Gingival Crevicular Fluid Levels Of SLIT3 And Its Correlation With RANKL And OPG

Background and objective:Periodontitis is a chronic infectious disease of the periodontal tissue,and subgingival plaque is its initiating factor,which triggers the local immune response of the body releasing a variety of cytokines,aggravating the destruction of periodontal tissue,and eventually leads to bone resorption.SLIT3 is an extracellular matrix protein secreted by osteoclasts,and its expression in patients with periodontitis and its relationship with periodontitis are unclear.In this study,the expression of SLIT3 in gingival crevicular fluid of patients with periodontitis was detected to analyze the relationship between the expression of SLIT3 and periodontal clinical indicators,RANKL,OPG and major periodontal pathogens.And also we explored the role of SLIT3 in the occurrence,development and possible mechanism of periodontitis.Methods:Fourty-five patients with periodontitis and another fourty-five periodontally healthy volunteers were recruited for the study.Clinical parameters,including clinical attachment level(CAL),the probing depth(PD),and bleeding index(BI)were examined for each participant.GCF sampling and subgingival plaque were assessed.Concentrations of SLIT3,RANKL and OPG in gingival crevicular fluid were detected by enzyme-linked immunosorbent assays.Subgingival plaque DNA was extracted and determined by real-time quantitative polymerase chain reaction was performed to detect Porphyromonas gingivalis(P.g),Tannerella forsythia(T.f)and Treponema denticola(T.d).We compared the differences in clinical parameters,biochemical parameters and the bacterial prevalence between healthy volunteers and periodontitis patients,and evaluated the correlations between the concentrations of SLIT3,RANKL and OPG and the clinical parameters of periodontal disease.Results:1 The periodontal clinical indexes BI,PD and CAL in the periodontitis group were 3.15�0.54,3.94�0.61 mm and 4.87�0.82 mm,respectively,and those in the control group were 0,1.69�0.22 mm and 0.04�0.03 mm,respectively.The mean values of BI,PD and CAL of periodontitis group were higher than those of the control group(p <0.05).2 The total amounts of SLIT3,RANKL and OPG in the gingival crevicular fluid of the periodontitis group were 0.26�0.07 ng,9.00�1.74 pg and 3.14�0.63 pg,respectively.The total amounts of GCF SLIT3,RANKL and OPG of the control were 0.12 �0.04 ng,5.10�0.82 pg,8.56�1.89 pg,respectively.The total amounts of SLIT3 and RANKL in the periodontitis group were higher than those in the control group,while the total amount of OPG was lower than that in the control group(p <0.05).3.The correlation coefficient r between the total amounts of SLIT3 and RANKL in the periodontitis group was 0.612(p=0.034<0.05),and the correlation coefficient with RANKL/OPG and OPG were 0.632(p=0.028<0.05)and-0.421(p=0.032< 0.05),respectively.SLIT3 was positively correlated with both RANKL and RANKL/OPG in the periodontitis group but negatively correlated with OPG.4 The correlation coefficient r between the total amount of GCF SLIT3 and CAL in periodontitis group was 0.598(p=0.033<0.05),and the correlation coefficient between the total amount of RANKL and CAL was 0.728(p=0.011<0.05).The total amount of SLIT3 as well as RANKL in the periodontitis group was positively correlated with CAL.5 The detection rates of P.g,T.f and T.d in the periodontitis group were 100%,93.33% and 97.78%,respectively.The detection rates of P.g,T.f and T.d in the control group were 55.56%,62.22% and 57.78%,respectively.The detection rates of P.g,T.f and T.d in periodontitis group were all higher than those in control group(p <0.05).Conclusion:The amount of SLIT3 in periodontitis patients was higher than that in healthy volunteers,and there was a positive correlation between SLIT3 and osteoclast differentiation factors RANKL and CAL,indicating that the amount of SLIT3 was correlated with alveolar bone resorption,which affected alveolar bone resorption in periodontitis patients.SLIT3 may be a potential marker for detection of periodontitis and a target for drug design to delay alveolar bone resorption.