Animal Health Solutions

13 Q3 2022 | Animal Health Solutions very few bacteria cause systemic infections in the healthy animal. This is the result of a highly efficient innate host defense system that monitors bacterial growth and prevents bacterial intrusion into the local tissues. At this point, rigorous tooth cleaning and oral hygiene procedures would reverse the course of gingivitis and return the periodontium back to a state of health. The primary etiological basis for periodontal disease is bacteria; however, the excessive host inflammatory response and inadequate resolution of inflammation is critical to the pathogenesis of periodontitis. Periodontal disease results from the body's failure to "turn off" its inflammatory response to infection. The result is chronic maladaptive inflammation. Progression of Periodontal Disease Inflammatory disease represents a disruption of tissue homeostasis. Any factor in its microbial or host base that can destabilize the homeostatic equilibrium can result in inflammatory disease. Keystone pathogens (eg. prophomonous gingivalis which can suppress the innate host response by paralyzing a key step in the host defense system resulting in increased commensal bacterial numbers and inflammation) create a dysbiosis between the host and dental plaque. Acute inflammation that is resolved within a reasonable time frame prevents tissue injury. Inadequate resolution of acute inflammation and failure to return to homeostasis results in chronic inflammation and subsequent tissue destruction. This amplification of the initial host response results in the propagation of the inflammation which leads to the destruction of soft and mineralized periodontal tissues (cementum, alveolar bone, gingival tissues and periodontal ligament). There are significant variations in host responses between animals in their presentation of periodontal disease. Microbial challenge is a primary initiating factor, but there are many other variables that modify disease expression. These risk factors interfere with the way the body responds to bacterial invasion and may shift the immune response beyond normal parameters. These risk factors could be environmental, genetic or epigenetic (how certain genes are expressed in specific tissues that change throughout life by external factors like stress). Once risk factors have been identified they need to be addressed. Microbial Challenge Biofilm/ Plaque/ Calculus Host-Immuno Inflammatory Response Connective Tissue and Bone Metabolism Clinical Signs of the Disease Tissue breakdown products and ecological factors Genetic risk factors Environmental and aquired risk factor Cytokines Prostanoids MMPs Antibody PMN Antigen LPS Other virulence factors

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