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Link with Tooth Decay and Organ Diseases
The Reason I Continue To Remind Owners of The Dangers of Dental Disease .
Periodontal disease is inflammation and infection of the periodontium (gingiva, periodontal ligament, alveolar bone and cementum) due to plaque bacteria and the host’s response to the bacterial insult. Gingivitis is reversible, affecting gingiva only. As inflammation continues, the gingiva detaches from the tooth, creating a periodontal pocket, and a shift occurs in the gingival flora from a gram-positive aerobic to a gram-negative anaerobic spectrum. Periodontitis is the more severe form of periodontal disease, affecting all periodontal tissues and resulting in attachment loss, gingival recession, periodontal pocket formation and alveolar bone loss. Bone loss is usually irreversible, causing the tooth to become mobile and ultimately to exfoliate. Periodontal disease affects 70-80% of cats and dogs over two years of age. Its systemic effects are well documented in humans (heart disease and stroke, diabetes, respiratory disease, and increased risk of premature delivery and low birth weight infants). Few studies have as yet been performed in companion animals. Examination Periodontal examination is performed under general anaesthesia and includes (1) probing of the gingival sulcus of all teeth with a periodontal probe; and (2) imaging of all teeth with dental radiographic film and a dental x-ray unit. The teeth are evaluated for the presence of plaque, calculus (mineralized plaque), gingivitis, gingival recession, sulcus (or pocket) probing depth, attachment loss, and mobility. Gingival enlargement may lead to the formation of so-called pseudo pockets, which is commonly seen in brachycephalic dogs. Treatment Options The goal of periodontal therapy is elimination of supra and subgingival plaque and reduction of periodontal pockets. Medicinal therapy includes the use of topical rinsing solutions (e.g., dilute chlorhexidine) or systemic antimicrobials (e.g., amoxicillin/clavulanic acid, clindamycin, spiramycin/metronidazole, doxycycline). Because of potential side effects and/or the possibility of bacterial resistance, systemic antimicrobials should only be used in selected cases to serve as an adjunct to local treatment. Mechanical/instrumental therapy can be categorized in two different concepts: (a) closed treatment (scaling, closed root planing, and polishing); and (b) open treatment. Closed treatment is indicated, when pocket depths do not exceed 4-5 mm, and consists of debriding the tooth and root surfaces of plaque and calculus as well as root planing and gingival curettage without reflecting a soft tissue flap. Open treatment is indicated when pocket depths exceed 5-6 mm and is performed following reflection of a gingival or mucoperiosteal flap. Closed Treatment Professional dental cleaning refers to scaling, smoothing the root surfaces (root planing), and polishing of all crown and subgingival tooth surfaces. The teeth are scaled with sonic or ultrasonic scalers. After gross power scaling, hand scalers are used to remove residual calculus in pits, fissures and developmental grooves of the crowns. The root surface is planed and smoothed with hand curettes, which are also used for (sub)gingival curettage that removes the inflamed and infected soft tissue lining of the periodontal pocket. Once scaling is completed, the tooth surfaces are polished with fine polishing paste and a rubber cup on a prophy angle that is attached to a low-speed hand piece. Debris and polishing paste are rinsed from the tooth surface with water from an air/water syringe or a dilute chlorhexidine solution. Low-dose doxycycline gel may be inserted into cleaned periodontal pockets greater than 4 mm after root planing and (sub)gingival curettage. Open Treatment The modified Widman flap procedure utilizes an internal bevel incision slightly apical to the gingival margin and down to the alveolar bone. However, no vertical incisions are made. The partially mobilized gingival flap is not reflected beyond the mucogingival junction with this flap design. More visibility to the surgical site is achieved by creation of a mucoperiosteal flap beyond the mucogingival junction into alveolar mucosa. This usually requires that one or two vertical releasing incisions are made. Osseous surgery (alveoloplasty) and placement of intraosseous implants are possible with this flap design. The flap is repositioned at varying locations (original, coronal or apical). Apical positioning flaps are used for crown-lengthening procedures of teeth fractured close to or below the gingival margin to allow
placement of prosthodontic crowns in working dogs. Gingivectomy and Gingivoplasty Gingivectomy is excision of gingiva to eliminate pseudopockets in patients with gingival enlargement. It is also used for crown lengthening procedures and exposing cavity margins. Gingivoplasty is a form of gingivectomy that serves in creation of a physiologic gingival contour. Gingivectomy is contraindicated when there is less than 2 mm of attached gingiva and when horizontal or vertical bone loss extends beyond the mucogingival junction. The depth of the pocket is marked on the outer gingival surface using a periodontal probe to create bleeding points. An external bevel incision is made slightly apical to the bleeding points with the blade held at a 45-degree angle to achieve a natural gingival contour. At least 1-2 mm of attached gingival tissue must be preserved after the procedure is completed. Home Oral Hygiene Plaque control is a critical component of periodontal disease prevention and in the maintenance of treatment success. The owner is given instructions on daily tooth brushing with a soft bristled toothbrush and pet dentifrice. In addition, home oral hygiene is enhanced by the use of treats, diets and products that meet preset criteria for effectiveness in mechanically and/or chemically controlling plaque or calculus deposition in companion animals.
Periodontal disease (PD) is an inflammatory disease involving the supporting structures of the teeth. The primary cause is plaque with the predominant bacteria in periodontitis being anaerobic in origin. Researchers now hypothesise that PD is a risk factor for other organ disease. Discussion: Links between PD and systemic illnesses have been discussed for many years, but with no real proof of such links. In the late 1800’s, the concept of “focus of infection” (Miller 1891) held that transient bacteraemias occurred from oral infections. It has been shown in veterinary medicine, that bacteraemias do occur following insults such as intestinal obstruction and GDV syndrome (Winkler et al. 2003). It is accepted that dental (Harari 1993) or oral surgery procedures, periodontal probing, toothbrushing and mastication cause transient bacteraemias, that, in the healthy patient, are quickly
cleared by the reticulo-endothelial system. Furthermore, the possible contribution of oral bacteria in periodontal pockets to bacterial endocarditis has been suggested for decades. But it wasn’t until Offenbacher and co-workers commenced their research in the 1990s, that links between PD and other organ disease were considered possible. The two-way relationship between PD and systemic health has now termed the phrase periodontal medicine (Offenbacher 1996). Recent research has shown a link between PD and cardiovascular disease, as well as pre-term/low birth weight babies in man. Pathways linkingPD to systemic diseases: Three pathways linking PD to systemic effects have been proposed. Infection theory: It has been reported that in patients with periodontal inflammation, a Streptococcus sanguis protein associated with platelet aggregation and bacteraemia associated with Porphyromonas gingivalis may contribute to some acute thromboembolic events (Meyer et al. 1998). Distant injury: Distant injury may occur directly from circulating oral microbial toxins or indirectly through the elevation of the acute-phase response, including C-reactive protein, haptoglobin, alpha 1-antitrypsin and fibrinogen. The liver, in response to the systemic challenge of organisms, secretes acute-phase proteins. This acute-phase response is triggered by blood-borne oral lipopolysaccharide, and oral bacteria which elicit the release of the cytokines interleukin-6 and tumour necrosis factor alpha. These mediators act in the liver to induce the acute-phase proteins. Acute phase proteins especially C-reactive protein appear to be associated with increased risk of myocardial infarction in “apparently healthy” individuals. (Ridker et al. 1998, Scannapieco 1998). Distant inflammation: PD can induce changes in immune functions that result in metabolic dysregulation of serum lipid metabolism through the proinflammatory cytokines. Locally produced proinflammatory cytokines and tumour necrosis factor alpha may exert systemic effects by predisposing the patient to a systemic disorder such as atherosclerosis. Periodontitis and Cardiovascular Disease. It has been hypothesized that one or more infectious agents may play a role
in atherogenesis (leading to atherosclerosis), either through a direct pro-inflammatory effect on the vessel wall or through a less specific, longdistance pro-inflammatory effect. In this context, it has been suggested that PD may be one such inflammatory foci (Honda et al. 2005). Periopathogens have been considered to be triggers of a systemic inflammatory response. Furthermore, it has been proposed that patients with PD may have elevated circulating levels of some of these inflammatory markers (Page 1998). In addition, low levels of endotoxaemia in apparently healthy subjects might result from chronic infection associated with the breaching of epithelial barrier function such as seen in PD (Rice et al. 2005). In the veterinary literature, a recent report (Tou et al. 2005) showed a possible link between dental prophylaxis and infective endocarditis in a dog with existing mitral regurgitation. The dog became ill and feverish soon after the dental prophylaxis, and it was suspected that a bacteraemia associated with the dental treatment induced infective endocarditis in this case. Blood cultures in this dog grew a heavy growth of Streptococcus bovis. Preterm/low birth
weight babies: PD is currently being investigated as a risk factor for premature and low birth weight babies. Pregnant women who have periodontal disease may be seven times more likely to have a baby that is born too early and too small. It appears that PD triggers increased levels of biological fluids that induce labour. Furthermore, data suggests that women whose periodontal condition worsens during pregnancy have an even higher risk of having a premature baby (Oral health information for the public: Preterm low birth weight babies, 2004). A study by Constanza (2005) and others showed that PD may be a potential independent risk factor for preterm low birth weight (PLBW) after adjusting for several known risk factors. A number of biologically active mediators such as prostaglandin E2 (PGE2) and tumour necrosis factor alpha (TNF alpha) are also involved in normal parturition. These mediators are raised to artificially high levels during infections and thus may foster premature labour (Gibbs et al. 1992). Lipopolysaccharides from gram-negative anaerobes found in periodontal pockets trigger release of PGE2 and TNF alpha, which may, in turn, affect the course of pregnancy. Evidence to support this hypothesis has been obtained in rodent models. In addition, a recent study of mothers of PLBW infants (Offenbacher, 1996), with otherwise low risk, had significantly more PD than a similar group of women with normal weight infants at birth. Diabetes mellitus: People with diabetes mellitus are 15 times more likely to be edentulous than people without the disease. Both type 1 (insulin controlled) and type 2 (noninsulin controlled) diabetes have the same effect. The likelihood of PD increases when diabetes is poorly controlled (Seppala & Ainamo 1994). People with well-controlled diabetes, with good oral hygiene and on a regular maintenance schedule have the same chance of developing severe periodontitis as people without diabetes. The mechanism is multi-factorial. The small blood vessels of people with diabetes have thickened basement membranes, leading to a reduction in transport across the vessel walls. There is a reduction in collagen production by gingival and periodontal fibroblasts. There is also an acquired neutrophil dysfunction associated with diabetes mellitus, leading to impaired host defence against bacterial assault. In addition, high levels of pro-inflammatory mediators responding to endotoxin from gram- negative bacteria lead to an increase in collagen breakdown (Matthews 2000). There appears to be a relationship between insulin resistance and active inflammatory connective tissue disease and acute infections. Tumour necrosis factor alpha and other inflammatory cytokines found to be associated with periodontitis have been reported to interfere with insulin’s actions and lead to metabolic alterations during infection (Hotarnisligil et al. 1993, Flier 1993). Diabetes mellitus in dogs and cats is often associated with PD. It is common practice that in those animals that show poor glycaemic control of their diabetes, periodontal management is seen as an essential component in restoring control of blood glucose levels and for the reduction in insulin dosage. This would therefore strenghthen the recommendation to incorporate a thorough oral examination and appropriate periodontal care in the management of dogs and cats with diabetes mellitus.
Periodontitis and pulmonary disease: Bacterial respiratory infections are thought to be acquired through aspiration (inhaling) of fine droplets from the mouth and throat into the lungs. These droplets contain organisms that can breed and multiply within the lungs to cause damage. Recent research suggests that bacteria found in the throat, as well as bacteria found in the mouth, can be drawn into the lower respiratory tract. Scientists have found that bacteria that grow in the oral cavity can be aspirated into the lung to cause respiratory diseases such as pneumonia, especially in people with PD. Periodontitis and systemic disease in dogs: Numerous studies have shown that a transient bacteraemia occurs in dogs after a dental procedure (Harari et al. 1993, Nieves et al. 1997). It is also accepted that during episodes of active periodontitis, periopathogens and their toxins enter the bloodstream. However, very few studies have been undertaken, looking at the association of PD and organ involvement in dogs and cats. DeBowes et al. (1996) showed an association between PD and morphologic changes in renal glomeruli and interstitium, myocardium and hepatic parenchyma. However, there was no significant association between PD scores and lung histopathology scores. The authors concluded that their results supported the hypothesis that PD can have systemic effects on other organs. A recent study conducted in thirtyeight client owned dogs (Rawlinson et al. 2005) looked at the association between the concentration of systemic inflammatory parameters (including serum C-reactive protein, urine protein:creatinine ratio, blood pressure, microalbuminuria), and severity of PD and then, after appropriate treatment of PD, the changes in these systemic parameters. The study showed that increases in concentrations of systemic inflammatory markers were positively related to the severity of PD. After periodontal therapy, there was a significant decrease in the concentrations of some of these inflammatory markers. The study showed that PD leads to systemic inflammation that is significantly reduced with appropriate periodontal therapy. The authors concluded that further research was required to fully understand the significance of these changes. Conclusion: Conclusion: Proving the link bet Conclusion: ween cause and effect of chronic diseases, such as PD, is not an easy task. As PD is generally slowly progressing, people/animals studied over a long period may be exposed to a multitude of potential causes making determination of a cause–effect link more difficult. However, there seems to be a growing body of evidence to suggest the PD is a true risk factor for other systemic diseases such as cardiovascular disease.
References : Constanza M., Segura-Egea J., Martínez-Sahuquillo A. : & Bullon P. 2005. Correlation between infant birth weight and mother’s periodontal status. J. Clin. Periodontol. 32(3):299-304. - DeBowes L., Mosier D., Logan E., Harvey C., Lowry S. & Richardson D. 1996. Association of periodontal disease and histologic lesions in multiple organs from 45 dogs. J. Vet. Dent. 13(2):57-60. - Flier J. 1993. An overview of insulin resistance, p.1-8. In: Moller D.E. (ed.), Insulin Resistance. Wiley, New York. 1-8. - Gibbs R.S., Romero R., Hillier S.L., Eschenbach D.A. & Sweet R.L. 1992. A review of premature birth and subclinical infection. Am. J. Obstet. Gynecol. 166:1515- 1528. - Harari J., Besser T., Gustafson S. & Meinkoth K. 1993. Bacterial isolates from blood cultures of dogs undergoing dentistry. Vet. Surg. 22:27-30. - Honda T., Yoshie H. & Yamazaki K. 2005. Effects of Porphyromonas gingivalis antigens and proinflammatory cytokines on human coronary artery endothelial cells. Oral Microbiol. Immunol.:82-88. - Hotarnisligil G., Shargill N. & Spiegelman B. 1993. Adipose expression of tumour necrosis factor alpha: direct role in obesity-linked insulin resistance. Science 259:87-91. - Matthews D. 2000. Periodontal disease: a new paradigm J. Can. Dent. Assoc. 66:488-491. - Meyer M., Gong K. & Herzberg M. 1998. Streptococcus sanguis-induced platelet clotting in rabbits and haemodynamic and cardiopulmonary consequences. Infect. Immun. 66(12):5906-5914. - Miller W. 1891. The human mouth as a focus of infection. Dental Cosmos 33:689-713. - Nieves M., Hartwig P., Kinyon J. & Riedesel D. 1997. Bacterial isolates from plaque and from blood during and after routine dental procedures in dogs. Vet. Surg. 26:26-32. - Offenbacher S. 1996. Periodontal diseases.
Pathogenesis. Ann. Periodontol.:821-878. - Offenbacher S., Katz V., Fertik G., Collins J., Boyd D. & Maynor G. 1996. Periodontal infection as a possible risk factor for preterm low birth weight. J. Periodontol. 67(10, Suppl.):1103-1113. - Page R. 1998. The pathobiology of periodontal diseases may effect systemic diseases: inversion of a paradigm. Ann. Periodontol. 3:108-120. - Rawlinson J., Goldstein R., Reiter A., Hollis N. & Harvey C. 2005. Tracking systemic parameters in dogs with periodontal disease. Conf. Proc. 19th Annu. Vet. Dental Forum and IX World Vet. Dental Congr., Orlando, Florida, p.49. - Rice J., Stoll L., Li W., Denning G., Weydert J., Charipar E., Richenbacher W., Miller F. & Weintraub N. 2003. Low-level endotoxin induces potent inflammatory activation of human blood vessels: inhibition by statins. Arterioscler. Thromb. Vasc. Biol. 23:1576-1582. - Ridker P., Cushman M., Stampfer M., Tracy P. & Hennekens C. 1998. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 97:425-428. - Scannapieco F. 1998. Position paper. Periodontal disease as a potential risk factor for systemic diseases. J. Periodonol. 69:841-850. - Seppala B. & Ainamo J. 1994. A site-by-site followup study on the effect of controlled versus poorly controlled insulindependent diabetes mellitus. J. Clin. Periodontol. 21:161-165. - Tou S., Adin D. & Castleman W. 2005. Mitral valve endocarditis after dental propyhlaxis in a dog. J. Vet. Intern. Med. 19:268-270. - Winkler K., Greenfield C. & Schaeffer D. 2003. Bacteria and bacterial translocation in naturally occurring canine gastric dilatation-volvulus patient. J. Am. Anim. Hosp. Assoc. 39:361-368.
References Lewis JR, Reiter AM. Management of generalized gingival enlargement in a dog – Case report and review of the literature. J Vet Dent 2005;22:160-69.

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