Photobiomodulation Therapy Reduces the Inflammatory Process without Inhibiting Bone Deposition in Rats in an Extraction Model.

Objective: We evaluated the influence of photobiomodulation therapy (PBMT) application during bone healing postexodontia in rats. Methods: We divided 84 male Wistar rats into a control group (CG), which received placebo treatment without PBMT, and a test group (TG), which was treated with PBMT. After exodontia, the animals were subjected to PBMT (TG) with an AsGaAI diode laser at 810 nm, 100 mW, 2 J, and 70 J/cm2 or placebo treatment (CG) every 72 h. After 1, 3, 7, 14, 21, and 28 days, the animals were weighed and euthanized to remove the left hemimandibles for radiographic (alveolar filling) and histomorphometric (inflammatory polymorphonuclear cell (PMN), mononuclear cell (MN), osteoclast (OC), and blood vessels counting) analysis. Statistic approach used two-way variance analysis followed by Bonferroni post hoc (p < 0.05, GraphPad Prism 5.0). Results: There was no significant difference in body mass variation (p = 0.828) and bone neoformation (p = 0.365) between the two groups, but the TG presented lower PMN (p < 0.001), MN (p < 0.001), and OC counts (p < 0.001) and higher blood vessels count (p < 0.001) throughout the repair process. Conclusions: PBMT attenuated the inflammatory process after exodontia without interfering with bone neoformation.

Chronic treatment with zoledronic acid alters the expression levels of inflammatory, bone, and apoptotic markers and Toll-like receptors 2 and 4 in rat dental pulp.

OBJECTIVE: The aim of this study was to evaluate the immunostaining of inflammatory, apoptotic, and bone markers, as well as Toll-like-receptors (TLRs) 2 and 4 in the dental pulp in rats treated with zoledronic acid (ZA). STUDY DESIGN: We administered 4 intravascular infusions of saline (control group) or 0.20 mg.kg-1 ZA in Wistar rats (n = 6/group). After 70 days, the 3 rights molars (n = 18/group) were microscopically evaluated (presence of ectasic/dilated blood vessels and inflammatory cells). Immunohistochemistry was performed for tartrate resistant acid phosphatase 5 (TRAP; cell counting), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), TLR2, TLR4, receptor activator of nuclear kappa B ligand (RANKL), osteoprotegerin (OPG), and caspase-3 (scored 0-3 in odontoblast and nonodontoblast dental pulp cells). Mann-Whitney and Fisher's exact tests and Spearman's correlation were used (GraphPad Prism 5.0). RESULTS: There was no alteration in ectasic/dilated blood vessels (P = .101) or inflammatory cells (P = .500), but the number of TRAP-positive cells was reduced in the ZA-group (P = .027). In ZA-group odontoblasts, immunostaining for COX-2 (P = .044), TLR4 (P = .003), OPG (P = .035) and caspase-3 (P = .039) increased, and that for RANKL (P = 0.045) decreased. In nonodontoblast dental pulp cells, RANKL immunostaining decreased (P = .009). In the ZA group, the RANKL/OPG ratio decreased in odontoblast (P = .022) and nonodontoblast dental pulp cells (P = .007). IL-6 did not differ between the groups. CONCLUSIONS: ZA increases the expression levels of inflammatory, apoptotic markers, and TLR4 and alters bone makers in the dental pulp of rats.

Effects of dexamethasone and nimesulide on bisphosphonate-related osteonecrosis of the jaw: An experimental study.

OBJECTIVE: To evaluate the effects of dexamethasone (DEX) and nimesulide (NIM) on Bisphosphonate-related Osteonecrosis of the Jaw (BRONJ) in rats. DESIGN: BRONJ was induced by zoledronic acid (ZA) infusion (0.2mg/kg) in Wistar rats (n=8), followed by extraction of the left lower first molar (BRONJ groups). Control groups (n=40) received saline (IV). For eight weeks, DEX (0.04, 0.4, 4mg/kg) or saline (SAL) were administered by gavage 24h before each infusion of ZA or saline (IV), or NIM (10.3mg/kg) was administered 24h and 12h before each infusion of ZA or saline (IV). The haematological analyses were conducted weekly. After euthanasia (day 70), the jaws were submitted to radiographic and microscopic analysis. Kidney, liver, spleen and stomach were analysed histopathologically. RESULTS: The BRONJ groups showed a higher radiolucent area compared with the control groups (p<0.05). Histomorphometric analysis revealed healing and new bone formation in the control groups, while the BRONJ groups exhibited devitalized bone with bacterial colonies and inflammatory infiltrate. The BRONJ-DEX 0.4 and 4mg/kg groups had a greater number of bacterial colonies (p<0.05) and an increased polymorphonuclear cell count compared to the saline-BRONJ group, while the BRONJ-NIM group had a lower polymorphonuclear count (p<0.05). The BRONJ groups had leucocytosis, which was reduced by DEX administration. Treatments with DEX with or without ZA caused white pulp atrophy. CONCLUSION: Thus, DEX or NIM therapy was not effective in preventing radiographic and histopathologic events associated with BRONJ. Treatment with DEX attenuated leucocytosis post-infusion with ZA.