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Periodontal Disease      985



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                  Figure 47-3. Host-bacterial interactions in the pathogenesis of periodontal disease. Periodontal disease is cyclic with bursts of tissue destruc-
                  tion followed by periods of healing and relative quiescence. Four stages in the pathogenesis of periodontal disease have been proposed: 1)
                  Microbial colonization. Salivary pellicle is deposited on the enamel surface and is soon colonized by oral bacteria that multiply forming plaque.
                  2) Microbial invasion. Plaque bacteria and their by-products invade the gingival tissues and initiate a host inflammatory response. 3) Tissue
                  destruction. Direct toxic effects of bacteria and their by-products and indirect host-mediated toxic responses lead to destruction of periodontal
                  tissue. 4) Healing. Periods of disease remission are characterized by a reduction in the inflammatory response and gingival healing. (Adapted
                  from Genco RJ, Goldman HM, Cohen WD, eds. Contemporary Periodontics. St Louis, MO: CV Mosby Co, 1990; 189.)

                    Although much of the evidence is based on documentation
                  of correlations between oral and systemic health, and the effect  Table 47-2. Stages of periodontal disease.*
                  of systemic diseases on the health of the oral cavity (particular-  Stage 0  Clinically normal
                  ly in the case of diabetes) (Mealey,1998; Levin et al,1996),data  No gingival inflammation or periodontitis clinically
                  are emerging that suggest a more causal and two-way relation-  evident.
                                                                        Stage 1  Gingivitis only
                  ship that makes a case for periodontal therapy as an adjunctive  No attachment loss. Height and architecture of the
                  treatment to classic disease therapies (D’Aiuto et al, 2004;  alveolar margin are normal.
                  Montebugnoli et al, 2005; Montebugnoli, 2004; Farooqi et al,  Stage 2  Early periodontitis
                                                                                Less than 25% attachment loss or Stage 1 furcation
                  2004; Kiran et al, 2005; Mealey, 2000; Miller et al, 1992;    involvement in multirooted teeth.
                  Pucher and Stewart, 2004; Taylor et al, 2004; Rahman et al,  Stage 3  Moderate periodontitis
                  2005; Mercanoglu et al, 2004).                                25 to 50% attachment loss or Stage 2 furcation
                                                                                involvement in multirooted teeth.
                    In dogs, numerous reports speculate on the association  Stage 4  Advanced periodontitis
                  between chronic periodontal disease and conditions affecting  Greater than 50% attachment loss or Stage 3 furca-
                  the heart valves and pulmonary airways (Hamlin, 1990;         tion involvement in multirooted teeth.
                                                                        *Adapted from AVDC.org. Wolf HF, Rateitschak EM, Rateitschak
                  Prueter and Sherding, 1985; Calvert and Dow, 1990; Bona-  KH, et al. Color atlas of dental medicine: Periodontology, 3rd ed.
                  gura, 1981). Furthermore, a positive correlation has been  Stuttgart, Germany: Georg Thieme Verlag, 2005.
                  found between the severity  of  periodontal disease and
                  histopathologic changes in the kidneys, myocardium and liver
                  (DeBowes et al, 1996). Periodontal infections allow bacterial  Ide et al, 2004; D’Aiuto et al, 2004, 2005; Joshipura et al,
                  migration into lymphatic and blood vessels, resulting in bac-  2004; Lowe, 2004; Holzhausen et al, 2004). The host defens-
                  teremia and are associated with increased levels of many of the  es of normal healthy pets can effectively clear transient bac-
                  systemic markers associated with the diseases described  teremia; however, blood-borne bacteria may colonize distant
                  above, including C-reactive protein, proinflammatory cyto-  sites in patients impairing immune function and/or compro-
                  kines, serum cholesterol, plasma fibrinogen, white blood cells  mising organ function, including development of atheroscle-
                  and blood glucose (Harari et al, 1993, 1991; Slade et al, 2000;  rotic lesions (Calvert and Green, 1986; Glurich et al, 2002).
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