A standard treatment for osteoradionecrosis (ORN) has not yet been established because of the diversity. Therefore, identifying the risk factors for a poor prognosis is essential. This study retrospectively investigated the factors associated with the prognosis of ORN in 68 patients. Relevant clinical data of all patients were obtained. Of the patients, 16 who underwent extensive surgery underwent histopathological analysis. The necrotic changes of the anterior and posterior margins in the cortical and cancellous bones were investigated. Multivariate analyses showed statistically significant associations between poor prognosis in patients with ORN and high radiation dose (hazard ratio [HR] 1.15), orocutaneous fistula (HR 2.93), and absence of sequestration (HR 2.49). Histopathological analysis showed a viable anterior margin of the middle portion of the cortical bone for all recovered cases; in contrast, most cases (75%) with a poor prognosis showed necrotic changes. The anterior margin of the cancellous bone was viable and resilient to high irradiation, regardless of the prognosis. These results suggest that patients with orocutaneous fistula should receive early surgical intervention, even if the affected area is limited or asymptomatic. In extensive surgery, a sufficient safety margin of necrotic bone, particularly in the anterior region, is required to improve the prognosis.

Purpose: This study aimed to evaluate the occurrence and treatment outcome of late complications after free fibula osteocutaneous flap reconstruction for mandibular osteoradionecrosis (ORN). Methods: We enrolled 15 consecutive patients (14 men, one woman; median age 65 years, range 57-80 years) who underwent free fibula reconstruction for advanced mandibular ORN during 2013-2017 with two or more years of follow-up. Late complications included infection, plate exposure, and recurrence at the resection margin. The effect of perioperative antibiotic administration on late complications was also assessed. Results: Late complications occurred in 33.3% (5/15) of patients, including two infections (local and distant), two plate exposures, and two recurrences (plate exposure and recurrence occurred in one patient). Perioperative antibiotic administration duration did not significantly affect the occurrence of postoperative late complications. All late complications were treated without problems. Conclusions: Late complications after ORN reconstructive surgery are not uncommon, but can be treated properly.

Background/Aim: Oral squamous cell carcinoma (OSCC) is a common malignancy with a poor prognosis, partly due to interactions within the tumor microenvironment. Cancer-associated fibroblasts (CAFs), key stromal components, promote tumor progression by enhancing cancer cell migration, angiogenesis, and extracellular matrix remodeling. Transforming growth factor-beta (TGF-β) is known to induce CAF differentiation from normal fibroblasts (NFs), but its functional contribution in OSCC remains to be fully elucidated. This study explored the role of TGF-β in inducing the transition of NFs into CAFs and its impact on progression of OSCC. Materials and Methods: In vitro, NFs were treated with TGF-β, and CAF induction was assessed by evaluating the expression of the CAF marker α-smooth muscle actin (α-SMA) using quantitative real-time PCR and fluorescent immunostaining. OSCC cell migration was analyzed using a scratch assay. In vivo, TGF-β-treated or untreated NFs were co-injected with OSCC cells. The tumor size and VEGF, MMP2, and MMP9 expression were analyzed via quantitative real-time PCR and immunohistochemistry. Results: In vitro, TGF-β-treated NFs exhibited significantly increased α-SMA expression and enhanced the OSCC migratory ability. In vivo, the TGF-β-treated group demonstrated a marked increase in tumor growth and up-regulated expression of VEGF, MMP2, and MMP9 compared to the untreated group. Conclusion: These findings suggest that TGF-β induces CAF differentiation and facilitates tumor progression by promoting angiogenesis and extracellular matrix degradation. This study highlights the potential of targeting TGF-β as a therapeutic strategy and underscores the need for novel approaches to counteract the tumor-promoting effects of CAFs.