The Effect Of Passive Smoking On Periodontal Tissue Of Rats With Experimental Periodontitis

Objective: Experimental periodontitis model of rats was established byperiodontal ligation, animal model of passive smoking was established bysmoking to observe variety of periodontal tissue, destroy of alveolar bone andthe expression of COX-2in periodontal tissue, exploring the effects of passivesmoking on periodontal tissue.Methods: One hundred and twenty6-month-old male SD rats wererandomly divided into four groups, each group had30rats: normal group,passive smoking group (smoking group), periodontitis group (ligation group),periodontitis and passive smoking group (ligation and smoking group). Ratsof ligation group and ligation and smoking group were anesthesiaed, thenligated the bilateral maxillary first molar teeth of cervical using a wirediameter of0.2mm. Ligation in rats of group S and group PS, then put them inthe “smoking case” made by self, passive smoking once every morning andafternoon,60minutes/once and8cigarettes/once. After ligated4weeks,8weeks,12weeks, randomly selected rats per group of10, killed the rats undergeneral anesthesia, taken maxillary, put into10%formaldehyde buffer solutionfor fixing48hours, then decalcified by10%EDTA solution for8weeks,periodontal tooth continuous slices was made for HE staining andimmunohistochemistry staining. Periodontal tissue was analysis imageanalysis system. The date was processed for statistical analysis.Results:1Appraisement of the rat periodontitis model:Taken the made maxillary first molar periodontal slices, under opticalmicroscope observed: when ligated in4weeks, obvious gingival flammationinfiltrated, epithelial nail apparent elongated and increased, showninflammatory cells infiltration, junctional epithelium move to the root, periodontal pocket was already to shamed, periodontal fibers were disordered,the alveolar bone was absorbed. All of them have indicated that: periodontitisof experimental rats’ model had been successfully established.2Observation of the rat periodontal tissue morphology by the HEstaining:Normal group: At the4th,8th,12thweeks junctional epithelium waslocated in the cemento-enamel junction boundaries. Gingival fibers andperiodontal ligament fibers arranged regularly and orderly. The frame ofalveolar bone was integrity, alveolar crest without absorption.Smoking group: At the4th,8thweeks junctional epithelium was located inthe cemento-enamel junction boundaries, small amounts of inflammatory cellswere infiltrated in the connective tissue, alveolar crest shape irregular, alveolarcrest to absorb. At the12thweeks junctional epithelium proliferation, morevisible within the connective tissue infiltration of inflammatory cells, alveolarcrest shape irregular, alveolar crest to absorb.Ligation group: At4thweek gingival flammation infiltrated, extendingto the deep part of connective tissue, junctional epithelium move to the root,shown inflammatory cells infiltration, alveolar crest to absorb. At8thweeknail of gingival epithelium bursting clear stretch, junctional epitheliumproliferation and extension to the root side, form a periodontal pocket, moreinflammatory cells infiltration, alveolar crest shape irregular, the alveolar boneheight could been seen and shown osteoclasts. At12thweek junctionalepithelium continue to move, formed deep periodontal pocket, visibleconcentration of inflammatory cell infiltration, Obvious alveolar boneabsorption and shown more osteoclasts.Ligation and smoking group: At4thweek junctional epitheliumproliferation and extension to the root side, form a periodontal pocket,infiltration of inflammatory cells in the connective tissue, alveolar crest toabsorb. At8thweek blood vessels dilatation, fibers arranged regularly,alveolarbone was absorbed vertically, shown osteoclasts. At12thweek junctionalepithelium proliferation and extension to the root side, fibers arranged regularly and broken, alveolar bone was absorbed vertically, shown moreosteoclasts.3Histology analysis:The loss of alveolar bone height: At the4th,8thweeks there was nosignificant change between smoking group and normal group(P>0.05), it wasmore significantly in the ligation group, ligation and smoking group than thatin the normal group(P<0.05), it was more significantly in the ligation andsmoking group than that in the smoking group(P<0.05), there was nosignificant change between ligation group and ligation and smoking group(P>0.05). At the12thweek it was more significantly in the smoking group,ligation group, ligation and smoking group than that in the normal group(P<0.05), it was more significantly in the ligation and smoking group than thatin the smoking group(P<0.05), it was more significantly in the ligation andsmoking group than that in the ligation group(P<0.05).4COX-2’s test4.1Immunohistochemical detection of the expression of COX-2in ratperiodontal tissue:The positive staining of COX-2in rat periodontal tissue was yellow orbrown granules, and mainly located in the fibroblasts, osteoblasts and bonecells. At the4th,8th,12thweeks, in rat periodontal tissue of normal group: alittle of positive cells, COX-2in some fibroblasts, osteoblasts showed weakand positive expression, COX-2in bone cells showed negative expression. Inrat periodontal tissue of smoking group and ligation group: the number ofpositive expression cells increased, showed positive expression. In ratperiodontal tissue of ligation and smoking group: the number of positiveexpression cells increased obviously, COX-2in fibroblasts, osteoblasts andsome bone cells all showed strong positive expression.4.2COX-2average light density value(OD) determination result:At the4th,8th,12thweeks, smoking group, ligation group, ligation andsmoking group to be higher than the normal group(P<0.05), ligation andsmoking group obviously to be higher than the smoking group(P<0.05), ligation and smoking group obviously to be higher than the ligation group(P<0.05).Conclusion:1Periodontitis of experimental rat model had been successfullyestablished by ligated the bilateral maxillary first molar teeth of cervical usinga wire.2Observation on pathological changes of periodontal tissues, passivesmoking increased the degree of inflammation of periodontal tissues.3By histology analysis, passive smoking increased alveolar boneabsorption and reduced the height of alveolar bone crest.4Passive smoking enhanced COX-2expression in the periodontal tissue,which prompted that PGE2increased, passive smoking increased the degreeof inflammation of periodontal tissues and increased alveolar bone absorption.