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Background:There are limited clinical experiments addressing the effects of photodynamic therapy (PDT) as an adjunct to conventional scaling and root planing (SRP) on clinical and biologic features of periodontitis. This trial compares the clinical parameters and cytokine profiles in gingival crevicular fluid of patients with moderate‐to‐severe chronic periodontitis (CP) who have been treated using SRP alone or SRP + PDT. Methods:Twenty‐two patients with two contralateral teeth affected with moderate‐to‐severe CP were selected. After SRP, the participants’ teeth were randomized to receive either no further treatment or a single application of PDT using a 638‐nm laser and toluidine blue. Although the change in probing depth was the primary outcome, bleeding on probing, clinical attachment level, gingival recession, interleukin‐1β, tumor necrosis factor (TNF)‐α, and matrix metalloproteinase 8 and 9 were also evaluated at baseline and 3 months postintervention. An oral rinse assay was also performed to determine the total levels of oral polymorphonuclear cells (PMNs) before and 3 months after the treatments. Results:Within each group, significant improvements (P<0.001) were found for all variables in 3‐month follow‐up compared with baseline. Only TNF‐α was significantly improved in the PDT + SRP versus SRP group. Total levels of PMNs were reduced for all patients compared with baseline levels (P<0.001). Conclusion:In patients with CP, a single application of PDT (using a 638‐nm laser and toluidine blue) did not provide any additional benefit to SRP in terms of clinical parameters or inflammatory markers 3 months following the intervention.

The role of interleukin (IL)-13, a Th2cytokine sharing many of the features of IL-4, has not previously been examined in patients with visceral leishmaniasis (VL). We examined sera from Iranian patients with VL caused by Leishmania infantum. Serum IL-13 was detected in 50% (22/44) of patients with active primary disease. In comparison, IL-10 was detected in 79.5% (35/44), interferon ? (IFN?) in 38.5% (17/44), and IL-4 in only 5% (2/44) of these patients. With few exceptions all 3 cytokines were undetectable after clinical recovery following antimony therapy. Five of 7 patients (71%) who failed antimony therapy and had relapsing disease had similar levels of IL-10 to patients with active primary disease. However, with only 1 exception, IL-13, IFN? and IL-4 were not detected in such patients. These data suggest that relapsing disease may result from defective cellular immunity, unrelated to immunosuppression mediated by IL-10.