Background:  The cause of mandibular third molar impaction is said to be due to inadequate space between the distal of the second mandibular molar and the anterior border of the ascending ramus of the mandible. The amount of space is determined primarily by facial growth. This study aimed to assess whether different patterns of facial growth lead to a different incidence of mandibular third molar impaction. It was hypothesized that those with predominantly horizontal (brachyfacial) would have lower incidence of mandibular third molar impaction compared with those with a predominantly vertical growth pattern (dolichofacial).Methods:  Ninety‐eight dental records were sourced from the records of orthodontic patients in the Royal Dental Hospital of Melbourne and all lateral cephalometric radiographs and orthopantomograms were assessed. The degree of impaction was determined by the Pell and Gregory system, and the facial type categorized by the facial axis angle.Results:  The overall rate of mandibular third molar impaction was 58.76 per cent. Those with a facial axis angle >93 (brachyfacials) demonstrated an almost two times lower incidence of mandibular third molar impaction as compared to subjects with a facial axis angle <87 (dolichofacials).Conclusions:  Within the limitations of the study, it was concluded that the greater horizontal facial growth pattern of brachyfacial subjects over dolichofacial subjects provides increased space for full eruption of the mandibular third molars.

Uncovering the inflammatory mechanisms underpinning initiation, progression, and promotion of oral squamous cell carcinoma (OSCC) development is fundamental to the rational pursuit of targeted therapeutics. Here we present a review of the current knowledge of the role of TNF-α in the aetiology, pathogenesis, and potential therapies with regards to OSCC. TNF-α is worthy of particular attention in OSCC, with its presence demonstrated to enhance cell proliferation and its downregulation demonstrated to inhibit proliferation and migration in other carcinomas in both in vitro and in vivo models and oral cancer patients. Increased TNF-α in the OSCC tumour microenvironment has been demonstrated to favour invasion through promotion of firstly the pro-inflammatory, pro-invasive phenotypes of OSCC cells and secondly its paracrine mechanism mediating recruitment and activation of inflammatory cells. Polymorphisms affecting the gene expression of TNF-α have been strongly associated with an increased risk for oral squamous cell carcinoma. A number of studies have considered TNF-α within biofluids, including saliva and serum, as a potential biomarker for the early detection of OSCC, as well as its staging, differentiation, and prognosis. The broad and multifaceted role that TNF-α plays in many inflammatory states presents an obvious confounder, particularly with demonstrated increased TNF-α levels in common oral disease states. Lastly, biologic agents targeting TNF-α are currently in clinical use for immune-mediated inflammatory rheumatological and gastrointestinal diseases. There is the potential that these biological agents might have an adjunctive role in OSCC prevention and treatment.

New anticoagulants are being introduced into the market. These drugs are orally administered, have predictable pharmacokinetics and dose response, do not require monitoring and have an acceptable safety profile when used appropriately, and so avoid many of the disadvantages and possible complications of warfarin and heparin. Dabigatran is the most widely used, and has been approved by the Therapeutic Goods Administration. The use of dabigatran will likely increase in the coming years, and so it is important for dentists to be aware of its mechanism of action, the possible complications, and how to reverse the bleeding if it occurs. This review discusses dabigatran and reports on our experience of five cases, and provides practical clinical advice on how to manage patients on dabigatran who require dental treatment, particularly extractions.