Preclinical assessment of leukocyte- and platelet-rich fibrin for inhibition of mandibular osteonecrosis.

Considering that osteonecrosis of the jaw may be due to the antiangiogenic effect of bisphosphonates and that leukocyte- and platelet-rich fibrin (L-PRF) releases proangiogenic factors, this study hypothesized that L-PRF could prevent mandibular osteonecrosis in the surgical alveoli of rats treated with sodium alendronate (ALE) or zoledronic acid (ZOL). A sample of 42 male Holtzman rats aged 3 months was divided into 3 experimental groups receiving different forms of treatment (n = 14): ALE, 1 mg/mL/kg weekly; ZOL, 0.3 mg/mL/kg weekly; or saline solution as a control vehicle, 0.009 mg/mL/kg weekly. After 8 weeks of drug or vehicle administration, the mandibular first molars were extracted, and the sockets were enlarged with a spherical drill. The left socket in each animal was filled with L-PRF, and the right socket was left empty in a split-mouth model. Administration of ALE, ZOL, and VEH continued weekly until 7 or 28 days postextraction, when the animals were euthanized (n = 7 per experimental group per timepoint). Repair of the surgical alveoli was evaluated by means of microcomputed tomography and histomorphologic analyses. The statistical significance value was set at P < 0.05. Micrographs showed no intergroup (Dunn test) or intragroup (Wilcoxon test) differences in bone volume density among the different groups at either time period (P > 0.05). According to the histomorphologic analyses, at both 7 and 28 days some expanded sockets in the ALE and ZOL groups exhibited nonvital bone with empty osteocytic lacunae surrounded by an amorphous material and/or an intense inflammatory infiltrate, regardless of the experimental condition of the socket (filled or not filled with L-PRF). In addition, the bone surface had rounded margins and no cells. The results of this study suggest that the presence of L-PRF did not prevent the occurrence of osteonecrosis of the jaw.