Abstract
Periodontal disease is one of the most common health problem affecting dogs. The disease is more prevalent in small breeds and brachycephalic breeds compared to large breeds, and incidence increases with advancing age. In first stage it affects only the gingival tissue and causes gingivitis. It later develops into periodontitis which involves changes in other periodontium tissues. Main etiological agents of periodontal disease are pathogenic bacteria of dental biofilm, and products of their metabolism. In human, Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia play a key role in the etiology of periodontal disease. Also, there are many other candidates as human periodontal pathogens, including Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Prevotella nigrescens, Fusobacterium nucleatum, Parvimonas micra, Eikenella corrodens, Capnocytophaga gingivalis, Eubacterium nodatum and Campylobacter rectus. Since periodontal diseases in dogs are similar to human diseases in terms of disease progression and clinical manifestation, we can assume their common etiology. This chapter is focused on review about canine dental biofilm and about members of biofilm as potential causative agent of canine periodontal disease.
Keywords
- dental plaque
- biofilm
- dog
- periodontal disease
- gingivitis
- periodontitis
1. Introduction
Periodontal disease is a significant veterinary health problem of companion dogs [1]. Periodontal disease refers to a group of inflammatory diseases. In both humans and dogs the initial stages of periodontal disease are observed clinically as red and inflamed gingivae, defined as gingivitis. Without treatment to remove, and disrupt the dental plaque, gingivitis may progress to periodontitis [2]. Periodontitis, the later, irreversible stage of the disease, is an inflammatory disease of supporting teeth tissues [3]. The primary etiological factor in the initiation and progression of periodontal disease is dental plaque [4]. Dental plaque is the community of microorganisms found on a tooth surface as a biofilm, embedded in a matrix of polymers of host and bacterial origin [5]. It is believed that enzymes secreted by dental biofilm bacteria as well as bacterial antigens activate the host inflammatory response initiating disease [6]. Dental calculus that represents mineralized bacterial dental biofilm is considered as secondary etiological factor in periodontal disease [7]. Dental calculus itself is relatively non-pathogenic and, despite its rough surface, is not the direct cause of inflammatory processes, but mainly has an irritant effect. 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 microorganisms [9].
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
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
3. Periodontal disease
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].
4. Periodontal pathogens
Although there is sufficient evidence that biofilm accumulation and maturation is essential for initiation and progression of periodontal disease, studies show that bacterial species colonizing periodontal pocket have different roles in the pathogenesis of this disease [36]. Microbial density is considered to be critical for the development of gingivitis, and some types of chronic periodontitis, while the species of the microorganisms may be of greater importance in the initiation of aggressive periodontitis [35]. Subgingival microbiota in periodontitis may contain hundreds of bacterial species, but only a small number is associated with disease progression, and is considered to be of importance etiologically [37]. The presence of
As with any other infection, identification of the microbial pathogens associated with the etiology of periodontitis is the first step towards the development of effective therapeutic approaches. The establishment of a microorganism as a true pathogen should be based on two main levels of evidence: (1) the organism should be present in higher prevalence and/or levels in disease than in health, and (2) its suppression or elimination should reduce or stop disease progression [39]. In human, the presence of three species of Gram-negative anaerobic bacteria within subgingival biofilm,
4.1 Genus Porphyromonas
The genus
4.2 Genus Tannerella
The genus
4.3 Genus Campylobacter
The genus
4.4 Genus Treponema
The genus
4.5 Genus Fusobacterium
The genus
4.6 Genus Parvimonas
The genus
4.7 Genus Prevotella
The genus
4.8 Oral protozoa
For several decades, research in periodontology is focused on the characterization of bacterial communities thought to be involved in canine periodontal diseases. However, other microorganisms are known to inhabit the oral cavity and could also influence the process of periodontal disease. There were identified two oral protozoa,
The species
The species
5. The possibility of transferring bacteria from the oral microbiome of dogs to human
Except for to the impact on animal health, bacteria from the oral cavity of animals may also have harmful effects on human health in the case of microbial transmissibility, for example, through dog bites. Dog bite wounds are polymicrobial, with a broad combination of aerobic and anaerobic microorganisms. The microbiology of infected bite wounds from dogs is similar to that of the organisms that colonize the dog’s oral cavity. Less frequently, isolates may also come from the environment and patients’ skin [82]. On average, a dog bite wound contains two to five different species of bacteria [83].
As transmission of oral bacteria during normal contacts between dogs and humans is also feasible one might expect correlations between the oral microbiota of dogs and humans [17]. Oral-to-oral transfer of
6. Conclusion
Review of literature showed that some bacterial species like
Acknowledgments
This publication was supported by the project of the Ministry of education science Research and sport of the Slovak Republic VEGA 1/0788/19 and VEGA 1/0081/17.
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