can either be protective, and provide an essential barrier through interactions with the host immune system, or be pathogenic, and cause diseases, such as periodontitis [15]. Oral microbiota varies greatly in healthy dogs and in dogs with disease of oral cavity, and also contains a high proportion of non-cultivable or unexplored species [23]. In healthy dogs, more common species are *Moraxella* spp., *Bergeyella zoohelcum*, *Neisseria shayeganii*, *Pasteurellaceae* spp., *Capnocytophaga* spp. and *Stenotrophomonas* spp. In dogs with periodontitis, species *Peptostreptococcaceae* spp., *Lachnospiraceae* spp. and *Clostridiales* spp. are signifi-

Periodontal disease occurs naturally in a wide range of species from rodents to humans [25]. Periodontal disease is one of the most common diseases of adult dogs, with up to 80% of animals affected [23]. All canine breeds are at risk of developing periodontal disease [26]. In general, the disease is more prevalent in small breeds compared to large breeds, and incidence increases with advancing age. In addition, brachycephalic breeds and dogs with teeth overcrowding have been reported to be especially vulnerable to developing the advanced stages of the disease [27]. There are four stages of periodontal disease, each of which is based on the severity of clinical lesions as follows: Stage 1—gingivitis, Stage 2—early periodontitis, Stage

Gingivitis is completely reversible, and is recognized by the classic signs of halitosis, bleeding, inflammation, redness and swelling of the gingivae. Periodontitis is irreversible, and attacks the deeper structures that support the teeth, permanently damaging the surrounding bone and periodontal ligament [23]. The breakdown of the collagen fibers of the periodontal ligament results in a periodontal pocket between the gingiva and the tooth. Periodontal pocket deepen due to further destruction of periodontal ligament fibers and alveolar bone resorption. Advanced periodontitis is characterized by gingival erythema and edema, gingival bleeding, gingival recession, tooth mobility, suppuration of periodontal pocket and loss of teeth [29]. We know two main categories of periodontal disease in which loss of supporting structures around the tooth occurs: chronic periodontitis and aggressive periodontitis [30]. Chronic periodontitis is chronic inflammation results in, mostly irreversible, loss of epithelial tissue, bone and ligament. Aggressive periodontitis is characterized by rapid rate of disease progression. It can be present in localized or generalized form; both are early-onset forms of chronic periodontal inflammatory disease. No disease-specific biomarkers exist that differentiate chronic periodontitis from aggressive periodontitis. Although current knowledge suggests that both have similar etiology and histopathology and might indeed be different ends of the same

Periodontal disease is caused by the accumulation of bacterial dental biofilm on the teeth and gingivae, toxic products of the metabolism of these microorganisms, and the host immune response against the infection that triggers the inflammatory

3—moderate periodontitis, Stage 4—advanced periodontitis [28].

*DOI: http://dx.doi.org/10.5772/intechopen.88305*

cantly more prevalent [24].

**3. Periodontal disease**

*Dental Biofilm as Etiological Agent of Canine Periodontal Disease DOI: http://dx.doi.org/10.5772/intechopen.88305*

and *Stenotrophomonas* are involved as primary colonizers in the formation of canine dental biofilm. The most common species of the genus *Neisseria* are *N. zoodegmatis*, *N. animaloris* and *N. weaveri*. Representatives of the genera *Actinomyces*, *Porphyromonas*, *Moraxella*, *Leucobacter*, and the families *Peptostreptococcaceae* and *Pasteurellaceae* probably play the roles of secondary colonizers. Species *Actinomyces canis* and *Porphyromonas gingivicanis* show high levels of biofilm incorporation. The species which featured most frequently in the role of third community member are *Peptostreptococcaceae* spp., *Porphyromonas gingivicanis* and *Leucobacter* spp. [22]. Bacteria from dental biofilm can either be protective, and provide an essential barrier through interactions with the host immune system, or be pathogenic, and cause diseases, such as periodontitis [15]. Oral microbiota varies greatly in healthy dogs and in dogs with disease of oral cavity, and also contains a high proportion of non-cultivable or unexplored species [23]. In healthy dogs, more common species are *Moraxella* spp., *Bergeyella zoohelcum*, *Neisseria shayeganii*, *Pasteurellaceae* spp., *Capnocytophaga* spp. and *Stenotrophomonas* spp. In dogs with periodontitis, species *Peptostreptococcaceae* spp., *Lachnospiraceae* spp. and *Clostridiales* spp. are significantly more prevalent [24].

## **3. Periodontal disease**

*Bacterial Biofilms*

microorganisms [9].

**2. Canine dental biofilm**

In addition, the presence of dental calculus leads to greater biofilm accumulation by creating a rough surface [8]. Dental calculus is always covered with a layer of dental biofilm, so it plays an important role as retention factor in the colonization of

The oral cavity is a host for a variety of microorganisms including bacteria, viruses, fungi and protozoa that colonize teeth, tongue, oral mucosa, hard palate, caries lesions, periodontal pocket and similarly. The distribution of microorganisms in the oral cavity is not random; most species prefer certain places to others due to the specific local conditions that these sites provide, for example, the anaerobic environment of the gingival sulcus [10, 11]. However, the oral cavity environment is also hostile to microbial life, so only a certain groups of microorganisms entering it are able to colonize it, and survive in this environment. Microorganisms must attach

Dog oral cavity hides a rich and diverse bacterial community and exceeds the estimates of culture-based studies. Of the cultivable oral microbiota, genera *Actinomyces*, *Streptococcus* and *Granulicatella* are most commonly isolated from saliva. Genera *Porphyromonas*, *Actinomyces* and *Neisseria* are most commonly isolated from plaque [13]. Genera *Porphyromonas*, *Fusobacterium*, *Capnocytophaga*, *Derxia*, *Moraxella*, *Bergeyella*, non-cultivable *Lachnospiraceae*, *Enhydrobacter*, non-classified *Peptostreptococcaceae*, *Xylanibacter*, *Parabacteroides*, *Tannerella*, *Neisseria*, *Treponema* and *Bacteroides* were identified by the pyrosequencing of the 16S rRNA gene [14]. In another oral microbiota study also by pyrosequencing the 16S rRNA gene, the bacterial genera *Actinomyces*, *Porphyromonas*, *Fusobacterium*, *Neisseria*, *Pasteurella*, *Lampropedia*, *Capnocytophaga*, *Frigovirgula*, *Filifactor*, *Conchiformibius*, *Eubacterium*, *Streptococcus*, *Corynebacterium* and *Derxia* have been identified with an abundance >1% [15]. Based on the sequencing of the 16S rRNA gene the presence of other genera in the oral cavity of dogs such as *Abiotrophia*, *Aerococcus*, *Campylobacter*, *Cardiobacterium*, *Clostridium*, *Curtobacterium*, *Dialister*, *Dietzia*, *Dysgonomonas*, *Eikenella*, *Enterococcus*, *Eubacterium*, *Gemella*, *Globicatella*, *Granulicatella*, *Haemophilus*, *Lactobacillus*, *Leptotrichia*, *Leucobacter*, *Micrococcus*, *Micromonas*, *Peptostreptococcus*, *Prevotella*, *Propionibacterium*, *Propionivibrio*, *Rothia*, *Selenomonas*, *Schwartzia*, *Sporocytophaga*, *Wolinella*, *Xanthomonas* and *Xenophilus* was confirmed [16]. Many of them are part of the biofilm formed on teeth surface. In dogs, also in humans, a subgingival biofilm includes colonies of anaerobic, Gram-negative (*Bacteroides* spp., *Capnocytophaga* spp., *Fusobacterium* spp., *Porphyromonas* spp., *Prevotella* spp., *Tannerella* spp. and *Treponema* spp.) as well as Gram-positive bacteria (*Actinomyces* spp., *Corynebacterium* spp., *Eubacterium* spp., *Peptostreptococcus* spp.

The formation of dental biofilm in the oral cavity is a multi-stage process [18]. It can be divided into four main stages: pellicle formation, initial bacterial adhesion, plaque maturation and finally bacterial dispersion [11]. Initially, a semipermeable layer called pellicle is formed on the tooth surface, which mediates the interaction between tooth, oral fluids and microorganisms [19]. Primary colonizers form biofilm autoaggregation (aggregation between the same species) and coaggregation (aggregation between different species) [20]. In addition, they facilitate the arrival of additional bacteria by providing multiple diverse adhesive sites. They also begin to build a matrix that holds the biofilm together. Some species are incapable of adhering to the surface, but are often able to anchor to a matrix or directly to earlier colonizers [21]. Representatives of the genera *Neisseria*, *Corynebacterium*

to the surface and form biofilms to remain in oral cavity [12].

**246**

and *Streptococcus* spp.) [17].

Periodontal disease occurs naturally in a wide range of species from rodents to humans [25]. Periodontal disease is one of the most common diseases of adult dogs, with up to 80% of animals affected [23]. All canine breeds are at risk of developing periodontal disease [26]. In general, the disease is more prevalent in small breeds compared to large breeds, and incidence increases with advancing age. In addition, brachycephalic breeds and dogs with teeth overcrowding have been reported to be especially vulnerable to developing the advanced stages of the disease [27]. There are four stages of periodontal disease, each of which is based on the severity of clinical lesions as follows: Stage 1—gingivitis, Stage 2—early periodontitis, Stage 3—moderate periodontitis, Stage 4—advanced periodontitis [28].

Gingivitis is completely reversible, and is recognized by the classic signs of halitosis, bleeding, inflammation, redness and swelling of the gingivae. Periodontitis is irreversible, and attacks the deeper structures that support the teeth, permanently damaging the surrounding bone and periodontal ligament [23]. The breakdown of the collagen fibers of the periodontal ligament results in a periodontal pocket between the gingiva and the tooth. Periodontal pocket deepen due to further destruction of periodontal ligament fibers and alveolar bone resorption. Advanced periodontitis is characterized by gingival erythema and edema, gingival bleeding, gingival recession, tooth mobility, suppuration of periodontal pocket and loss of teeth [29]. We know two main categories of periodontal disease in which loss of supporting structures around the tooth occurs: chronic periodontitis and aggressive periodontitis [30]. Chronic periodontitis is chronic inflammation results in, mostly irreversible, loss of epithelial tissue, bone and ligament. Aggressive periodontitis is characterized by rapid rate of disease progression. It can be present in localized or generalized form; both are early-onset forms of chronic periodontal inflammatory disease. No disease-specific biomarkers exist that differentiate chronic periodontitis from aggressive periodontitis. Although current knowledge suggests that both have similar etiology and histopathology and might indeed be different ends of the same disease spectrum [31].

Periodontal disease is caused by the accumulation of bacterial dental biofilm on the teeth and gingivae, toxic products of the metabolism of these microorganisms, and the host immune response against the infection that triggers the inflammatory

process [32]. In case of chronic periodontitis usually have abundance of plaque and calculus, which match with the amount of periodontal destruction. On the other hand, in case of aggressive periodontitis, there is usually a mismatch between the amount of local factors and the periodontal destruction [33]. Periodontal disease affects more frequently and more severely regions of premolars and molars than regions of maxillary and mandibular incisors. Missing of teeth is observed at a high and increasing incidence with age. The tooth most commonly lost is the first premolar, followed by the other premolars and molars, where severe periodontitis is frequently found [34]. Periodontitis is a serious infection that can have medical consequences such as anorexia and weight loss, chronic pain, swollen gums, dental caries, breakage or loss of teeth and breakage of the maxillary or mandibular bone [35]. Unfortunately, the damage from periodontal disease is not confined to just loss of teeth. Oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as chronic bronchitis, pulmonary fibrosis, endocarditis, interstitial nephritis, glomerulonephritis and hepatitis [1].
