Interpersonal Violence and Maxillofacial Fractures.

PURPOSE: Accident Compensation Corporation statistics shows that maxillofacial fracture affects 11,000 people with an approximate $90 million annual cost in New Zealand dollars (NZD). Previous studies have demonstrated interpersonal violence (IPV), road traffic accidents (RTAs), sports injury, and falls being the common causes of maxillofacial fracture. This study investigated the causes and associated alcohol and/or drug use and fracture patterns in patients presenting with maxillofacial fractures in the Wellington region. SUBJECTS AND METHODS: Demographic data of the patients, the cause of maxillofacial fracture and associated alcohol and/or drug use, and the fracture patterns were culled from our prospective maxillofacial fracture database at Hutt Hospital for a 5-year period from January 01, 2013, to December 31, 2017 and analyzed. RESULTS: A total of 1535 patients were referred with maxillofacial fractures during the study. 38% of the maxillofacial fractures were caused by IPV, followed by sports injury (24%), falls (24%), and RTA (6%), with 33.4% associated with alcohol and/or drug use. Males were six times more likely to present with IPV-related maxillofacial fractures, compared to females. The 16-30-year age group was the most prevalent in the IPV group with NZ Maori attributing to significantly more maxillofacial fractures compared to NZ European, 54.6% vs. 32.0% (P < 0.0001). CONCLUSIONS: IPV, especially involving alcohol and/or drug use, is the most common cause of maxillofacial fractures in the Wellington region, especially in NZ Maori males aged 16-30 years. Public health strategies are needed to decrease IPV as a cause of maxillofacial fractures.

Phosphaturic mesenchymal tumor without osteomalacia: additional confirmation of the "nonphosphaturic" variant, with emphasis on the roles of FGF23 chromogenic in situ hybridization and FN1-FGFR1 fluorescence in situ hybridization.

Phosphaturic mesenchymal tumor (PMT) is a rare, histologically distinctive neoplasm that classically presents with phosphaturia and tumor-induced osteomalacia (TIO; ie, oncogenic osteomalacia). Both the phosphaturia and the TIO are due to paraneoplastic production of FGF23 (a phosphatonin) by the neoplastic cells, which are genetically characterized by rearrangements of FN1 (most often with FGFR1, and less frequently with FGF1). However, rare cases of PMT present without phosphaturia and TIO (ie, the "nonphosphaturic" variant) and are therefore much more challenging to diagnose. Here, we report the first case of a genetically confirmed, nonphosphaturic PMT, in which the correct diagnosis was established through a combination of careful histologic evaluation, FGF23 chromogenic in situ hybridization, and fluorescence in situ hybridization testing for FN1-FGFR1.