Background and Aim:The immunocompromised condition is considered a defect in the immune system. This condition tends to increase the risk of oral candidiasis, due to the inability of the immune system to eliminate the adhesion of Candida albicans and leads to systemic candidiasis with a mortality rate of 60%. Green tea (Camellia sinensis) contains potential antioxidant and immunomodulatory which acts as anticancer, antifungal, and antivirus agent. The aim of this study was to invent herbal-based medicine, which acts as an immunomodulator and antifungal agent to treat fungal infection in immunocompromised patients.Materials and Methods:Thirty-five immunocompromised Wistar rats induced with C. albicans were divided into 7 groups (n=5): Control group (C+); treated for 4 days with green tea extract 1.25% (GT 4), epigallocatechin gallate (EGCG) 1% (EGCG 4), EGC 1% (EGC 4); and treated for 7 days with green tea extract 1.25% (GT 7), EGCG 1% (EGCG 7), and EGC 1% (EGC 7). Tongue tissue was collected and analyzed with immunohistochemistry staining using monoclonal antibody; interleukin (IL)-17A, IL-8, and human beta-defensin 2 (HBD)-2. Data were analyzed using analysis of variance test and Tukey honest significant differences test.Results:The expression of IL-17A, IL-8, and HBD-2 was significantly increased (p=0.000) after green tea extract administration in 7 days, whereas in 7 days, the expression of IL-8, IL-17A, and HBD-2 after EGCG and EGC administration did not give a significant result (p>0.005).Conclusion:Within the limits of this study, green tea extract has the ability as an immunomodulatory agent in an immunocompromised patient infected by C. albicans through expression augmentation of IL-8, IL-17A, and HBD-2 compared to EGCG and EGC.

The aim of this study was to find the role of TLR2 signaling pathway in reducing osteoclast activity and promoting osteoblast growth by inducing a combination of Aloe vera and cancellous bovine xenograft (XCB) into dental extraction socket. Forty-eight Cavia cobayas were used. They were divided into eight groups (n=6). For control group, their mandibular incisors were extracted and filled with PEG. For treatment groups, they were extracted and filled with XCB, Aloe vera and the combination of Aloe vera and XCB. The first four groups were sacrificed after 7 days and the other groups after 30 days. Immunohistochemistry and histopathology examination were conducted to examine TLR2, TNFα, OPG, collagen-1, and the osteoblast and osteoclast expressions. The expressions of TLR2, OPG and Collagen-1, as well as the number of osteoblast were increased. Meanwhile, the expressions of TNFα and osteoclast were decreased. The study finding was that TLR2 signaling pathway influenced alveolar bone osteogenesis process by reducing osteoclast activity and stimulating osteoblast growth induced by the combination of Aloe vera and XCB.

Objective The aim of this study is to analyze the low-intensity laser therapy (LILT) biostimulation mechanism as adjuvant therapy within orthodontic treatment as a means of accelerating bone remodeling by transforming growth factor β1 (TGF-β1), bone alkaline phosphatase (BALP), and osteocalcin (OSC) expression. Materials and Methods An analytical experimental method incorporating a posttest only randomized the control group design. The sample consisted of 24 3- to 4-month-old male Cavia porcellus weighing between 300 and 500 g divided into three groups (group 1: control, group 2: received orthodontic treatment, and group 3: received orthodontic treatment with irradiation LILT). LILT biostimulation at a dose of 4 joule/cm2 was performed daily for 3 min on the mesial-distal labial-palatal of the first dextra and sinistra incisor for 2 weeks. The TGF-β1, BALP, and OSC expression was subjected to immunohistochemical analysis. An analysis of variance with multiple comparison, a Tukey's honestly significant difference test, a Kruskal–Wallis test, and a Wilcoxon–Mann–Whitney test were all performed (p < 0.05). Results TGF-β1 expression was significantly different (p = 0.047; p < 0.05) in the tension area, but not in the compression side (p = 0.154; p > 0.05). BALP expression was significantly different in both the tension (p = 0.009) and compression areas (p = 0.005; p < 0.05). OSC expression was significantly different (p = 0.034; p < 0.05) in the tension side, but not in the compression area (p = 1.194; p > 0.05). Conclusion LILT biostimulation can increase TGF-β1, BALP, and OSC expression during orthodontic tooth movement.

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Background: Inflammation is a mechanism or reaction of the natural immune system to defend from external hazards. All foreign objects that enter the body will trigger an immune response in the form of antibodies. In Indonesia, the prevalence of diseases that involve the inflammatory process in the body is high. Freeze-dried hydroxyapatite gypsum puger (HAGP) scaffold is a gypsum powder which is currently under development as a bone replacement material. Freeze-dried hydroxyapatite bovine (HAB) scaffold is a bone substitute material available on the market. Objective: To analyze the inflammatory and immunogenic responses in the tissue after application of freeze-dried HAGP scaffold compared to freeze-dried HAB scaffold through mediators of tumor necrosis factor alpha (TNF-α) and immunoglobulin G (IgG) in rats. Materials and Methods: This study used Wistar rats. HAGP group and HAB group were applied subcutaneously, settled for 7 and 14 days, then the levels of TNF-α and IgG were measured using enzyme-linked immunosorbent assay. Statistical analysis was done using nonparametric test with the Kruskal–Wallis test. Results: TNF-α levels at day 7 in the HAGP group were nearly equal to the control group, while those in the HAB group were higher. Statistically, the significance was P = 0.184 ( P > 0.05). At the 14 th day, the level of IgG on the HAGP and HAB groups the level was higher than the control group, statistically it was found P = 0.127. Conclusion: freeze-dried HAGP scaffold compared to freeze-dried HAB scaffold did not cause inflammatory and immunogenic response on rats through mediators of TNF-α and IgG.