Periodontitis (periodontal disease) in the dog and cat

The term periodontal disease (paradontosis, periodontitis, parodontopathy, pyorrhoea) covers several pathological conditions, specifically gingivitis and periodontitis, which in its turn is classified in various degrees. Periodontal disease is probably the condition encountered most often in domestic carnivores; over eighty percent of dogs are affected by it and it is commonly present also in the feline population (Fig. 1). Not all subjects are affected to the same degree; there is in fact an individual predisposition to developing this disease, and a predisposition linked to the breed and size of the animal has been confirmed; in the dog, for example, small-sized and toy breeds (e.g. Yorkshire terriers, Malteses, etc.) and brachycephalic dogs (e.g. Pugs) are affected most. The normal defence mechanisms of healthy subjects (integrity of the epithelium, leaching action of the saliva, tongue and lip movements, chewing, action of bacteriostatic and bactericidal substances of the gingival fluid, etc.) keep the bacterial plaque, which accumulates on the surface of the teeth, in the gingival groove and on the gums, under control. When these mechanisms do not work, or work only partially, periodontal disease sets in; this is a chronic, recurrent and continuously progressing disease (Fig. 2).

AETIOLOGY AND PATHOGENESIS

The aetiology of periodontal disease is bacterial; the response of the tissues to the pathological presence of bacteria, which accumulate on the teeth and in the gingival groove, causes an inflammatory reaction of the gingiva and of the gingival groove (gingivitis), or of all the structures that support the tooth (periodontitis) Fig. 3. The bacterial aetiology of periodontal disease is not limited to a single bacterial species; more than 400 different species have been identified in the oral cavity in the plaque alone; some of these, mainly anaerobes of the subgingival flora (Porphyromonas, Prevotella, Peptostreptococcus, Spirocheta and Fusobacterium), are considered responsible for the disease. Local factors, mainly plaque and tartar, which are the real culprits responsible for the disease, and systemic factors, which can predispose the periodontium to the onset or worsening of periodontal disease, also play a role in the aetiology of the disease. Apart from the presence of plaque and tartar, other additional contributing local factors are the amount and composition of the saliva, the oral respiration of certain breeds (e.g. brachycephalics), malocclusions, persistence of deciduous (milk) teeth and inflammatory forms of the oral cavity;  among the systemic factors, besides the previously cited heritability, the list includes the presence of severe systemic diseases, endocrine dysfunctions, altered immune responses, diet and, finally, age. The acute phases of the disease are characterised by an inflammatory response with predominance of neutrophils and by the consequent formation of a purulent exudate (dental abscess) (Fig. 4); if the pus finds a draining tract (dental fistula), the disease tends to enter into the chronic phase, markedby the presence of lymphocytes and plasma cells. The alternation of acute and chronic phases is at the basis of a progressive destruction of periodontal structures (Fig. 5); such phases often go undiagnosed, as the greatest damage is to the alveolar bone, which remains invisible.

In the course of a periodontal disease the following phenomena may be observed:

• Film: a protective layer on the tooth surface formed by saliva and debris (it favours bacterial adhesion, its presence is however normal).
• Plaque: plaque is composed of a glycoprotein matrix in which bacteria are immersed; if it is not highlighted on purpose, in general, it is invisible; it causes halitosis and can be removed with the daily use of toothbrush and toothpaste.
• Tartar: tartar is the product of the mineralisation of plaque and is mainly composed of calcium and phosphorus salts. The calcium salt supply mainly originates from the saliva, consequently more tartar deposits are present at the openings of the salivary ducts (last premolars and molars of the maxillary arch). Although it plays a minor role in the pathogenesis of periodontitis, tartar, with its irregular surface, favours plaque adhesion. The daily use of a toothbrush and toothpaste does not remove tartar effectively; for a complete removal professional cleaning is required.
• Stains:these are composed of a thin film of yellow-brown, difficult to remove proteins. Though anti-aesthetic, in veterinary medicine these stains are not a special reason for concern.
• Gingivitis: with the exclusion of cases in which the inflammatory stimulus causes gingival hyperplasia or epulis, or in the presence of alveolar bone lesions, gingivitis is a reversible disease. However, if not treated, gingivitis may develop into a periodontitis, thanks to the migration of bacteria, present in the gingival groove, towards the apex; as the lesion reaches the deepest tissues, the O2 gradient decreases and, as a result, anaerobe bacteria tend to predominate; these are the ones responsible for the transformation of the gingival pocket into a periodontal pocket.
• Periodontitis: unlike gingivitis, this is an irreversible pathological condition characterised by migration of the epithelial attachment, destruction of the alveolar-dental ligament and loss of bone tissue.

CLASSIFICATION OF PERIODONTAL DISEASE

Of the many existing classifications, the one that follows can be easily applied in the veterinary clinic.

• Clinically healthy gum: if not pigmented, gums should have a rosy pink colour;  probing of the gingival groove is normal (< 3 millimetres in the dog, < 0.5 mm in the cat); there is no bleeding during probing and no plaque or tartar is noticed.
• Gingivitis: the gum appears reddened; probing of the gingival groove gives a normal measurement but easily causes bleeding; no plaque or tartar is visible.
• Chronic gingivitis: also in this case the probing depth of the periodontal pockets is normal, however the reddened gum shows signs of chronic inflammation due to the presence of plaque and tartar (Figs.  6 and 7); halitosis is a constant symptom of this pathological condition, which can persist indefinitely or develop into a periodontitis (irreversible condition).

• Moderate periodontitis:this term should not be taken to indicate a benign stage of the disease: all forms of periodontitis should be considered dangerous for the health status of the subject. The inflammation of the gums is moderate or severe; probing of the pockets gives values that are clearly above the norm (< 7 millimetres in dogs, < 2 mm in cats) (Fig. 8); a clinical attachment loss (CAL) under or equal to 50% is present. Plaque extends to the gingival groove, while tartar may be both supragingival and subgingival. Tooth mobility is visibly increased (up to 0.5 mm of lateral oscillation) and provoked or spontaneous bleeding is always present. Radiologically, reabsorption phenomena involving up to 50% of the alveolar bone around the tooth are present (Fig. 9).
• Severe periodontitis:  the inflammation of the gums is generally severe; probing of the pockets gives high values (> 7 millimetres in dogs, > 2 mm in cats); a clinical attachment loss (CAL) above 50% is present. Plaque penetrates into the gingival groove, while tartar abounds both above and below the gum (Fig. 10). Tooth mobility goes from 1 mm of lateral oscillation up to values that make the tooth non-functional. Provoked or spontaneous bleeding is always present. Radiographically, reabsorption phenomena equal to or greater than 50% of the alveolar bone around the root are present. The dental elements affected by severe periodontitis (Fig. 11) must be extracted.

DIAGNOSTIC/THERAPEUTIC STRATEGIES

Given the complexity of the disease and  the various degrees of severity, a rigorous investigation plan should be adopted together with a treatment plan appropriate for the degree of disease detected:

DIAGNOSIS

Strict compliance with the diagnostic approach is necessary in order to allow a careful study of the disease, to make a prognosis and to formulate a therapeutic plan.

• Clinical history: it is necessary to collect information on the patient’s diet, past and present systemic and dental diseases, behavioural habits and previous treatments.
• Signalment:attention should be focused on the species, age, breed and size, all factors which affect the development of periodontal disease.
• Physical examination: aimed at verifying the general state of health of the patient and fundamental for assessing the feasibility of a possible general anaesthesia.
• Special physical examination with the patient unsedated: this allows to assess facial asymmetries, fistular tracts (Fig. 12), draining of fluids from the oral cavity; when possible, the study of grasping and chewing behaviour also provides useful information. Finally, if the subject is docile, a complete inspection of the oral cavity is performed.
• Special physical examination with the patient sedated or under general anaesthesia:
  • plaque, gingivitis and the presence of tartar are assessed by means of a visual examination. Tartar, although present, is sometimes not particularly visible; in such cases it can be highlighted  by drying the tooth with a gentle jet of air; when, on the other hand, tartar is so abundant as to cover the gum, its mechanical removal becomes necessary in order to view the underlying tissues and to correctly probe the periodontal pockets (Fig.  8);
  • a periodontal probe is used to determine the depth and bleeding of the gingival pockets and the consistency of the gingival tissue. The depth detected by the probe is considered normal when it does not exceed 3 millimetres in the dog and 0.5-1 millimetres in the cat. The resulting values must be correlated with the breed and with the pathological variations of the height of the adherent gum, such as in the case of hyperplasia or gingival retraction (Fig. 13). Tooth mobility is estimated using the probe handle. The dental furcation is evaluated using a pointed probe.
• Radiological investigation: radiographs allow to evaluate the tissues which are normally covered by the gums and by the mucosae; this investigation can be used to verify any rounding of the alveolar crest at the cemento-enamel junction, expansions of the periodontal space (Figs. 14, 15, 16, 17, 18), erosion of the lamina dura, lysis of the perialveolar bone, erosion of the alveolar crest and presence of abscesses.
• Cytology and biopsy: these are necessary whenever masses or inflamed tissues are noticed during examination of the periodontium.

TREATMENT

Pharmacological treatment

Antibiotics. Regardless of the reason leading to the administration of antibiotics in an attempt to control oral pathologies, the choice of the drug should be based on the assessment of the nature and severity of the disease in progress, on the knowledge of the bacterial flora present in the specific pathological situation and on laboratory tests aimed at identifying the species of anaerobes most represented on a percentage basis. Prophylactic use of antibiotics may be useful in immunocompromised animals, in animals with metabolic and/or organic insufficiencies, in heart disease patients and in all situations in which the bacteraemia, induced by the periodontal disease, can predispose to the development of systemic diseases. In addition, antibiotics can be recommended when healthy tissue has been exposed. Surgical treatment of parodontopathies, through ablation of the supra- and subgingival tartar, periodontal surgery, tooth extractions and other interventions may sometimes be combined with an antibiotic therapy, which may however be linked to the occurrence of undesired reactions (like bacterial resistance or superinfections).

Although periodontal disease is characterised by an inflammation sustained by bacteria, the antibiotic therapy is far from being curative. On the contrary, it is often not necessary, if not actually contraindicated; in case of use, these chemotherapeutic agents must be chosen based on clinical trials, supported by the execution of microbiological tests before and after treatment.

Disinfectants. Chlorhexidine can be used for local treatments at a concentration of 0.12-0.06% after brushing with toothbrush and toothpaste. The possible ingestion of the active ingredient by the patient should not be cause for particular alarm, as the oral LD50 is very high (1800 mg/Kg in mice). Higher doses (0.5%) may be used to prepare the operating field before dental treatments. In any case, it remains incontrovertible that chlorhexidine by itself is not capable of controlling all types of inflammation of the oral cavity, but it can be used together with medical-surgical treatments.

Other drugs. Many drugs can be administered in the attempt to control oral diseases, but only a few of them have demonstrated a sure efficacy and the absence of severe side effects.

Instrumental treatment of parodontopathies

The instrumental treatment of parodontopathies should be the last resort in a programme agreed on with the owner, aimed at providing the patient with the best possible quality of life. It is not only the degree of parodontopathy that determines the treatment, but also the owner's willingness to carry out the home treatments (diet, oral hygiene, etc.) on his/her animal, which, on its part, must be docile enough to put up with them.

Several manual interventions, variously combined together, are useful for resolving periodontal diseases, and their correct execution generally requires a considerable amount of time.

Subgingival curettage: the portion of tartar and plaque that forms below the gum line (subgingival tartar) is the one that is most difficult to remove and that damages the health of the oral cavity to the greatest degree. Ultrasonic scalers with special inserts are undoubtedly the fastest and most effective means for removing subgingival tartar; periodontal curettes may be used as an alternative.

Ablation of supragingival tartar with extraction forceps and scalers: in the presence of a considerable amount of tartar, most of it can be removed using normal extraction forceps. The block of tartar is grasped between the jaws of the forceps and broken up using slight pressure. Supragingival tartar can be removed with specific instruments, like scalers. These instruments have a working part which, with its triangular section, makes two sturdy blades available for removing supragingival tartar and plaque.

Ablation of supragingival tartar with ultrasonic equipment and polishing of the treated surfaces (Fig. 19): one of the manual methods most often adopted in veterinary odontostomatology is ultrasonic scalingto remove supragingival tartar; when the enamel of the crown comes into contact with the scaler it is damaged (only visible using an electron microscope). This situation can be remedied by polishing the tooth surface with the special pastes that are applied with a dental prophylaxis handpiece

Ablation of supragingival tartar with powder scalers: using the outlet of a hose of the dental unit, an instrument can be connected that mixes micronised sodium bicarbonate powder with air and water which, coming out under pressure, generate a spray capable of removing plaque and tartar from the surface of the tooth. Powder scalers make it possible to reach every recess and, if used with an angle of incidence of 30–60 degrees, do not damage the enamel.

PREVENTION AND CONTROL OF PARODONTOPATHIES

• Diet: the diet used should have a balanced protein content; diets poor in proteins do not in fact reduce plaque production, while an excess in proteins leads to an increase in plaque production. Diets containing excess minerals (calcium and phosphorus) lead to a greater concentration of minerals in the saliva and, therefore, they affect tartar formation. Shape, consistency, direction of the fibres and other physical characteristics of the food affect plaque and tartar formation: sticky foods should therefore be discouraged, while those designed to maintain a healthy oral cavity should be encouraged.
• Behaviour: another factor to be monitored and corrected concerns any abnormal behaviours of domestic carnivores, like gnawing on hard (bones, wood, etc.) or strongly abrasive (tennis balls, etc,) materials.
• Home treatments: daily oral hygiene is the most important and effective method for the prevention of oral diseases. Bacterial plaque can only be removed mechanically, with a toothbrush. Daily oral hygiene should be performed using suitable instruments: the optimal situation would be to perform two oral hygiene treatments daily using toothbrush and toothpaste designed for animals.

Suggested readings

1. Emily P.P., Penman S., (1992) Manuale di odontoiatria dei piccoli animali. Ediz. SCIVAC. Cremona, Italia, 1992. pp. 39-54
2. Gorrel C. (2001) Periodontal disease in the cat - EVDS Forum vol. 10 N. 1 2001 pp 13-14
3. Gorrel C. (2001) Periodontal disease in the cat – prevention is the key! - EVDS Forum vol. 10 N. 1 2001 pp 14-16
4. Gorrel C. (2008) Small animal dentistry - Saunders solutions in veterinary practice
5. Harvey C.E, Emily P.P., Small Animal dentistry. Ediz. Mosby 1993
6. Harvey C.E, Shofer F.S., Laster L., (1994) Association of age and Body weight with periodontal disease in north American dogs- Journal of Veterinary Dentistry vol. 11 n. 3 1994 pp. 94-105
7. Holmstrom S.E., Frost P., Gammon R.L. (1992) veterinary dental techniques for the small animal practitioner, W.B. Saunders Company 1992
8. Logan E.I., Finney O., (2002) Effects of a dental food on plaque accumulation and gingival health in dogs. J. Vet. Dent. Vol. 19 N. 1 2002 pp.15-18
9. Ingham K.E., Gorrel C., (2002) Il trattamento delle affezioni orali nel cane e nel gatto anziani – Waltham Focus Vol. 12 N. 1, 2002 pp. 21-27
10. Wiggs R.B., Lobprise H.B., (1997) Veterinary dentistry – Principles & practice. Ediz. Lippincott – Raven. Philadelphia, Pennsylvania, 1997
11. Winkel EG, van Winkelhoff AJ, Barendregt DS, van der Weijden GA, Timmerman MF, van der Velden U (1999) Clinical and microbiological effects of initial periodontal therapy in conjunction with amoxicillin and clavulanic acid in patients with adult periodontitis – J Clin Periodontal 1999;26:461-68