Although a number of inflammatory cytokines have been shown to be associated with periodontal pathogenesis, it is important to investigate further whether these biomarkers are associated with the degree of success in nonsurgical treatment of chronic periodontitis. The aim of the present study was to quantify the total levels of interleukin (IL)-1α, -1β, -6, -10 and tumour necrosis factor (TNF)-α in gingival crevicular fluid (GCF) of chronic periodontitis patients prior to and following nonsurgical periodontal therapy. In total, 52 GCF samples from disease sites of patients with chronic periodontitis, prior to and following periodontal therapy, and ten non-disease sites from non-periodontitis subjects, were collected and cytokine concentrations were determined using a multiplex method. Periodontal parameters, including bleeding on probing, probing pocket depth and the clinical attachment level, in all the sites were recorded. Untreated disease sites exhibited higher cytokine levels in the GCF when compared with the non-disease sites. Nonsurgical periodontal therapy resulted in a statistically significant decrease in the total levels of IL-1α, -1β and -6 in the GCF, but not in IL-10 or TNF-α. The results support the hypothesis that proinflammatory cytokines, including IL-1α, IL-1β and IL-6, are likely to be involved in the pathogenesis of periodontitis and are good markers to evaluate the success of nonsurgical therapy in disease sites of patients with periodontitis.

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Summary Pathological ocular manifestations result from a dysregulation in the balance between proinflammatory type 1 cytokines and regulatory type 2 cytokines. Interleukin‐10 (IL‐10) is an anti‐inflammatory cytokine with potent immunosuppressive effects. We have examined the efficiency of viral IL‐10 adenovirus (Ad‐vIL‐10)‐mediated gene transfer on experimental autoimmune uveoretinitis (EAU) induced in mice and rats by purified retinal autoantigens, respectively, interphotoreceptor binding protein (IRBP) and S‐antigen (S‐Ag). B10‐A mice that received a single unilateral injection of Ad‐vIL‐10 in the retro‐orbital sinus venosus performed 1 day before immunization with IRBP in the footpads showed high levels of circulating vIL‐10 in their sera and a significant reduction in pathological ocular manifestations. Lower levels of IFN‐γ and IL‐2 were found in cellular supernatants from IRBP‐stimulated splenic cells in these treated mice. The local effect on ocular disease of vIL‐10 was neutralized completely by injection of a monoclonal anti‐vIL‐10 antibody, demonstrating the specificity of the treatment. To determine whether the transfer of the vIL‐10 gene within the periocular tissues of the eye could prevent acute EAU, a subconjunctival injection of Ad‐vIL‐10 was performed in Lewis rats simultaneously with S‐­antigen in the footpads. This injection determined in situ vIL‐10 expression with very low circulating vIL‐10 and led to a significant reduction of EAU without affecting the systemic immune response. The present results suggest that Ad‐mediated gene transfer resulting in systemic and local expression of vIL‐10 provide a promising approach for the treatment of uveitis.

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