Page 611 - WSAVA2018
P. 611

WSV18-0159
WSAVA GLOBAL NUTRITION
CHEW ON THIS – NUTRITION FOR DENTAL DISEASE
M. Chandler1, B. Niemiec2
1Vets Now Referrals, Clinical Nutrition, Glasgow, United Kingdom
2Veterinary Dental Specialists, Veterinary Dentistry, San Diego, USA
CHEW ON THIS: IMPLICATIONS OF NUTRITION AND DENTAL HEALTH
Brook Niemiec, DAVDC, DEVDC, FAVD & Marge Chandler DVM, MS, MANZCVS DACVN, DACVIM, MRCVS
Introduction
Periodontal disease is the number one health problem in small animals. By two years of age, 70% of cats and 80% of dogs have periodontal disease. There are generally little to no outward signs of early disease process, so therapy typically comes late. Consequently, periodontal disease may be the most undertreated disease in our patients. Unchecked periodontal disease has numerous local and systemic consequences.
Pathogenesis:
Periodontal disease is initiated by oral bacteria which adhere to teeth in a substance called plaque. Plaque
is a biofilm, made up almost entirely of oral bacteria, contained in a matrix of salivary glycoproteins and extracellular polysaccharides. Calculus (tartar) is basically plaque which has secondarily become calcified by the minerals in saliva. Plaque and calculus may contain
up to 100,000,000,000 bacteria per gram. Bacteria within a biofilm do not act like free living or “planktonic” bacteria; they are 1,000 to 1,500 times more resistant to antibiotics than planktonic bacteria. Plaque on the tooth surface is supragingival plaque. Once it extends under the free gingival margin and into the gingival sulcus (between the gingiva and the teeth or alveolar bone),
it is subgingival plaque. Supragingival plaque likely affects the pathogenicity of the subgingival plaque in the early stages of periodontal disease; however, once the periodontal pocket forms, the effect of supragingival plaque and calculus is minimal. Therefore, control of supragingival plaque alone is ineffective in controlling the progression of periodontal disease.
Bacteria in the subgingival plaque secrete toxins as well as metabolic products. Cytotoxins and bacterial endotoxins can invade tissues causing inflammation of the gingival and periodontal tissues. This inflammation damages the gingival tissues and initially results in gingivitis. Eventually, the inflammation can lead to periodontitis, i.e. the destruction of the attachment
between the periodontal tissues and the teeth. In addition to directly stimulating inflammation, bacterial metabolites elicit a host inflammatory response. The progression of periodontal disease is determined by the virulence of the bacteria combined with the host response. It is the host response that often damages periodontal tissues.
The inflammation produced by the combination of the subgingival bacteria and host response damages the tooth’s soft tissue attachment and decreases bony support via osteoclastic activity. This causes the tooth’s periodontal attachment to move apically (towards the root tip). The end stage of periodontal disease is tooth loss; however, the disease creates significant prior problems.
Periodontal disease is generally in two stages, gingivitis and periodontitis. Gingivitis is the initial, reversible stage in which inflammation is confined to the gingiva. The gingival inflammation is created by plaque bacteria and may be reversed with a thorough dental prophylaxis and consistent homecare. Periodontitis is the later stage of the process defined as an inflammatory disease of the deeper supporting structures of the tooth (periodontal ligament and alveolar bone) caused by microorganisms. The inflammation results in the progressive destruction of the periodontal tissues, leading to attachment loss. This can be seen as gingival recession, periodontal pocket formation, or both. Mild to moderate periodontal pockets may be reduced or eliminated by proper plaque and calculus removal. However, periodontal bone loss
is irreversible (without regenerative surgery). Although bone loss is irreversible, it is possible to arrest its progression.
Clinical Features:
Normal gingival tissues are coral pink in color (allowing for normal pigmentation), have a thin, knife-like edge, and a smooth and regular texture. There should be
no demonstrable plaque or calculus on the dentition. Normal sulcal depth in a dog is 0 to 3mm and in a cat is 0 to 0.5mm.
The first clinical sign of gingivitis is erythema of the gingiva. This is followed by edema, gingival bleeding during brushing or after chewing hard/rough toys, and halitosis. Gingivitis is typically associated with dental calculus but is primarily elicited by PLAQUE and can be seen in the absence of calculus. Alternatively, widespread supragingival calculus may be present with little to no gingivitis. Calculus itself is essentially non-pathogenic; therefore, the degree of gingival inflammation should be used to judge the need for professional therapy. As gingivitis progresses to periodontitis, the oral inflammatory changes intensify.
The hallmark feature of established periodontitis is attachment loss. As periodontitis progresses, alveolar
Your Singapore, the Tropical Garden City
          609
            







































































   609   610   611   612   613