Periodontal disease is a disease of the supportive structures of the teeth.
Periodontal disease is a disease of the supportive structures of the teeth. Periodontal disease includes: gingivitis, acute or chronic, and, periodontitis simplex or complex. Gingivitis is an inflammatory response to the oral microorganisms in the gingival sulcus, without pocket formation. Periodontitis is an inflammatory extension of gingivitis to the periodontal ligament with pocket formation and bone loss. The disease may be localized to a single tooth or a group of teeth with progression at a varied rate. It is progressive, and usually non-regenerative, effecting eighty-five per cent of dogs beyond three years of age, presenting the most frequently seen malady in the Veterinary hospital. Untreated and undiagnosed periodontal disease deprives the practitioner of potential income, client confidence and complete therapy to the patient.
NOTE: The total periodontium consists of the connective and supporting tissues of the tooth. These are the gingival, periodontal ligament, cementum, and alveolar bone.
The attached gingiva is the part of the oral mucosa that covers the alveolar processes of the jaw and surrounds the necks of the teeth. The gingival sulcus is the shallow crevice or space around the tooth bounded by the surface of the tooth on one side and the epithelium lining the free margin of the gingiva on the other.
The attached gingiva is the most important oral mucosal tissue. It is the first line of defense against periodontal disease, protecting the subjacent bone and supporting tissues. Without an adequate zone of gingiva (a minimum of 1.5 to 2mm) to maintain support to the tooth and protect the alveolar bone, the crestal and alveolar bone will be lost to disease. The width of the attached gingiva is a very important clinical parameter. It is defined as the distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or the periodontal pocket. It is firm, resilient, and tightly bound to the underlying periosteum of alveolar bone. The facial aspect of the attached gingiva extends to the relatively loose and movable alveolar mucosa from which it is demarcated by the mucogingival junction.
The mucogingival junction remains stationary throughout adult life. Changes in the width of the attached gingiva are due to modifications in the position of the coronal end. The gingival sulcus is the shallow V-shaped space or groove between the tooth and gingiva that encircles the newly erupted tooth - only the junctional epithelium persists. The sulcus consists of the shallow space that is coronal to the attachment of the junctional epithelium and is bounded by the tooth on one side and the sulcular epithelium on the other. The coronal extent of the gingival sulcus is the gingival margin.
Periodontitis begins as an inflammatory infiltrate subjacent to the epithelium of the gingival margin and rapidly extends throughout the marginal gingiva to affect the connective tissue underlying both the oral and the sulcular epithelium. There are pathologic alterations that take place in both the sulcular and the oral epithelium of the marginal gingiva. The inflammatory lesion is found throughout the entire thickness of the marginal gingival tissue.
There is a significant correlation between inflammatory deposits periodontal pocket depths and the amount of hyperplastic tissues. The additional factor of infection by periodontal pathogens worsens the disease. The size of hyperplastic tissue mass and pocket depth increases as the disease becomes more severe.
Bone loss begins at the bifurcation of the second premolars and around the first premolars. As the disease progresses, the third and fourth premolars and then the first molars become involved. Bone resorption appears sooner and more severely in the bifurcation regions than interproximally. The first and second premolars are the teeth most frequently lost from periodontitis usually exhibiting bilateral symmetry in the disease process.
The clinical features and pathogeneses of periodontitis in dogs is characterized by conversion of the normal gingiva to acutely inflamed, highly vascular, collagen poor granulation tissue. The disease begins as an acute vasculitis upon which a lymphoid cell response becomes superimposed. At an early stage, proliferation of the tissues of the gingival margin and the soft tissue wall of the gingival sulcus occurs and enlargement becomes apparent. With time, this area, which presents early as a rolled margin, enlarges in cross section, this enlargement appears as a mushroom-like structure with a cauliflower-like surface. The structure is comprised of collagen poor, highly vascular granulation tissue with a dense infiltrate of lymphoid cells and a variable population of PMNs. Enlargement continues until no normal gingiva remains. During this process, extensive bone resorption occurs. The soft tissues behave in one of two ways, either the hyperplastic granulation tissue remains located near the cemento-enamel junction and a deep periodontal pocket forms comparable to the situation usually seen around human teeth. Alternatively, the soft tissue retreats along the root surface as the bone resorbs. In cases of the latter type, the disease may progress to the point of tooth exfoliation without significant pocket formation.
Periodontal disease is an ongoing process rather than individual stages. A break down as to stages or grades of periodontal disease defines particular problems that occur during the disease process.
A healthy mouth free of periodontal disease presents gingival tissue with sharp gingival margins and pink or coral in color. There is normal stippling, which is a pebble like orange peel appearance, and an absence of marginal exudates, and mouth odor. This is a mouth frequently seen in adult dogs one to one and one half years of age.
Marginal gingivitis: created primarily from a lack of adequate home care resulting in the accumulation of plaque. This stage of periodontal disease is reversible with simple tooth polishing procedures.
Beginning edema, swelling of the marginal gingival tissues, and inflammation of the entire attached gingiva: This stage of periodontal disease is still classified as gingivitis and is reversible with total dental prophylaxis.
Edema coupled with gingivitis and beginning pocket formation. With pocket formation there is an extension of gingivitis to periodontitis. Most of early grade three periodontal cases are reversible with total prophylaxis, subgingival curettage and root planing.
Severe inflammatory response, deep pocket formation, pus formation, beginning of bone loss, and mobility to the teeth. True periodontitis.
Advanced bone loss, pocket formation and tooth mobility: Grades four and five require surgical intervention to perfect some sort of periodontal disease control
To summarize, periodontal disease progresses from the marginal gingiva to the gingival sulcus with loss of epithelial attachment, periodontal ligament and supporting alveolar bone. The loss of supporting bone results in loosening and eventual loss of the tooth.
The ultimate and total remission, prevention, or control of all periodontal prophylaxis, disease and surgery is directly proportionally controlled by the elimination of plaque. An absolutely plaque free condition is unattainable, but all prevention measures succeed with plaque control as does the remission of periodontal disease and the advancement of a proper periodontal surgical end result. Without plaque control all measures and methods will eventually fail.
Microbial plaque is a structured, resilient, yellow-grayish substance that adheres tenaciously to teeth. It is comprised of bacteria in a matrix of salivary glycoproteins and extracellular polysaccharides like glucans (e.g., dextrans, mutans) and fructans (e.g., levan). This matrix makes it impossible to rinse plaque away with water; it must be removed mechanically by means of hand instruments, a toothbrush or other oral hygiene aids. Supragingival plaque and subgingival plaque are two distinct morphological and microbiological entities. Supragingival plaque seen above the free gingival margin and subgingival plaque occurring below the free gingival margin.
The relationship of plaque is quite clear that "marginal" plaque and subgingival plaque are directly responsible for the initiation and progression of periodontal diseases. It is probable that supragingival plaque strongly influences the growth, accumulation, and pathogenic potential of subgingival plaque, especially in the early stages of gingivitis and periodontitis. Once the disease has progressed and periodontal pocket formation has taken place, the influence of supragingival plaque on all but the most coronally located subgingival plaque is minimal.
In the subgingival region it is possible to differentiate between adherent and non-adherent plaque. A dense plaque layer of varying thickness adheres to the tooth (root) surface. The composition of this adherent layer resembles the supragingival plaque associated with gingivitis: some gram-positive cocci but primarily filaments and Actinomyces species. The adherent plaque can become mineralized to form subgingival calculus.
Calculus is mineralized plaque. By itself it is not pathogenic, but due to its rough surface it is an ideal substrate for retention of pathogenic microorganisms.
Mouth breathing leads to dehydration of the oral cavity, rendering the plaque tougher and stickier. The TCA-protective function of saliva is reduced.
Before dental prophylaxis is undertaken a thorough oral examination of the entire mouth for other problems must be undertaken at this time. Other maladies are noted and prophylactic procedures are begun. Prophylaxis begins with the gross removal of calculus with either a hand or mechanical instrumentation.
Ultrasonic cleaning devices, used in the mechanical removal of calculus and plaque, are of two types, those whose functional tips work in a linear pattern (Peizo scalers), or those whose functional tips work in an elliptical pattern (Cavitron types). Linear patterns are preferred for there is less tooth damage or scarification. All ultrasonic cleaning devices are designed to remove supragingival plaque and calculus. Subgingival plaque and calculus (below the free margin of the gingiva) is removed with hand instrumentation (subgingival curettage). Curettes remove the soft substrate and hard substrate subgingivally as well as the diseased sulcular lining. Subgingival curettage or Closed Curettage is the most basic form of periodontal surgery.
Calculus and plaque may be removed with the use of a rotosonic bur (Roto-Pro) placed in a high-speed dental hand piece. Roto-pro burs are used supragingivally and subgingivally. This is a controversial method of calculus and plaque removal since it entails the use of high-speed mechanical instrumentation that can remove sections of crown and root unless care is taken. In using all mechanical cleaning devices care must be taken not to introduce the tip of the ultrasonic device directly to the tooth surface producing additional tooth scarification.
Ninety percent of all veterinary offices do not polish teeth after gross removal of plaque and calculus. Tooth surface irregularities are created by hand and mechanical instrumentation during plaque and calculus removal. These irregularities serve to trap and retain plaque at a much more rapid rate than polished teeth. Polishing is very simple matter. It entails the use of a rubber polishing cup and dental pumice in a slow speed dental hand piece. The slow speed hand piece can either be belt, air, or electrically driven. A complete rubber cup and pumice polishing will include, the coronal aspect and the subgingival root surfaces of the teeth. Care must be exercised when using the rubber cup on the tooth surface not to create undo heat. Excessive heat can produce pulpal necrosis.
After a thorough polishing or pumicing has been accomplished on all supra and subgingival surfaces of the teeth, the gingival sulcus must be flushed or irrigated. Rather recent studies in periodontology have shown that there is an immediate reorganization of the bacterial component in the gingival sulcus post prophylactically. If the bacteria are allowed to pool in the gingival sulcus, the pooled bacteria must be flushed from the gingival sulcus as a final prophylactic procedure. The flushing or irrigating device can be either a blunt 18 gauge needle and a 40cc syringe or a water irrigation type device. The flushing solution can be saline, a mixture of 50% hydrogen peroxide and water, or a diluted antiseptic solution. All are equally effective.
General and oral health consists of maintenance on a regular basis through diet and proper hygiene. Frequent tooth brushing is essential for gingival health, plaque control and the reduction of halitosis. Brushing is especially indicated for the cheek teeth, a primary site of periodontal disease due to the location of the perotid duct and its discharge over the upper third and fourth premolars. Proper canine and feline dentifrice and mouth solutions are available. Avoid the use of human toothpaste and sodium bicarbonate.
There are many additives to the water available to help control periodontal disease and halitosis.
One of the most effective water additives is Breathalyzer. This solution has shown great potential for disease control and halitosis prevention.
NOTE: An initial solution of water and a trace amount of garlic salt will make a palatable introductory brushing solution for dogs and cats.
Proper brushing techniques must be shown to the client. They should be taught how to retract the cheek, place the toothbrush in the mucobuccal fold, brushing the lateral surfaces of the teeth in a circular motion debriding the gingival sulcus and the crowns of teeth. Instruct the client not to remove the calcareous deposits themselves with dental scalers or hand instruments available through pet stores. They can create a tremendous amount of damage not only to the periodontium but the tooth surface as well as rendering the dog or cat mouth shy. Prophylaxis is best left in the hands of veterinarians and their staff.