5.2 Periodontal Anatomy and Physiology

To recognize and understand periodontal disease and its treatment requires a familiarity with the normal anatomy and physiology of the periodontium. The alveolar mucosa is separated from the gingival mucosa by the mucogingival junction. The gingiva is divided by the free gingival groove into the free gingiva and the attached gingiva [14]. The free gingival margin has a flat knife‐edge or more curved edge in young and old dogs, respectively [14]. The attached gingiva is not mobile and is firmly attached to underlying structures. It is thickest in the regions of the canine teeth, maxillary fourth premolars, and mandibular first molars [15, 16]. Likewise, the entire gingival width from the free gingival margin to the mucogingival margin is widest at the canine teeth compared to the premolars [17]. The interdental papilla is formed by gingiva between adjacent teeth. Where the buccal and lingual gingival papilla meet, a non‐visible col is formed. Most the gingival epithelium is parakeratinized stratified squamous epithelium although the col and gingival sulcus are lined by non‐keratinized stratified squamous epithelium. This epithelium can be easily irritated, leading to gingivitis [18]. The normal space between the free gingiva and the tooth is the sulcus. The sulcular epithelium continues to the junctional epithelium (JE) at the apical portion of the sulcus. The junctional epithelium attaches the gingiva to the tooth, acts as a barrier to the apical periodontal structures, allows passage of gingival crevicular fluid, and allows diapedesis of inflammatory cells. Every 4–6 days and 9–12 days the junctional epithelium and gingival epithelium are replaced, respectively [19, 20]. In healthy periodontal tissues the apical boundary of the junctional epithelium ends at the cementoenamel junction (CEJ). Once the cells reach the bottom of the gingival sulcus, they are sloughed. Replacement of the sulcular epithelium is at a rate between junctional and gingival epithelium replacement rates.

The extensions of the gingival epithelium (rete pegs) and the connective tissue extensions (dermal papilla) interdigitate in order to form a strong attachment. The resulting clinical appearance is gingival stippling in some animals. However, the interdigitation may not correlate in stippling in dog gingiva [14, 21]. The most prominent stippling may be found in the same regions of the widest and thickest gingiva (i.e., the strategic canine teeth, mandibular first molars, and maxillary fourth premolars) [21]. Stippling can be present or absent in healthy or diseased gingival tissue.

The cementum is both a mineralized portion of the tooth and the periodontium. It is approximately 45–50% mineralized and 55–50% connective tissue receiving blood supply from the PDL [22–24]. This avascular tissue lacks innervation and the organic tissue is composed of primarily Type I collagen. The cellular layers of cementum are thickest apically and thinnest coronally [14]. Cementum is divided into acellular (referred to as primary) and cellular (referred to as secondary). Cementum is further divided into six types by the origin of the collagen fibers from fibroblasts (extrinsic fiber cementum) and cementoblasts (intrinsic fiber cementum) [19]. The densely packed Sharpey’s fibers inserting into cementum function to anchor the PDL to the tooth.

The PDL anchors the tooth to the alveolar bone, is actively involved in periodontal maintenance, and dampens occlusal forces. The PDL contains Sharpey’s fibers primarily of type I collagen [22]. Alveolodental fibers that anchor the cementum to the alveolar bone are divided into six groups [19]. The PDL has a good supply and the polygonal mesh vascular network and unique oxytalan fibers provide shock absorption for occlusal forces [25, 26]. The rete venosum in alveolar bone may act as the reservoir of displaced blood during occlusal loading forces [25]. Connective tissue cells of the PDL include fibroblasts, osteoblasts, cementoblasts, and undifferentiated cells that can uniquely differentiate into any of those cells [19, 27, 28]. The fibroblast is the most abundant cell and can synthesize and phagocytize collagen of the PDL for normal physiological maintenance and attachment to alveolar bone [19, 26]. In some species (e.g., aradicular hypsodont and radicular hypsodont teeth), immature teeth, an interdigitating fiber arrangement called the intermediate plexus, have been demonstrated traversing the periodontal space allowing for continual growth and/or eruption [27].

Alveolar bone serves as the anchor for Sharpey’s fibers holding the teeth in the maxillofacial skeleton. The bone is continuously remodeled as it distributes occlusal forces of mastication. Plates of cortical bone (compact bone), with spongy cancellous bone (trabecular bone) in between, compose alveolar bone [29]. Bundle bone, produced by osteoblasts, is the location of Sharpey’s fiber insertion [30]. The inner cortical bone is denser, compared to trabecular bone, and appears radiographically as the lamina dura. The marginal alveolar bone is the thinnest portion of the alveolar process, especially facially, as there is no underlying trabecular bone supporting it. In the maxilla of the dog, this facial surface closely follows the contour of the roots, forming palpably distinct juga over the roots.

The alveolar bone is under constant remodeling by osteoclasts and osteoblasts [30]. The coordinated removal of bone by osteoclasts is regulated by the RANK (receptor‐activated nuclear factor κβ)/RANKL (receptor‐activated nuclear factor κβ ligand)/OPG (osteoprotegrin) [28]. The macrophage‐colony stimulating factor must be present in addition to osteoblasts to regulate osteoclasts. RANK is found on osteoclast precursor cell membranes and RANKL on osteoblasts. OPG is produced by osteoblasts to bind the RANKL in order to prevent activation of osteoclasts and balance bone removal, by osteoclasts, and bone production, by osteoblasts. However, inflammatory cytokines in periodontitis change the balance and allow induction of osteoclasts and associated bone resorptive activity.

5.3 Etiology and Pathophysiology of Periodontal Disease

The pathophysiology of periodontal disease is similar between veterinary patients and humans [11, 31, 32]. Periodontitis is active inflammation of the periodontium. It begins with the accumulation of the dental pellicle (0.1–0.8 mm) (e.g., salivary glycoproteins) that occurs within seconds of a tooth being cleaned. Within hours, Gram positive oral bacterial first colonize the pellicle and the plaque biofilm is formed. With the addition of extracellular polysaccharides (i.e., bacterial byproducts), plaque takes on its classic ivory to yellow to grayish appearance. The plaque biofilm is established in 24 hours and matures within days. Maturation of the plaque biofilm to a stage where anaerobic organisms are supported is within 24 hours [33, 34]. Mineralization of the plaque biofilm results in calculus (Figure 5.2). Periodontitis is caused by the bacterial biofilm (plaque) and the associated inflammatory response. Significant periodontal disease can be present without calculus. Likewise, some patients can have significant calculus with minimal periodontal disease. Additionally, periodontal disease may be quiescent or have periods of active inflammation (i.e., periodontitis).

The plaque is an organic matrix of salivary glycoproteins, oral bacteria, lipids, cellular debris, and extracellular polysaccharides that adhere to the tooth surface. The glycoproteins and polysaccharides provide the adherence for the bacteria [35]. Dental plaque is not a food residue. It forms more readily during sleep when there is no food taken in and has been shown to form in humans when parenteral feeding is being utilized for nutrition [36]. The mechanical action of food and stimulated saliva deters and slows plaque formation. Plaque is a biofilm [37, 38].

The plaque biofilm is a complex, cooperative community of bacteria that can resist host defenses and is shaped by the local environmental and host factors in the oral cavity [39]. The biofilm inhibits antimicrobial penetration, prevents desiccation, and limits the host immune system [40, 41]. Additionally, the biofilm bacteria benefit from cooperation and altered gene expressions, adding to the tenacity of the protective biofilm. Furthermore, there is no host blood supply to the tooth surface to deliver oxygen and inflammatory cells to directly target the biofilm. The inflammatory cells must first move into the gingival crevicular fluid or periodontal exudate in order to reach the outer surface of the biofilm. Biofilms in medicine and surgery cannot be seen visually, require disruption in order to treat, and require a robust blood supply to heal [42]. Mechanical removal and disruption of the plaque biofilm professionally and with tooth brushing is necessary in order to treat and prevent periodontal disease, respectively.

Supragingival plaque influences the growth accumulation and pathogenicity of subgingival plaque in the early stages of periodontal disease. The plaque biofilm protects the subgingival plaque and reduces the oxygen available deeper in the plaque matrix, thereby allowing Gram negative anaerobes to proliferate. Although the supragingival and subgingival bacterial communities are a continuum, during maturation delineation occurs, separating the two different communities [43]. The oral bacteria and those bacteria in the biofilm community may be aerobic bacteria (e.g., require oxygen), facultative bacteria (e.g., survive in aerobic or anaerobic conditions), and anaerobic bacteria (e.g., require oxygen‐free environments). Bacteria can also be found in the gingival crevicular fluid (i.e., planktonic bacteria) and some can actively invade gingival tissue. The black pigmented anaerobic bacilli have virulence factors such as direct epithelial invasion, collagenase production, protease production, release endotoxins, impair neutrophils, and activate the host inflammatory cytokines [44]. The activated neutrophils release cytokines and produce metalloproteinases that recruit additional inflammatory cells and destroy the periodontal tissues while fighting the bacteria. The pathogenic bacteria in primate, canine, and feline periodontal disease arise from similar bacterial families and although some genus and species are found in the comparative species, specific bacteria have been identified in carnivores with cultures and molecular cloning and sequencing. Black‐pigmented Gram negative anaerobes and spirochetes have been incriminated in canine periodontal disease [45, 46]. Oral bacteria incriminated in periodontal disease in the dog and cat include, at this time, Bacteroides sp., Porphorymonas sp., Prevotella intermedia, Tannerella forsythensia, Campylobacter rectus, Peptostreptococcus sp., Treponema denticola, Fusebacterium canifelinum, Pseudomonas sp., Capnocytophaga sp., and Desulfomicrobium sp. [45–57]. As the biofilm matures the population of the anaerobic bacteria and spirochetes increases, changing the ratio of anaerobic and aerobic bacteria in the biofilm.

As the plaque biofilm matures, early bacterial colonizers, Gram positive aerobic cocci, become less predominant as the biofilm switches to Gram negative anaerobes and spirochetes located more apical in the periodontal pockets. Bacterial products such as ammonia, volatile sulfur compounds, and proteolytic enzymes contribute to the destruction of the periodontium. The host inflammatory response, matrix metalloproteinases that degrade collagen of the PDL, elastase, and prostaglandins (PGE₂) are directly responsible for tissue damage and/or stimulate osteoclastic bone resorption (PGE₂, IL‐1β, IL‐6, TNF‐α). Cytokines affect immune cells and resident cells of the periodontium, integrating aspects of the innate and adaptive immune response to plaque pathogens [58]. This host inflammatory response substantially contributes to destruction of the periodontium.

The theories of periodontal disease continue to evolve [59]. The “specific plaque hypothesis” explains that periodontitis is caused by specific strains of virulent bacteria. This type of hypothesis could explain the nature of certain forms of aggressive periodontitis. When reduced host resistance allows facultative pathogens found in the normal oral flora to proliferate, periodontitis results. The “non‐specific plaque hypothesis” best explains chronic periodontitis. This mixed bacterial population in the plaque biofilm, with lack of professional and home care, proliferates and induces an inflammatory response resulting in periodontitis and attachment loss.

Calcium carbonate and calcium phosphate, with small amounts of magnesium, potassium, and sodium in the saliva mineralize the plaque biofilm to form calculus [44]. Accumulation begins hours after plaque formation and is clinically detectable in 48–72 hours. Calculus is mineralized dental plaque adhering to the tooth root and crown. Plaque and calculus accumulation appears to be more severe on the buccal surface of the maxillary teeth, with the carnassial being the worst affected. Calculus increases the surface area for further plaque biofilm accumulation and can mechanically irritate the gingiva [34]. Calculus adheres supragingivally and subgingivally and is not easily removed with home care and dentifrices. Therefore, professional dental cleanings are necessary to remove the deposits.

5.4 Histological Changes in Periodontal Disease

Inflammation of the gingiva (i.e., gingivitis) is considered reversible with treatment. However, periodontal attachment loss from periodontitis is not reversible with the exception of added osseous surgery such as guided tissue regeneration. It is normal to have small numbers of neutrophils in relatively healthy gingiva and gingival crevicular fluid. As inflammation begins the junctional epithelium will have lateral proliferation in the coronal region and more neutrophils, plasma cells, and other inflammatory cells accumulate. An increase exudate in the sulcus occurs and connective tissue loss begins. Edematous gingivitis is common. However, fibrous gingival response to plaque occurs in some breeds (Figure 5.3).

The time frame for initial gingivitis is two to four days once the plaque starts to accumulate. The earliest clinically observable gingivitis is considered to be an established gingivitis. Within one to three weeks the junctional epithelium continues to proliferate, inflammatory cells and exudate accumulate, and collagen loss increases. Early in gingivitis, the migration of neutrophils and exudate flow moves parallel to the tooth surface, similar to the movement and sloughing of junctional epithelial cells, providing the host with another defense against bacteria by moving bacteria and exudate out of the sulcus. However, bacteria move through the large spaces in the JE and into the connective tissue of the PDL, resulting in bacterial colonization of the PDL and related cementum and bone. With periodontal pocket formation exudate flow changes to a perpendicular flow in relation to the tooth surface, diminishing the normal cleansing flow. Pocket formation and attachment loss occurs and spontaneous healing is no longer possible.

5.5 Cofactors in Periodontal Disease Pathophysiology

Many of the smaller breeds of dogs and purebred breeds have been subjectively and anecdotally been associated with an increased predilection toward crowding of the teeth and malocclusions, both of which predispose for the development of periodontal disease [5]. The thinner gingiva and alveolar bone in toy breed dogs contributes to the likelihood of a poor periodontal stage [16]. In the cat, the Somalis and Abyssinian both are well known for their predilection for aggressive forms of periodontal disease. Additionally, many lines of Miniature Schnauzers, Maltese, and Sight Hounds have a similar propensity for aggressive periodontitis. Genetics can also predispose to oral disease by affecting structure size, immune system, organ health, and numerous other body systems. The overall patient general health is important. Animals in poor health are more susceptible to infections and disease. Animals with underlying systemic problems, such as diabetes mellitus, immunosuppressant diseases, or those that are receiving commonly used immunosuppressive medications for various dermatological and systemic diseases (e.g., cyclosporine, corticosteroids) have an altered immune response and can be expected to have more periodontal health problems. With improved diets and medical care, animals are living longer, healthier lives. Unfortunately, it has also been demonstrated that as animals age, dental and periodontal disease increases [5, 60]. As pet owners take better care of dogs and cats, the pets have longer life spans and increases in age‐related chronic diseases such as periodontal disease occur. Without professional dental care and daily home care, the pets, clients, and veterinarians are reacting and extracting teeth rather than focusing on prevention and wellness. Additionally, awareness of dental disease and oral pathology in companion pets is a relatively recent evolution in veterinary medicine, making owners and veterinarians aware of the health issues that were ignored generations before.

Home dental care can dramatically affect the development and control of periodontal disease. Home care encompasses diet, chew toys, chemicals, oral solutions and gels, and brushing [61–88]. Chewing behavior affects the oral cavity, teeth, and periodontium. Pet food nutrients and food components have been involved with the changes in general health and longer life expectancies [89]. These have generally required less chewing, thereby reducing the need for a functional dentition.

However, appropriate chewing is beneficial for the gingiva and teeth. Some dental chews help reduce calculus and plaque that can lead to periodontal disease. However, inappropriate chewing of various hard chew toys such as bones, antlers, hard nylon bones, cow hooves, and other devices frequently can cause tooth fractures resulting in endodontic disease and/or endodontic‐periodontal disease [3, 90, 91]. Finally, many dental chews may make no difference in controlling plaque and calculus.

Abnormal chewing from behavioral or dermatological problems may cause damage to the periodontium. With dermatologic problems, animals may chew excessively, resulting in abrasion, at times exposing the pulp canal. This can result in endodontic disease. Second, hair wrapped around teeth or even small pieces caught in the gingival sulcus act as local irritants, leading to gingivitis and periodontitis. Separation and storm anxiety may cause a pet to chew various articles, or attempt to chew out of confining areas, causing damage to the teeth and periodontium.

Textures of diets may influence chewing if the pet has dentition and dentition that is pain free. Chewing can help with the natural cleaning effects of the teeth. Textures deal not only with the coarseness of a food, but its compressibility and resistance to tearing. Soft diets compared to hard diets have been debated. However, at this time there is no strong evidence that either soft diets or hard diets preferentially lead to greater plaque accumulation in dogs and cats [61, 92].

The nutritional components of a diet (e.g., vitamins, minerals, carbohydrates, sugars, fats, proteins) and variation can produce numerous tooth, alveolar bone, and periodontium problems. Vitamin C and the mineral selenium deficiencies have both been shown to result in a weak PDL that is easily damaged. Increases in sugars, decreased minerals, and increased pH can all have effects on the development of caries.

Saliva quality and quantity have an influence on supragingival plaque formation in humans. Individuals with reduced salivary flow or “dry mouth” have a higher rate of supragingival plaque development. Anatomically and histologically the salivary glands in dogs and cats have been characterized [93, 94]. However, very little is known about the constituents (e.g., proteonome, hormone, transcriptome) of saliva in dogs and cats.

Local trauma such as trauma of occlusion, bruxism, and foreign bodies influence periodontal disease. Hair in the gingival sulcus is a foreign body, stimulating inflammation, ulceration, and profuse exudation. Likewise, small fragments from chew toys can break off and lodge between teeth and/or in the gingival sulcus.

5.6 Periodontal Disease and Local Sequelae

Periodontal disease and the associated periodontal pockets can cause oronasal fistulas (ONFs). The ONF may not be apparent and only identified with an anesthetized examination, periodontal probing, and intraoral radiographs. Furthermore, these hidden ONFs are a cause for chronic inflammatory rhinitis [95, 96].

The juxtaposition of the maxillary molars to the incomplete orbit in the dog and cat allows periodontal disease to contribute to periocular/ocular diseases such as retrobulbar cellulitis and ophthalmic inflammation [97–99]. The proximity of the teeth (e.g. canine tooth) to the nasolacrimal canal can be a contributing factor to nasolacrimal disease and epiphora [100–105]. These conditions are more pronounced in brachycephalic dogs and cats.

The tooth‐to‐jaw ratio has not remained proportional as dogs have been bred smaller (Figure 5.4a and b) [106]. Not only are these crowded teeth more predisposed to periodontal disease but when attachment loss occurs it predisposes the mandible to “pathological” fractures [107]. A relatively normal force may lead to mandibular fractures in small and toy breed dogs.

5.7 Periodontal Disease and Systemic Health

Periodontal disease in humans has shifted from the Focal Infection Theory to Periodontal Medicine, where there is a two‐way relationship between the periodontium and the rest of the body. It is accepted that infection and inflammation of periodontal disease in humans leads to systemic ramifications such as premature and low birthweight babies, cardiovascular disease, systemic inflammatory disease, cerebrovascular events, neurological disease, pulmonary disease, and male reproductive disorders. Diabetes mellitus (DM) is a complicated bidirectional relationship with glycosylation of the microvasculature and inhibition of the local immune response in the oral cavity. Oral infection is a factor in systemic resistance to insulin in diabetic patients. In the opposite direction from oral inflammation leading to systemic disease, systemic disease can lead to oral disease. It is known that systemic neutrophil disorders, connective tissue disorders, genetic diseases, and calcium phosphate disorders can lead to aggressive periodontitis in humans [108].

Dogs have been used as models for human periodontal disease for many decades [109, 110]. Since the pathophysiology of periodontal disease and these conditions are similar in dogs and cats, systemic ramifications are possible in these species. Evidence of distant organ changes, systemic inflammation, and bacteremia associated with periodontal bacteria has been documented in dogs and cats [111–121]. Both human literature and veterinary literature conclude associations between dental infection and systemic disease. However, a direct causal relationship cannot necessarily be drawn. Caution is necessary as the pathophysiology of some systemic diseases in humans (i.e., cardiovascular disease) is different when comparing dogs and cats. The veterinary profession needs to be cautious in evaluation of the evidence in animals. Although in some cases human associations can be extrapolated.

Mechanisms of distant systemic changes include (i) direct spread of bacterial pathogens, (ii) systemic spread of bacterial endotoxin, and (iii) systemic inflammatory cytokines. Periodontal bacterial pathogens migrate through the sulcular epithelium and into the periodontal connective tissues, thereby gaining access to the pets’ vascular system. The regional tissues and reticuloendothelial system are then continuously challenged. A local and systemic inflammatory response occurs and continues until the source of infection/inflammation is controlled. Inflammatory cytokines (e.g., Interleukin‐1β, Interleukin‐6, Interleukin‐10, Prostaglandin E₂, Tumor Necrosis Factor‐α) and lymphocytes accumulate in the periodontal pocket and increase in the systemic system. Furthermore, Gram negative bacteria produce endotoxin (i.e., Lipopolysaccharide), which will induce a systemic inflammatory response and acute phase proteins from the liver [117, 118]. Although bacteria may be a contributing factor to distant organ effects, the chronic inflammatory mediators associated with periodontal disease are known to cause histological changes in organs and are as, or more, important in distant effects compared to the bacteria [116–118].

Chronic systemic inflammation associated with periodontal disease has been documented in dogs and cats with c‐reactive protein [111, 119, 121]. Hepatic parenchymal inflammation, changes in renal interstitial and glomerular tissue, and some cardiac tissue have been associated with periodontal disease in dogs [116–118]. Cardiovascular changes in dogs are more controversial at this time, due to a single case report, flawed retrospective studies, and the pathophysiology of canine heart disease [112–115]. Different methods for assessment of “periodontal disease,” “tooth abscess,” etc., question the accurate assessment of dental/periodontal disease whereas accepted American Veterinary Dental College (AVDC) staging methods with intraoral radiographs would be more accurate. Furthermore, different methods of “assessment” do not lend themselves for future meta‐analysis.

It will be difficult to find direct large causal relationships between dental infection and inflammation and distant systemic disease in dogs and cats. Veterinary medicine does not lend itself to prospective large studies (i.e., thousands to tens of thousands of patients). When the numbers are attempted it is retrospective with poorly controlled definitions and criteria written in medical records [112, 113, 120]. Small conflicting studies and case reports blur potential associations [113]. Confounding factors in small clinical veterinary studies makes interpretation of data challenging. Financial costs for a well‐designed clinical study with large numbers of patients seems almost unrealistic unless comparative translational medical research grants or industry partnerships are achieved in which human health care and/or businesses have a potential return on investment. Furthermore, periodontal disease has a complex pathophysiology with periods of quiescence and active periodontitis, and establishing research during the active phase is necessary. Nevertheless, the current human and veterinary literature does support the contention that dental infection is associated with many current systemic diseases and organ changes.

5.8 Clinical Signs Associated with Periodontal Disease

The clinical signs of periodontal disease are often hidden and insidious. Halitosis, gingivitis, supragingival plaque and calculus, reluctance to chew, head shyness, pawing at the mouth, dropping food, sneezing, nasal discharge, exaggerated jaw movements while eating, food and water bowl aversion, are clinical signs. The complaint of halitosis is the result of volatile sulfur compounds (e.g., hydrogen sulfide, methyl‐mercaptans, dimethyl sulfide, volatile fatty acids) produced by oral bacteria [120–126]. Unfortunately, many of these clinical signs require astute client observation and/or careful questioning from the clinician. Other clinical signs occur late in the disease course after the patient has suffered silently for months or years with chronic pain and infection. Commonly, there may be no obvious clinical signs to the owner and untrained veterinarian. Almost all the patients are still eating and many pet owners are unaware their pets have significant infection, inflammation, and pain in the oral cavity.

The American Animal Hospital Association (AAHA) Dental Guidelines and Canine and Feline Life Stages Guidelines recommend annual evaluations of the oral cavity [127–129]. The recommended time to start professional evaluations and cleanings, in order to prevent disease, is in the first to second year of life. Veterinary medicine needs to focus on prevention and wellness and not sickness when treating pets [129]. Periodontal disease is a preventable disease!

5.9 Clinical Examination Findings Associated With Periodontal Disease

5.10 Periodontal Charting

Knowledge of the dental formula of the permanent teeth will help in recognition of abnormalities. There are 42 and 30 teeth, in the adult canine and feline mouth, respectively. Many methods for charting are available; consistency in charting is the key. With general anesthesia the patient can receive a full oral examination, periodontal probing, intraoral radiographs, and dental charting.

The normal gingival sulcus depth in a dog is less than 3 mm and less than 0.5 mm in a cat. The edema, inflammation, and bleeding of the gums are noted (gingivitis). Purulent debris around the teeth, buccal mucositis, glossitis, palatitis, and caudal mucositis are investigated and recorded in the patient record.

While attachment loss and its measurement are the focal aspect of evaluating periodontal disease, there are many other indices and stages that may be used to quantify the extent of inflammation and disease. It is virtually impossible to cover every index available, that could be adapted from human periodontology, and some assessments may have numerous evaluation schematics to choose from. Current AVDC nomenclature is presented below with other periodontal indices [135].

When assessing and recording disease various categorical criteria can be applied. It is important to understand the assignment of the disease description [135] (reprinted with permission, AVDC).

“A stage is the assessment of the extent of pathological lesions in the course of a disease that is likely to be progressive (e.g. stages of periodontal disease, staging of oral tumors) A grade is the quantitative assessment of the degree of severity of a disease or abnormal condition at the time of diagnosis, irrespective of whether the disease is progressive (e.g. grading mast cell tumors based on mitotic figures). An index (indice) is a quantitative expression of predefined diagnostic criteria whereby the presence and/or severity of pathological conditions are recorded by assessing a numerical value (e.g. gingival index, plaque index, calculus index).”

Gingival inflammation is assessed. Gingival index (Loe and Silness) [136]:

• Gingival indice of 1. Inflammation and swelling of the gingiva with no bleeding during periodontal probing.
  
• Gingival indice of 2. Inflammation and swelling of the gingiva with bleeding during periodontal probing.
  
• Gingival indice of 3. Inflammation and swelling of the gingiva with spontaneously bleeding of the inflamed gingiva prior to periodontal probing.

Swelling of the gingiva will increase pocket depth. After resolution of gingivitis, either spontaneous or after therapy, the acute inflammation in the gingiva will resolve, and gingival shrinkage may occur, returning the probing depth to a measurement consistent with a normal sulcus. Shrinkage and resolution of the gingival edema should be differentiated from true gingival recession, which is measured from the level of the CEJ.

Furcation exposure (involvement) occurs when a periodontal probe can extend between the roots, under the crown, of multirooted teeth as a result of attachment loss (Figure 5.5) [135–138]. Extensive problems can occur with attachment loss in these areas, including increasing food and plaque retention, rapid attachment loss, and external inflammatory resorptive lesions. Pathologic invasion of a furcation is best determined by careful probing with a curved explorer, although radiographs finalize the diagnosis.

The following is the AVDC furcation staging system used in veterinary dentistry [135] (reprinted with permission, AVDC):

• “Stage 1 furcation (F1). The periodontal probe extends less than halfway under the crown in any direction of a multirooted tooth with attachment loss.
  
• Stage 2 furcation (F2). The periodontal probe extends greater than halfway under the crown of a multirooted tooth with attachment loss but not through and through.
  
• Stage 3 furcation (F3). The periodontal probe extends under the crown of a multirooted tooth, through and through from one side of the furcation to the other.”

The presence of furcation involvement generally results in a poor prognosis. It is difficult to clean the furcation area clinically and with daily home care. If these problems can be reasonably resolved and daily home care with tooth brushing can be administered, some teeth with furcation exposure can be treated and maintained with a client committed to daily brushing and semi‐annual and annual periodontal cleanings, as indicated. However, most teeth with furcation 3 exposure require extraction.

Mobility of the tooth refers to the movement of the tooth within the alveolus. Mobility of teeth is a critical diagnostic and prognostic tool. As mobility increases, so does the proportional chance of tooth loss. Some degree of tooth movement is considered normal and is termed physiologic mobility. The physiologic mobility of a tooth is limited to the width of the PDL and the elasticity of the periodontal support. Pathologic mobility is defined as the displacement of a tooth, either vertically or horizontally, beyond its physiologic movement [139]. However, a tooth that is mobile does not necessarily denote the presence of periodontal disease. Mobility can be present in a clinically normal periodontium as the result of previously applied stress, such as orthodontics, or due to a fibrous alveolus, such as seen in mandibular first incisors in the fibrous connective tissue symphysis. In addition, some transient mobility may occur following traumatic injuries, endodontic treatment, and periodontal therapy.

The following is a classification for stages of mobility used in veterinary dentistry [135] (reprinted with permission, AVDC):

“Stages of Tooth Mobility:

• Stage 0 (M0). Physiologic mobility up to 0.2 mm.
  
• Stage 1 (M1). The mobility is increased in any direction other than axial over a distance of more than 0.2 mm and up to 0.5 mm.
  
• Stage 2 (M2). The mobility is increased in any direction other than axial over a distance of more than 0.5 mm and up to 1.0 mm.
  
• Stage 3 (M3). The mobility is increased in any direction than axial over a distance exceeding 1.0 mm or any axial movement.”

While mobility of a tooth is primarily influenced by the degree of bone loss associated with periodontal disease, occlusal forces can also contribute to progressive mobility [140, 141]. Parafunctional occlusal habits such as bruxism and cage biting can result in mobility problems. The mobility itself can be detrimental and perpetuate periodontal disease and inhibit healing [141]. Periodontal splinting may be required in addition to periodontal treatments to control the inflammation and mobility. Severe mobility nearly always results in tooth loss while the patient has been suffering months or years with chronic infection, inflammation, and pain. The elimination or even control of pathologic tooth mobility can only be gained by the interference with the causative pathology. In the majority of cases, once the tooth is actually lost, the inflammation around the region lessens or even resolves, as the plaque retentive surface is no longer present. Too little too late!

Gingival recession (root exposure) is measured from the location of the CEJ to the free gingival margin (Figure 5.6). Any probing depths, whether normal or not, are recorded because an additional probing depth is additive to periodontal attachment loss. For example, if there is 3 mm of gingival recession and a 2 mm probing depth (normally, 2 mm would be considered within the normal probing depth of a dog), then total attachment loss is 5 mm. Generalized recession does occur, but more commonly one to several teeth are often involved. Periodontitis, labial frenulum tension (e.g., brachycephalic breeds), improper tooth brushing techniques, orthodontic therapy, breed (e.g., Greyhound), and even overall aggressive scaling can contribute to the recession.