Proceeding of the NAVC North American Veterinary Conference Jan. 8-12, 2005, Orlando, Florida

Transcription

1 Proceeding of the NAVC North American Veterinary Conference Jan. 8-12, 2005, Orlando, Florida Reprinted in the IVIS website with the permission of the NAVC

2 Small Animal - Dentistry PREVENTION OF PERIODONTAL DISEASE A DIFFERENT APPROACH Colin E. Harvey, BVSc, FRCVS, DipACVS, DipAVDC School of Veterinary Medicine University of Pennsylvania, Philadelphia, PA Periodontal disease is the most common disease in domestic dogs and cats. This manuscript describes what causes periodontitis, and how to put that understanding to use to prevent this disease. Periodontium refers to the tissues that hold the tooth in the mouth, including the alveolar bone, periodontal ligament and gingiva. Periodontal disease = plaque-induced disease of any part of the periodontium. It is often separated into two conditions, defined as: Gingivitis = Inflammation of the gingiva, which is reversible. (Conclusion: If it is reversible, it cannot be not a big deal..) Periodontitis = Loss of attachment. (This also does not sound like a big deal, compared with Alveolar bone osteomyelitis, which is a more accurate definition of periodontitis.) Periodontitis is sometimes divided into active or passive periodontitis. However, periodontitis ( itis = inflammation of) is by definition active. Passive periodontitis really means loss of attachment (= evidence of past periodontitis, with no current evidence of active disease) so by definition it is not periodontitis! TEETH Teeth are used to prehend and perform mechanical work on food material. Not surprisingly, they vary greatly depending on the natural food sources of each species (herbivore, omnivore, carnivore). Whether the teeth tear, cut or crush the food material, a hard surface is required. As the hardest tissue in the body, enamel is very suitable. The crowns of teeth are the head of the hammer, the face of the rasp, or the points and blades of a pair of scissors. No matter how hard they are, teeth cannot be effective without a platform or handle from which force can be directed. The jaws are the handles. When one hard structure is struck against another hard structure with sufficient force, one of the two is damaged it cleaves. This would be true of occluding teeth if they were rigidly fixed to jaws. Fortunately, there is the periodontal ligament sandwiched between them. PERIODONTAL LIGAMENT The periodontal ligament has three primary functions: 1. Hold the tooth in the jaw. The collagen fibers of the periodontal connective tissue are the laces knitting the tooth to the bone, and are locked into the cementum and alveolar bone. 2. Provide a shock-absorbing effect to prevent fracture of teeth during biting. It spreads the mechanical force generated by occlusal action around the full surface area of the root. 3. Maintain and repair the periodontal ligament tissues. Vascular tissue, fibroblasts. Remember Wolff s Law from orthopedics? We usually think of Wolff s Law as Bone gets stronger if the mechanical work it is required to do increases, and assume that it involves healthy mineralized bone structure. Wolff s law also holds true for soft tissues, and this is particularly noticeable in the periodontal ligament. If there is no or significantly reduced on-going occlusal work, the quality of collagen is degraded. ALVEOLAR BONE The alveolar bone has the most rapid turn-over of any bone in the body, followed by the cortices of the mandible and maxilla. This is why we observe rubber jaw in hyperparathyroidism, instead of rubber leg. It is a reflection of the rich blood supply of the jaws. The crestal bone is a critical area. Think of the periodontal ligament as a zipper the crestal attachment is the open end of the zipper. If it is not fully closed and locked by the zipper tab, the entire zipper closure is at risk. GINGIVA The gingiva is the locking tab at the open end of the periodontal ligament zipper, and it provides a thick protective cap to the crestal bone. The marginal gingiva, which is unattached to bone, moves with the tooth to keep the cemental attachment protected. It is held in place by the hemidesmosomal attachment of the sulcular epithelium to the enamel surface a chemical glue. The glue layer is itself protected by the external shape of the crown (dental or supragingival bulge there is no thickening of enamel, so enamel bulge is incorrect). This finely-engineered system works very well under normal conditions. Of course, normal conditions include the daily janitorial work of occlusion in wild carnivores. But the mouths and teeth of many companion animals do not work under normal conditions. The unattached surfaces of the teeth (normally just the enamel) are inert, unlike every other part of the body surface (except the nails). Enamel has no epithelium, and no basement layer and vascular supply that react to surface contamination or trauma. THE ENVIRONMENT The teeth live in an open environment. Any inert surface exposed to the environment is covered with microorganisms. Think of the tongue as a dish rag and the nose as a vacuum cleaner and you realize why there is such a rich microflora in the oral and nasal cavities. A moist surface supports more microorganisms than a dry surface. A warm environment encourages many organisms to grow faster. A fluid loaded with microbial nutrients encourages growth. The mouth is constantly moist, warm and very often loaded with nutrients. The teeth are constantly covered by oral fluid spread by the tongue and lips. Intermittent evaporation causes the fluid to become thicker, resulting in deposition of a glycol-protein layer (the pellicle ) on the crowns of the teeth. Think of it as fly-paper. Perfect conditions for development of a biofilm. When if occurs on the inert surfaces of the teeth, the biofilm is called dental plaque. 205

3 The North American Veterinary Conference 2005 Proceedings The microbes do not have completely free rein. The fluid the teeth are bathed in has antibacterial properties (lysozyme, lactoferrins, antibodies), and the combination of this antibacterial activity and daily occlusal scrubbing works well to keep the enamel biofilm from getting out of hand. Excellent long-term oral health is easy to achieve in dogs if daily oral care is impeccable. When oral care is less than optimal, and the biofilm is allowed to accumulate, the biofilm becomes thicker and more complex. THE CONSTRUCTION SITE The rigid, non-vascularized enamel tooth surface is the ideal platform for development of a biofilm (plaque), and its cousin, calculus. Calculus forms when calcium carbonate and calcium phosphate salts in salivary fluid crystallize on the surface of the teeth, mineralizing soft plaque. It takes 2-3 days for plaque to become sufficiently mineralized to form calculus that is resistant to being readily wiped off. This is the window that we work with in oral home care planning. Calcium salts are more likely to be deposited on plaque in an alkaline environment. Unfortunately, the mouths of dogs and cats are slightly alkaline (oral fluid in humans is usually slightly acidic). Thus, dogs and cats are more prone to deposition of calculus than humans. (There is some good news - probably because of the ph difference, caries is uncommon in dogs and cats compared with humans.) The bacteria found in dental plaque are not required for deposition of calculus - germ-free dogs develop calculus deposits. But germ-free dogs do not develop the gingival inflammation and bone loss that occurs in many pet dogs as a result of deposition of plaque and calculus. The bacteria in plaque are the real cause of gingivitis and periodontitis. However, there are two clinically important attributes of calculus: 1. Although calculus itself does not cause disease, it provides a protected physical location for development of plaque, including deep crevices that promote growth of anaerobic bacteria. 2. Once formed, calculus cannot be removed except by mechanical action on the surface of the tooth. When the occlusal scrubbing is insufficient, the biofilm on the enamel thickens and matures. Think of a biofilm is a microbial village, constantly under-going changes the longer it is allowed to grow, the more complex it becomes. A tooth with thick calculus deposits and deep periodontal pockets has expanded beyond a village it is a thriving microbial city, with neighborhoods each unique unto themselves. The thicker the biofilm, the more likely it is that the oxygen gradient will result in an anaerobic environment at its base. PERIODONTAL INFECTION Gingivitis and periodontitis are often referred to as bacterial infections. The usual definition of an infection is that Koch s postulates can be applied: A sample from an example of spontaneous clinical disease yields a specific microorganism. The organism is identified and grown in pure form in a laboratory. It is introduced into unaffected tissues of a healthy individual. The disease develops at the site of inoculation. A sample from the area of induced disease is obtained, and the organism is cultured and identified from the sample. Without fulfilling each of these five steps, we cannot prove that gingivitis and periodontitis are the result of infection by specific organisms. The reason we cannot is that plaque, the dental biofilm, is a complex mixture of organisms. Around 500 bacterial species have been identified to date in this microbial city. Note that the bugs are not there to seek opportunity to infect the periodontal tissues they are just obeying laws of nature, because the conditions are right for growth in this environmental niche. Plaque development over the first few days following dental scaling: 1. Colonization of the pellicle by cocci (they are short, so are not readily displaced by the tongue, and are aerobic, growing well in the well oxygenated environment of the thin pellicle). 2. Adhesion of aerobic rods on the sticky and irregular surface provided by the coccal layer. The thickening biofilm allows them to hold on and grow. 3. Further thickening and maturation of this aerobic mix. The aerobic cocci and rods multiply, and as they do so, the oxygen gradient changes, so that at its deepest point, oxygen is no longer available. The occasional facultative and obligate anaerobes caught in the biofilm start to grow. The maturation of plaque to the point where it will support anaerobic organisms takes about 24 hours in the dog. 4. The biochemical environment changes as the biofilm continues to mature, and gingival inflammation results. The mixture of microbial detritus and products of inflammation results in a physical and chemical environment that allows spirochetes to thrive. 5. In biofilm parlance, a Climax Community - a semistable state in balance with available nutrients and oxygen. PERIODONTOPATHOGENS Periodontal microbiology is a unique sphere of microbiology because many of the organisms now known to be important are difficult to grow and are rarely looked for in samples from other parts of the body. No veterinary microbiology laboratory has the experience and expertise to identify many of these organisms, and specimens submitted for routine veterinary culture and sensitivity testing will miss the most important bugs. Periodontopathogens are the putative cause of gingivitis and periodontitis. Challenges to achieving expertise in veterinary periodontal microbiology: Anaerobic culture techniques are absolutely essential. Many of the organisms of interest are obligate anaerobes. Spirochetes, which are very common (seen on electron-microscopic examination, they are densely lined up perpendicular to the root surface in pockets), are notoriously difficult to culture. A subgroup of spirochetes called Pathogen-Related Oral Spirochetes (PROS) is now recognized. Carnivore and humans mouths have some important microbiological differences, and Porphyromonas 206

4 Small Animal - Dentistry spp. may favor a slightly alkaline ph, which is found in the mouths of carnivores. 1. Porphyromonas gingivalis is listed as a key human periodontopathogen. Canine and feline P. gingivalis -like bacteria are catalase-positive, and are now identified as Porphyromonas gulae. 2. Other recently-recognized canine and feline Porphyromonas organisms include: Porphyromonas cangingivalis, Porphyromonas canoris, Porphyromonas cansulci, Porphyromonas crevioricanis, Porphyromonas gingivicanis. Identifying the bugs is only the first step. In the absence of being able to prove Koch s postulates, factors important in demonstrating periodontopathogenic significance are: 1. The bug is found more commonly in diseased areas of the mouth than in healthy areas. 2. The bug produces products known to be toxins and tissue-destructive enzymes. 3. Cytotoxic effects are seen on tissue culture. Periodontopathogens work collectively, whether by enhancing aggregation in the biofilm or attachment to epithelial cells. Human P. gingivalis have fimbriae that play an important role in adherence of the organisms to gingival cells as the initial step in the progression of periodontitis; canine and feline P. gulae have the same fimbrial protein, which may be a significant antigen for development of antibody protection. CLINICAL AND PATHOLOGICAL EFFECTS As with bacterial infections in any other tissue, the initial effect is inflammation of the gingival tissues. What happens then depends on whether the local tissues are overwhelmed by the bacterial burden. Neutrophils are attracted to the site, move onto the epithelial surface, ingest the bacteria and then digest the bacteria. Many of these neutrophils are over-full and they burst. Some retire into the adjacent tissue before they burst. These bursting neutrophils release bacterial toxins and destructive enzymes including metalloproteinases such as collagenase within tissue, causing breakdown of the integrity of the epithelium and connective tissue. The bursting neutrophils also release cytokines that propagate the inflammatory response. When oral hygiene is poor (i.e. the maturing plaque is not wiped off the surface of the tooth), the bacterial load is constantly enlarged, ratcheting up the response, and the mixture of bacterial and cell degradation products becomes destructive. Thus the neutrophils the body s firemen contribute to the development of periodontitis. The epithelial layer is breached, exposing the more vulnerable connective tissue to the onslaught. As the destructive mixture descends deeper into the tissue, inflammation-induced resorption nibbles away at the alveolar bone to produce periodontitis (alveolar bone osteomyelitis). The ability of animals (including humans) to resist a given gingival bacterial load varies greatly, depending on immunological competence, individual differences in protective constituents of saliva, age, stress, nutritional status, concurrent infections (e.g. FIV), non-oral health status and probably several other factors that are incompletely understood or not yet known. Continuing bone loss causes instability of the attachment of the tooth. The result is mobility, which causes the tooth to be pushed against the remaining bone during chewing. This enhances tissue destruction by stretching the soft tissues and squeezing the blood vessels adjacent to the tooth. If the process continues for long enough (which varies greatly from patient to patient), the eventual result is loss of the tooth. This is actually a defense mechanism - finally, the remaining tissues can recover because there is no longer the constant presence of the overwhelming bacterial burden. In a old Yorkie, by then there may be only a match-stick of mandibular bone present adjacent to the roots of the first mandibular tooth. In the often long period between the initial gingivitis and the final exfoliation of the tooth, bacteria that find themselves adjacent to capillaries may end up causing bacteremia by diapedesis. Bacteremia is frequent in patients with gingivitis and active periodontitis, and it is rapidly cleared by the reticulo-endothelial system in otherwise healthy patients. But what are the long-term consequences of frequent bacteremic showering? It has been known for several years that there is an association between severity of periodontal disease and distant organ abnormalities, in both humans and dogs. Studies are underway to determine whether the suspected cause (gingivitis/periodontitis) and effect (distant organ damage) hypothesis is correct. Bacteremia is not be the only likely cause of distant organ effects chronic body-wide release of inflammatory mediators and bacterial and cellular degradation by-products may produce immune-mediated distant organ pathology. Periodontitis is not a simple infection story. As veterinarians, we should emphasize the clinical importance of recognizing not just the extent of plaque and calculus deposition, but the reaction of the periodontal tissues. In one patient, a tooth with extensive plaque/calculus build-up may be amenable to conservative treatment (scaling and polishing with follow-up home care), and another patient with the same extent of plaque/calculus build up may have such severe tissue response that extraction of the tooth is the only practical option. Scheduling a patient for a 'dental' without appreciation of the severity of the disease, and without pretreatment discussion with the owner of the details of the treatment and the number of teeth that may need to be extracted, are common causes of consumer complaints about veterinary care. How can we recognize the extent of periodontitis? We cannot probe the bottom of pocket in an awake patient. We can recognize gingivitis and gingival recession; however, in dogs particularly, there is often poor correlation between the severity of visible gingivitis and the extent of periodontitis. In a non-mobile tooth, the periodontal probe or a radiograph are the only accurate means of determining the severity of periodontitis, which creates a particular challenge for veterinarians compared with human dentists. PREVENTION 1. Prevent accumulation of plaque. Daily is best, every other day is very helpful in slowing down the progression of disease. Anything less frequent than this is of doubtful long-term value because of calculus deposition. Brushing is the gold standard. Oral home care is easy to describe to owners, and difficult for many owners to practice over the long-term. 207

5 The North American Veterinary Conference 2005 Proceedings Mechanical cleansing. In the wild, mechanical cleansing resulting from natural chewing activity achieves moderate life-time control of periodontitis in carnivores. In most pet dogs and cats, similar effectiveness can be achieved with consistent use of chew products and diets that are effective in removing plaque and calculus. The Veterinary Oral Health Council (VOHC) recognizes products that achieve pre-set standards of plaque or calculus control in dogs and cats ( Chemical anti-plaque effect. Chlorhexidine, and possibly others with less documentation available. Use of anti-plaque chemicals will not prevent the accumulation of calculus. Extend the benefit of scaling by polishing, and delay subsequent accumulation by applying silicone or wax to the surface of the tooth. 2. Prevent accumulation of calculus. Mechanical cleansing. Chemical effect. Sodium hexametaphosphate as Ca ++ chelating agent. 3. Suppress the periodontal inflammatory reaction. It is know that long-term use of NSAIDs reduces periodontitis in dogs. 4. Correct host factors that may be exacerbating periodontitis (diabetes, stress). 5. Prevent accumulation of or reduce severity of the effects of pathogenic bacteria. Antimicrobial treatment. Frequent or intermittent use of systemic antibacterial drugs simply to control gingivitis and periodontitis is not recommended. Replace pathogenic bacteria with non-pathogenic bacteria in this ecological niche. Good bug displacing bad bug is now a serious topic in human dentistry. Anti-collagenase drugs, such as the tetracycline group. Bacterin made from important periodontopathogens as a vaccine, to induce antibody reaction to specific pathogenic bacteria. TREATMENT When there is extensive loss of attachment, treatment beyond scaling and polishing is required. There are 42 separate decisions to be made in the mouth of an adult dog one for each tooth. Triage each tooth: Extent of periodontitis does not require any treatment other than scaling and polishing. Tooth can be retained, but requires specific procedure in addition to scaling and polishing. Too diseased to retain extraction is the only option. Prevention is a much more efficient option! 208