| Periodontitis, which is one of the two main oral diseases, is mainly responsible for adult teeth loss; and its incidence rate is going up. So the treatment of periodontitis is of great significance. Conventional therapies, including oral hygiene instruction, scaling, root planing and pocket irrigation, aim to eliminate the local stimulating factors, but fail to arrest or stabilize attachment sites during initial therapy or maintenace. Local antimicrobial therapy has been shown to be an effective treatment for periodontitis as an adjunct to mechanical debridement, but has some side-effects, for example, inaccess to biofilm bacteria and microbial resistence. Difficulties in access, extent of periodontal destruction, unfavourable anatomy and tissue architecture, and difficulty of plaque control may all limit the effectiveness of mechanical and antimicrobial therapy. Furthermore, all the above therapies could not block the inflammatory cascade reaction in a timely way. Suppression of the bacterial challenge remains the sine qua non of treatment. Nevertheless, recognition that the host response to pathogens is mainly responsible for tissue destruction has led to host modulation therapies in the management of the periodontal patients. In recent years, many researches have been made to explore the host response modulators. Chitosan is the deacetylated (to varying degrees) form of chitin. They both carry positive charge. Chitosan is a linear polymer of N-acetyl-D-glucosamine and deacetylated glucosamine that shares some characteristics of glycosaminoglycan and hyaluronic acid. It exhibits not only excellent biocompatibility and biodegradability, but also various promising biological activities, such as hemostatic activity, antimicrobial activity, the ability to accelerate the reformation of connective tissue, angiogenesis and bone formation, the ability to promote the production of transforming growth factorβ1(TGF-β1)and platelet derived growth factor (PDGF) by human monocyte Mφ, the ability to inhibit the overproduction of prostaglandin E2(PGE2), and many other immune stimulating activities. Applications of chitosan to medical and pharmaceutical domains have received considerable attention in recent years. According to its properties, it is assumed that chitosan produce a marked effect on periodontitis. The aim of this study is to investigate the therapeutical effect of chitosan-ascorbate on periodontitis by clinical evaluation and histological observations on Wistar rat model of periodontitis and to analyze the involved mechanisms, thereby to provide foundation for further investigation into chitosan as a new agent of pocket local delivery. Methods: Fifty-six Wistar rats weighing 175 to 185g, obtained from JiLin University experimental animal facilities, were housed in conventional condition. Three days later, we induced an experimental periodontitis model in rats, with minor modifications, as described by Kimura. Briefly, rats were anesthetized with ketamine hydrochloride and a nylon(000) thread ligature, drawn from petri dish when the porphyromonas gingivalis subsisted at the end of logarithmic phage, was surgically placed through gingival embrasure of the first and second maxillary teeth. The ligature was knotted on both sides of the embrasure, with the stumps pressed into gingival groove. Two days after ligation, acetic acid mtacortandralone was given intramuscularly on interval day for 4 times. The rats were divided into 2 groups of half male and half female each at random when periodontitis was established. The ligatures were removed and treatment was carried out. The trial group were treated with chitosan-ascorbate injected into the pocket bottom; while the control group with saline. Five clinical parameters, namely dental plaque index(PLI), gingival index(GI), pocket depth(PD), attachment level(AL) and tooth mobility(TM) were evaluated or measured on every ligation unit containing the first and second maxillary teeth after 0,2,4,8,14,28 days of treatment respectively.
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