Gingivitis and Periodontitis

Inflammation and recession of perialveolar gum margins are common findings in dogs and cats.²⁹¹ These lesions are initially caused by excessive accumulation of dental plaque resulting from deposition of by-products from breakdown of food and saliva by normal resident microflora. Plaque is an organic matrix of salivary glycoproteins and polysaccharides adhering to the tooth surface that provides sites for oral bacteria to proliferate. Microflora involved with supragingival and subgingival plaque in healthy mucosal sites in dogs are resident streptococci and Actinomyces species.^171,172 At first, these gram-positive, nonmotile aerobic cocci and bacilli predominate. These bacteria produce a glycopolysaccharide referred to as a glycocalyx, which facilitates the attachment of other bacteria. This biofilm is further consolidated into a film, or plaque. Plaque accumulation results in inflammation of the gums. Plaque can become mineralized, resulting in calculus (tartar) (Fig. 88-1). As periodontal inflammation progresses with associated calculus formation, gram-negative motile, obligate anaerobic rods and spirochetes proliferate.^310,515 Pups have very few Porphyromonas species in their dental plaque; however, bacterial numbers increase as the pup matures and inevitably periodontal disease develops.¹⁹⁹ Supragingival plaque is visible as is its associated calculus formation. However, subgingival plaque incites an inflammatory response in the gingival tissue that can lead to periodontitis and chronic periodontal disease with eventual loss of teeth. Early bacterial damage occurs in the subgingival epithelial tissues with penetration of the interdental rete pegs. Proliferating spirochetes may disrupt the intercellular junctions, creating a portal of entry for other bacteria.³¹⁰ Many of these bacteria possess proteolytic enzymes that allow them to colonize and invade periodontal tissues. Periodontal pathogens destroy the integrity of the dentition and oral mucosae and can also cause bacteremia or distant tissue embolization. Unfortunately, periodontal disease is irreversible when pockets form and teeth loosen, and damaged gum tissue cannot be restored to health. In humans, periodontitis, which results from bacterial proliferation in the gingival sulcus, has been associated with an increased population of Porphyromonas (Bacteroides) gingivalis.¹³⁹ In comparison, microflora from anaerobic plaque and gingival crevices of dogs with periodontal disease are Porphyromonas denticanis–Porphyromonas gulae and Porphyromonas salivosa¹⁵⁴; Prevotella and Wolinella species that are pigmented, gram-negative rods; Actinobacillus actinomycetemcomitans; and Clostridium and Fusobacterium species. Reduced numbers of streptococci, enterococci, and staphylococci are found compared with resident flora (Table 88-3).^198,199 To reverse this imbalance, periodontal application of selected beneficial bacteria (Streptococcus sanguinis, Streptococcus salivarius, and Streptococcus mitis) after removal of dental plaque and scale in dogs inhibits pathogen recolonization of periodontal pockets,⁴⁷⁵ presumably through competitive or immunologic means. In cats, differences in the microflora between clinically healthy animals and those with gingivitis have not been appreciated; however, they have not been as extensively studied (see Table 88-2). P. gingivalis is the most likely periodontal pathogen associated with progressive periodontal disease in cats.^331–334 Salivary microflora, which differs from plaque microflora, remain relatively constant in the presence of periodontal disease.

Periodontitis can also develop whenever tooth damage occurs, exposing the dental pulp. Acute periapical periodontitis begins within 20 days of pulp exposure in dogs and progresses with time.²⁴² Fractures of teeth usually result in pulp infection before revascularization of the canal by vital tissue can occur. Although facultative bacteria predominate at first in root canal infections, anaerobes displace them with time.²² Filling the canal with a triple antibacterial paste (ciprofloxacin, minocycline, and metronidazole) in a resorbable matrix base early after injury has been shown to avert the problem of endodontic infection and promote revascularization of the pulp canal.⁵³⁰

Calculus is mineralized dental plaque that adheres to tooth surfaces, facilitating additional plaque formation and periodontal inflammation. Complete removal of all supragingival and subgingival calculi is essential in control of periodontal disease. Long-term intermittent periodontal care for dogs is highly recommended because it slows the progression of gingival recession and depth of periodontal crevices that develop in dogs not receiving dental hygiene.¹⁹³ Gingival hypertrophy and alveolar abscess formation are sequelae of calculus formation.^324,327 The type of microflora present, the diet, and the animal’s chewing habits may be important in the formation of calculus.^265,503 Advancing age is a predisposing factor in dogs.¹⁸⁰ Leukopenia and bacteremia occasionally develop as secondary effects.²⁷⁰

Radiographic examination of the teeth and associated bony structures is required to determine the condition of the tooth roots and secondary bone resorption before treatment. Furthermore, endodontic involvement, neoplastic destruction of bone, and nasal and sinus passages can be evaluated to determine the extent of disease and feasibility of resolving it.

Surgical or mechanical debridement of diseased teeth or surrounding tissues may be required. Although bacterial pathogens are important in periodontitis, antimicrobial therapy alone does not eliminate progression of disease. Proinflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin (IL)-1, have been important in the progression of periodontal disease in experimental animals.84,131 Cats with more severe periodontal disease have greater serum antibody titers to P. salivosa and P. gingivalis than those with less severe periodontal disease.^{274,330,334,335} Inhibition of IL-1 and TNF with specific blockers has been beneficial in inhibiting inflammation and preserving bone in the periodontal tissues. Oral IFN-α4, administered to dogs with naturally occurring gingivitis, reduced both periodontal bacterial counts and associated gingival inflammation.²⁰⁰ Other anti-inflammatory drugs, such as metalloproteinase matrix (e.g., tetracyclines), adelmidrol (an aliamide), and prostaglandin inhibitors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), have been beneficial in this regard. These findings support the concept that periodontal tissue loss is caused by an exaggerated host response to certain species of bacteria with the ability to grow on the tooth surface and in periodontal structures and the triggering of an inflammatory cascade.

Adjunctive management methods such as providing hard diets, regular tooth brushing, and oral hygiene chews have been shown to reduce the incidence of calculus accumulation.* Diets or supplements with Omega-3 fatty acids reduce the local gingival inflammatory response in P. gingivalis infection and may provide some benefit.²³⁴ Treatment includes the extraction of severely affected teeth, debriding necrotic or proliferative gum margins, root planing with curettes, and scaling calculi from the remaining involved supragingival and subgingival dental surfaces by manual or ultrasonic means. More aggressive surgical debridement is needed for advanced periodontal disease.⁴¹⁹

Systemic antimicrobials such as tetracycline, metronidazole, and tinidazole (Table 88-4) and topical chlorhexidine have been evaluated for treatment of periodontitis in experimentally affected dogs.^367,377 Clindamycin treatment for 5 days after dental prophylaxis reduced subsequent oral odor and dental plaque formation when dogs were monitored for up to 70 days.⁵⁰¹ Treatment of clinically healthy beagle dogs with clindamycin for 14 days reduced the amount of gingival crevicular fluid, dental plaque, and gingivitis.⁵³⁸ Tetracycline and metronidazole have been beneficial in reducing dental calculus or preventing its reformation when they have been given with or without mechanical cleansing. After 1 year of tetracycline therapy, dogs with periodontal disease had less alveolar bone resorption than untreated controls.⁵²⁸ Metronidazole therapy has had similar beneficial effects.³³⁶ Tinidazole had good efficacy against P. gingivalis–like bacteria.⁴⁰⁴ The use and efficacy of systemic antimicrobial therapy for this purpose has been questioned as an alternative for indicated dental procedures¹⁷⁸ and may lead to antimicrobial-resistant strains. Systemic antimicrobial therapy is not indicated as a long-term solution to periodontal infections. For example, in dogs with periodontitis and periodontal bone defects, reestablishment of the oral microflora with beneficial species of microorganisms, after dental scaling and root planing, facilitated the healing process in the perialveolar bone and controlled progression of periodontal infection.³¹⁸

Perioceutics are pharmaceutical formulations that are placed into periodontal pockets to allow for sustained antimicrobial activity against periodontal pathogens. They are used as an adjunct to scaling and cleaning the dental surfaces. These perioceutics, consisting of tetracyclines and having antibacterial and anticollagenase activity, are delivered into the periodontal pocket via a blunt cannula. Once there, the biodegradable polymer gels coagulate, allowing for sustained release of the drug for up to 13 weeks.63,233 Dogs with periodontal disease that had dental cleaning followed by doxycycline polymer applied to their gingival crevices had less periodontal disease than untreated animals after 12 weeks of monitoring.^165,175,175 In addition to a reduction in the depth of alveolar pockets, a reduction in aerobic microaerophilic and anaerobic bacterial microflora and proteolytic enzymes, such as collagenase, have been observed.⁵³⁹ Topically applied polymers containing doxycycline (Heska, Fort Collins, CO; Pharmacia Animal Health, Piscataway, NJ) or minocycline (Sunstar Inc., Takatsuki, Japan) are available for treatment and control of periodontal disease in dogs. Flushing dental surfaces once daily with 0.1% to 0.2% chlorhexidine¹⁴⁹ or alternate-day brushing⁴¹⁰ may delay accumulation of calculi. Unfortunately, chlorhexidine may stain teeth light blue, but a commercial product formulated especially for dental purposes (Nolvadent, Fort Dodge Labs, Fort Dodge, IA) does not stain. Monoperoxyphthalic acid applied before chlorhexidine was used resulted in less dental staining.⁵⁹ Daily application of chlorhexidine gel was effective in reducing recurrence of dental plaque in dogs.¹⁷⁰ Twice-daily applications of nisin, an antimicrobial peptide, were as effective as chlorhexidine in preventing calculus in dogs.¹⁸⁸ Numerous cleansers and brushes have been developed for daily brushing of dogs’ teeth, and they warrant consideration when a dog has a tendency to form calculi. Special diets are also available that may help to reduce calculus formation. Daily feeding of a commercial dental food significantly reduced plaque and gingivitis by 39% and 36%, respectively, compared with daily feeding of a control dry-food diet.²⁶⁶

The oral administration of probiotics may also benefit oral health by preventing the growth of pathogenic bacteria or by modulating mucosal immunity in the oral cavity. A small number of in vitro and in vivo studies have been performed on the role and effects of probiotics on oral health. There are several important modifications for “oral probiotics” that should be considered when compared to probiotics used for promoting intestinal health. For example, oral probiotic bacteria should adhere to and colonize on dental tissue and should be part of the biofilm. They should not ferment sugars, which subsequently lowers the pH and is detrimental to dental health.³⁰⁸ Consumption of products containing probiotic lactobacilli was shown to successfully reduce the risk of caries and the number of mutans streptococci in the oral cavity.⁴⁹ A few studies also revealed that probiotic lactobacilli strains were useful in reducing gingival inflammation and the number of black-pigmented rods including P. gingivalis in the saliva and subgingival plaque.^196,243 A split-mouth, double-blind randomized pilot study, involving eight beagle dogs with moderate experimentally induced periodontitis, documented the impact of multiple subgingival applications of pellets containing S. sanguinis, S. salivarius, and S. mitis.³¹⁸ The bone density within periodontal pockets treated with the beneficial bacteria improved significantly after 12 weeks, whereas there was a nonsignificant change in the control group that received a single root planing at baseline. In addition, there was a significant increase in the alveolar bone level at the end of the study based on repeat radiographs compared to the control group. These studies clearly illustrate that the probiotic route clearly has potential for improving oral health, but much more needs to be known about the oral microbiota in health and which organisms are capable of restoring and maintaining health when delivered in a probiotic format.

A P. denticanis-gulae-salivosa bacterin that was commercially available as an aid in preventing periodonal disease in no longer licensed¹⁵⁵ (see Immunoprophylaxis for specific diseases, Chapter 100 and Web Appendix 3). In addition, recombinant protein vaccines targeting extracellular proteinases and adhesins of Porphyromonas spp. have been effective in attenuating Porphyromonas infection in mice.¹¹⁶

In cats with naturally occurring periodontal disease, clindamycin, doxycycline, or spiramycin-metronidazole, but not amoxicillin-clavulanate, reduced the numbers of P. gingivalis.³³³ Furthermore, improvement was observed in the degree of periodontal inflammation. This occurred despite the fact that all isolated organisms showed susceptibility to all the tested drugs. These drugs should probably be selected for adjunctive treatment along with mechanical debridement in cats. The use of special diets supplemented with dental chews may be effective in reducing calculus formation on cat teeth.^191,194 Cats were fed either a dry diet only or a dry diet supplemented with dental chews.¹⁹⁴ A two-period, crossover design was used, and the test phase lasted 4 weeks. Results indicated that the daily addition of dental chews to a dry diet was effective in reducing plaque and calculus accumulation and the severity of gingivitis. In other studies, cats fed large kibbles with mechanical cleaning qualities had less gingivitis and tartar than cats on small kibble diets with or without daily brushing.⁴⁹⁴ Dental brushing has also been helpful in the prevention of periodontal disease in cats.^191,194 Daily application of zinc ascorbate gel has also been effective in decreasing bacterial growth, plaque formation, and gingivitis in cats when it was used after dental prophylaxis.⁶²

Systemic Effects of Oral or Periodontal Infections

Ophthalmic manifestations can occur from dental disease because of the close proximity of the caudal maxillary teeth and the orbit (Box 88-1). Systemic complications of periodontal disease, including cerebral and myocardial infarction, systemic hypertension, and early mortality, have been linked in people.^89,358 A large body of evidence in humans suggests that patients with diabetes, in particular when inadequately controlled, are at an increased risk of developing periodontal disease³⁰⁵ and show accelerated alveolar bone loss.⁴⁷² From the opposite viewpoint, the presence of periodontal disease itself in diabetic patients may influence their glycemic control.⁴⁷¹ There is evidence that resolution of periodontal inflammation can improve metabolic control of blood glucose in diabetics,²⁴¹ and the mechanism underlying the effect is likely due to resolution of inflammation from the periodontal tissues.

Similar relationships of periodontal inflammation to heart, liver, and kidney disease have been made in dogs.⁷⁹ However, controversy has been addressed in veterinary publications as to the role of oral cavity infections and systemic disease.¹⁶¹ In some retrospective studies, no statistical association was found between bacterial endocarditis in dogs and either dental or oral surgical procedures or oral infection.^352,460,460 Unfortunately, detailed prospective screening and grading of oral cavity changes were not undertaken in these studies. In contrast, a statistical association was found between periodontal disease severity in dogs and degenerative changes in the left atrioventricular valves and pathologic changes in the liver and kidney.³⁵¹ Other studies involving whole-mouth periodontal scoring show a correlation of the severity of oral disease with microscopic lesions in distant organs⁷⁹ and increased mediators of inflammation in serum.³⁷⁵ Further focused prospective studies with suitable control animals will be needed to make conclusive assessments.

Bacteremia associated with dental manipulations may be clinically asymptomatic, cause acute septicemia, or subsequently result in bacterial endocarditis or localized embolic tissue infections (see Chapter 86).³⁷⁸ The severity of bacteremia frequently correlates with the degree of periodontitis present. In people, use of antibacterial prophylaxis during dental procedures in patients predisposed to infective endocarditis is accepted, but also debated.¹⁴⁶ In cats with periodontitis undergoing dental scaling and extraction, 36% had positive blood culture results at the time of the dental procedures.¹⁵³ Bacteria most commonly isolated were Propionibacterium acnes, Pasteurella multocida, and Staphylococcus epidermidis. None of the cats became ill after the dental procedures. Septic pericarditis in a cat was attributed to presumed bacteremia from a prior dental procedure.²⁶³ Positive blood culture results of resident microflora have also been found in up to 40% of dogs with periodontal disease undergoing dental scaling and tooth extraction, and none showed clinical evidence of bacteremia.¹⁵² Dental procedures should not be performed at the same time as other surgical procedures, because the release of bacteria from the dental procedure can infect surgical wounds. Oral microflora may establish themselves in tissue injured or devitalized by routine surgical procedures, sutures, or foreign implants. When dentistry is performed on immunocompetent animals with clinical oral cavity infections, prophylactic administration of antimicrobial drugs has been recommended (see Table 88-4). Routine use of antimicrobials for dental procedures should be mandatory in immunocompromised animals. Amoxicillin is the drug of choice for humans undergoing dental cleaning where prophylactic administration is indicated. Intravenous administration of aqueous penicillin during ultrasonic dentistry in dogs did not alter the prevalence of bacteremia before or after dental manipulation.³⁶ In dogs and cats, pretreatment with clindamycin at 5.5 mg/kg for 5 days decreased plaque and reduced aerosolization of bacteria during ultrasonic teeth cleaning.⁵⁴¹ Ampicillin (amoxicillin) has been recommended empirically beginning 1 hour before dental procedures.¹⁸² On the basis of in vitro susceptibility testing of periodontal disease–associated bacteria, chloramphenicol, cephalosporin, erythromycin, or gentamicin have also been recommended. With the exception of erythromycin, all can be given parenterally while the animal is anesthetized. Gentamicin should never be administered alone because it is relatively ineffective against anaerobic bacteria. For these reasons, ampicillin (amoxicillin), chloramphenicol, clindamycin, metronidazole, or cephalosporin with or without gentamicin or a quinolone (although rarely used) are recommended for dental prophylaxis. Prerinsing the oral cavity with chlorhexidine solutions can also be performed just before the sealing and cleaning procedure. The Drug Formulary in the Appendix and Table 88-4 should be consulted for drug information and appropriate dosages. Therapy should begin no earlier than 4 hours before the dental procedure and should preferably be continued throughout the procedure by intravenous infusion. The most critical period is during the procedure. Drug administration should be terminated no longer than 12 hours after the dental procedure because no additional benefits are gained, and the risk increases for antibacterial-resistant bacterial infections.

Because of the large numbers of bacteria in the oral cavity and especially the gingival crevices, public health considerations are important. Face masks and ocular shields should always be worn by humans who clean animals’ teeth. In addition, biofilms that form on the inside surface of water lines of ultrasonic scalers may harbor Legionella species, which might produce acute pneumonia in susceptible individuals.⁵²⁷

Glossitis

Inflammation of the tongue from infection is common among lingual lesions.⁸⁷ Primary viral causes in dogs include canine distemper virus, canine calicivirus,¹⁰⁴ canine parvovirus, and feline calicivirus (FCV) (see Chapters 3, 8, and 14). Bacterial, fungal, and protozoal organisms can also involve the tongue, producing suppurative or granulomatous lesions.³⁵⁷ Primary physical injury can occur via trauma, bite wounds, burns, caustic substances, and foreign bodies. Metabolic conditions such as diabetes mellitus, hyperadrenocorticism, uremia, and niacin deficiency can induce lingual ulcerations. In addition, autoimmune diseases such as pemphigus vulgaris, bullous pemphigoid, and systemic lupus erythematosus are associated with ulceration of the tongue. Secondary infections develop in these ulcers with opportunistic organisms such as Candida spp. or oral bacterial microflora. Organisms are not often found on histologic examination; however, suppuration and overlying ulceration are usually apparent. Foreign material such as hair, bone, or plant matter can be present in lingual wound infections.

Gingivostomatitis and Pharyngitis

In humans, necrotizing ulcerative gingivostomatitis (NUG), or “trench mouth,” is a syndrome with multiple causes and is characterized by oral ulcerations and secondary infections. NUG may be a manifestation of systemic or immunosuppressive illness. Opportunistic overgrowth of oral microflora occurs in many diseases when immune defenses are impaired or oral ulcerations develop.391,470 Similar to periodontitis, motile (predominantly anaerobic) bacteria, including spirochetes, often proliferate and may invade tissues before the development of necrotic lesions.³⁸⁵ NUG may also be observed in dogs or cats and has been well documented in Maltese terriers¹⁶² (Fig. 88-2). It is caused by a similar proliferation of anaerobic and spirochetal bacteria (Borrelia and Treponema).³²⁹ The histopathologic infiltration in the oral lesions of immunocompromised animals consists primarily of leukocytes, in contrast to the lymphoplasmacytic infiltrates seen in immune hyperresponsive disorders²⁷⁹ (see Feline Lymphocytic Plasmacytic Ulceroproliferative Gingivostomatitis, later). As in humans, the causes of NUG in dogs and cats are equally diverse and include many acquired immunosuppressive conditions, such as diabetes mellitus, persistent neutropenia, feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) infections, and canine Cushing’s disease. Exogenous glucocorticoid administration in dogs also increases susceptibility to NUG.³¹⁰ As in humans, psychologic and physical stresses may be involved in some animals. Bristles of plant awns can induce a similar syndrome when they become embedded in gingival tissues.³⁰³ Fungal stomatitis can result from infection with Candida species. Candidiasis can be associated with diffuse oral inflammation, especially on the tongue and at mucocutaneous junctions. See Chapter 63 for additional information concerning its diagnosis and treatment.

Cats subclinically infected with FCV and feline herpesvirus (FHV-1) can develop oral ulceration with or without respiratory signs after stress or immunosuppression, such as with concurrent FIV infection. Stress also appears to reduce the amount of fibronectin, a receptor protein, on epithelial cells for gram-positive organisms. Thus, overgrowth with gram-negative bacteria may develop.

The pattern of oral ulceration may be helpful in determining its underlying cause (Table 88-5). Regardless of its cause, oral ulceration has a particular clinical syndrome characterized by reluctance to eat, hypersalivation, halitosis, and evidence of pain on opening the mouth. Hemorrhage may occur spontaneously or after oral manipulation. Although rare, systemic signs may include fever, lymphadenomegaly, and lethargy. Ulcers may be distributed throughout the oral cavity but are usually concentrated on the dental, labial, and gingival surfaces. Ulcers may be covered by a pseudomembranous exudate. White pseudomembranous plaques can be found in cases of candidal stomatitis. In many neutropenic cats infected with FeLV, the ulcers characteristically have minimal exudation; some can progress rapidly, with sloughing of large portions of the caudal oropharynx or larynx.

Feline Lymphocytic Plasmacytic Ulceroproliferative Gingivostomatitis (Faucitis)

Chronic faucitis in cats is a multifactorial disease thought to be caused by a variety of persistent microbial organisms in the oral cavities of cats with immunologic hyperresponsiveness. Although a variety of infectious agents have been associated with this disorder, direct causation has not been proven.³⁶⁵ FeLV, FIV, FCV, FHV-1, and Bartonella species can be present subclinically, making correlations difficult. FCV can be detected in many cats with this condition; however, the disease has not been experimentally reproduced.^24,91,91 The presence of a persistent infectious agent such as FCV and an aberrant host immune response, with or without a co-infecting agent such as FIV,^236,477,477 is likely responsible for disease manifestations. Hard, dry cat food also appears to have a role in exacerbating palatine ulceration in cats with acute FCV infection.²²² The prevalence of FeLV infection in affected cats with stomatitis is lower than that of FIV.

Faucitis is characterized by vesicular, ulcerative, and later, proliferative lesions in the mucosa, usually accompanied by mucosal ulceration and lymphoplasmacytic or eosinophilic infiltrations in the tissue of the caudal pharynx at the glossopharyngeal arch (fauces).218,477,477 Faucitis frequently appears among a number of cats within a household and tends to be recurrent after the initial treatment or is unresponsive to treatment. In chronic stages, proliferation of granulation tissue forms large masses in the caudal pharynx (Fig. 88-3). FCV has been isolated in a high percentage of cats with this syndrome compared with clinically healthy cats or those with oral ulcers at other locations. Cessation of FCV shedding was associated with resolution of chronic gingivostomatitis in one cat.¹ It is likely a hypersensitivity phenomenon to persistent FCV infection. Co-infections with FIV or FeLV result in the most severe lesions. CD8+ T cells, representing cytotoxic and suppressor T cells, have been in the high reference range for all cats. In one study, cats with chronic gingivostomatitis were more likely to shed FCV and FHV-1 together than either virus alone.²⁶⁹ Compared with nondiseased cats, affected cats showed a significant increase in the relative messenger RNA (mRNA) expression of IL-2, IL-4, IL-6, IL-10, IL-12 (p35 and p40), and interferon (IFN)-γ. These results suggest that the normal feline oral mucosa is biased toward a predominantly (T_h) type 1 profile of cytokine expression and that during the development of lesions seen in feline chronic gingivostomatitis, a shift in the cytokine profile from a type 1 to a mixed type 1 and type 2 response occurs.¹⁵⁸

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