| Periodontitis, which is one of the widespread human being diseases, ismainly responsible for adult tooth loss. As the criterion of the world healthorganization the incidence rate of gumtis is 71% and that of periodontitis is50% in our country. So the treatment of periodontitis is of great significance.Conventional therapies, including oral hygiene instruction, scaling, rootplanning and pocket irrigation, aim to eliminate the local stimulating factors,but fail to arrest or stabilize attachment sites during initial therapy ormaintenace. Local antimicrobial therapy has been shown to be an effectivetreatment for periodontitis as an adjunct to mechanical debridement, but hassome side-effects, for example, inaccess to biofilm bacteria,microbialresistence .Difficulties in access, extent of periodontal destruction,unfavourable anatomy and tissue architecture, and difficulty of plaque controlmay all limit the effectiveness of mechanical and antimicrobial therapy.Furthermore, all the above treatments could not block the inflammatorycascade reaction in a timely way. Suppression of the bacterial challengeremains the sine qua non of treatment. Nevertheless, recognition that the hostresponse to pathogens is mainly responsible for tissue destruction has led tohost modulation therapies in the management of the periodontal patient. Inrecent years, many researches have been made to explore the host responsemodulator.Chitosan is the deacetylated (to varying degrees) form of chitin. Theyboth carry positive charge. Chitosan is a linear polymer ofN-acetyl-D-glucosamine and deacetylated glucosamine that shares somecharacteristics of glycosaminoglycan and hyaluronic acid. It exhibits not onlyexcellent biocompatibility and biodegradability, but also various promisingbiological activities, including hemostatic activity, antimicrobial activity, theability to accelerate the reformation of connective tissue, angiogenesis andbone formation, the ability to promote the production of transforminggrowth factorβ1(TGF-β1)and platelet derived growth factor (PDGF) byhuman monocyte M φ, the ability to inhibit the overproduction ofprostaglandin E2(PGE2),and many other immune stimulatory activities.Applications of chitosan to medical and pharmaceutical domains havereceived considerable attention in recent years. According to its properties, itis assumed that chitosan should produce a marked effect on periodontitis. Theaim of this study is to investigate the therapeutical effect of chitosan-ascorbate on periodontitis by clinical evaluation and histological observationson Wistar rat model of periodontitis and to analyze the involved mechanisms,thereby to provide foundation for further investigation into chitosan as a newagent of pocket local delivery.This study is composed of 3 parts: molecule modification and para-metermensuration of chitosan; restraining experiment of chitosan to Actinobacillusactinomycetemcomitas Aa.; The effect of local delivery of modifiedchitosan-ascorbate gel in treating periodontitis in the rat model.Methods: sixty Wistar rats weighing 175 to 185g,obtained from JiLinUniversity experimental animal facilities, were housed in conventionalcondition. Three days later, we induced an experimental periodontitis model inrats, with minor modifications, as described by Kimura. Briefly, rats wereanesthetized with ketamine hydrochloride and a nylon(000) thread ligature,drawn from petri dish when the Actinobacillus actinomycetemcomitassubsisted at the end of logarithmic phage, was surgically placed throughgingival embrasure of the first and second maxillary teeth. The ligature wasknotted on both sides of the embrasure, with the stumps pressed into gingivalgroove. The rats were divided into 3 groups of half male and half female each atrandom when periodontitis was established. The ligatures were removed andthe treatment began. Trial 1 group were treated with chitosan-ascorbateinjected into the pocket bottom; Trial 2 group were treated with modifiedchitosan-ascorbate and control group were treated with saline. Five clinicalparameters, namely dental plaque index(PLI), gingival index(GI), pocketdepth(PD), attachment level(AL) and tooth mobility(TM) were evaluated ormeasured about every ligation unit containing the first and second maxillaryteeth after 0,2,4,8,14,28 days of treatment. The rats were sacrificed after0,4,8,14,28 days of treatment by dislocation under anesthesia, 2 rats eachgroup each time, and maxillae were excised for histological analysis. In thesame way, maxillae derived from trial and control group after 0,2,4,6,8 weekswere used to determine the degree of bone loss(morphometric and X-ray filmanalysis ). Results: Intergroup analysis: Statistically significant difference in clinicalparameters exist between trial and control group. PLI in trial group was lowerthan that in control group, and their difference increased throughout treatment.The greatest difference in GI came up after 4 and 8 days of treatment. Thedifference of the two groups in TM and AL became more and more obviousfrom 8 days of treatment. PD in trial group was slightly lower than that incontrol group only after 4 and 8 days of treatment. Inter trial group analysis:PLI and GI of T1 group were lower than T2 group at 2,4,8 d and the healingtime of T2 was shorten about 1 week. TM of them had occurred evidentdifference from the 2d after treating and that of T1 was lower than T2.PD andAL of them had no evident difference . Intragroup analysis: The varying tendencies of clinical parameters weredifferent between trial and control group. All the parameters in trial groupdescended, range larger and emergence earlier than those in control, especiallyPLI and GI. In control group, TM and AL raised with the time of treatment onthe contrary.Alveolar bone loss: ABL of control group was assumed of ascending and itincreased obviously at 2w (P<0.001) and increased opposite reductive at 4w(P<0.05). And the increase was not significant during 6-8w. ABL of trial groupwas assumed of descending and it descended obviously at 2w (P<0.05) thenthe decrease was not significant. Intragroup analysis did not reveal astatistically significant difference in trial group, but ABL in control groupincreased after 2 (P<0.001) and 4(P<0.05) weeks of treatment. X films showedthat alveolar bone destruction stopped or plerosis occurred in trial group, butbone was destructed to greater extent in control group. Histological observations: inflammatory infiltration in perio-dontalconnective tissue, epithelia ulceration, bone adsorption, pocket formation wereobserved before treatment. In trial group, inflammatory infiltrate regressedearly after 4 days of treatment, cementum and alveolar process were wellpreserved and restored compared with that before treatment. In contol group,the extinction of cell influx and osteoclast retarded after 8 days of treatment,bone destruction was more severe than that before treatment. Conclusions: Clinically and histologically, the experimental outcome fulfilled thelandmark of periodontitis; inflammatory infiltrate, attachment level decrease,bone destruction, pocket formation all emerged. Thus the Wistar rat models ofperiodontitis were induced successfully. According to the statistical analysis ofclinical parameters and bone measurements in combination with histologicaland X-ray films observations, it is evident that chitosan-ascorbate, deliveredinto pocket, not only improve the clinical symptoms of periodontitis, but alsoblock the continuous destruction of periodontal tissue to preserve periodontaltissue as much as possible. In this study, there was no piece of evidence ofnew attachment formation, though not to deny the ability of chitosan topromote periodontal tissue regeneration. In conclusion, chitosan-ascorbate is apromising local delivery agent for periodontitis. From the curative effect...
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