Influence on binding of third-order torque to second-order angulation

Using an earlier model, which described the critical contact angle for binding from second-order angulation alone, a more generalized model is derived that combines the effects of angulation and torque. From this vantage point, the onset of binding is evaluated for 3 scenarios: second-order angulation alone, third-order torque only, and a combination of second-order angulation and third-order torque. These scenarios are detailed by plotting the critical contact angle for binding against the torque angle as a function of 10 wire dimensions (16 x 16, 16 x 22, 17 x 17, 17 x 22, 17 x 25, 18 x 18, 18 x 22, 18 x 25, 19 x 25, and 21 x 25 mil), 4 bracket widths (70, 100, 130, and 160 mil), and 4 bracket slots (18, 20.5, 22, and 24.5 mil). From these plots, we learn that each wire base dimension (eg, an 18-mil base as found in 18 x 18-mil, 18 x 22-mil and 18 x 25-mil archwires) has a common maximum critical contact angle for binding. Moreover, each wire-slot combination has a common maximum torque angle, which is independent of bracket width. Finally, we learn that archwire-bracket combinations that use a metric 0.5-mm slot might have some advantages with regard to torquing--given the current philosophy that light, continuous forces are more favorable.     

The αvβ6 integrin plays a role in compromised epidermal wound healing

The alphavbeta6 integrin is an exclusively epithelial integrin that is highly expressed during fetal development. In adult tissue, alphavbeta6 integrin is expressed during inflammation, carcinogenesis, and in wound healing. We previously reported that alphavbeta6 integrin is highly expressed in poorly healing human wounds and its over-expression is associated with chronic wounds in a mouse model. The objective of this study was to investigate the role of alphavbeta6 integrin in compromised wound healing induced by hydrocortisone treatment or aging by using young and old mice deficient in or overexpressing the beta6 integrin subunit in the epidermis. Untreated aged beta6 integrin-deficient (beta6-/-) animals showed a significant delay in wound healing when compared to their age-matched controls or younger beta6-/- mice. The most significant delay was observed at the stages where granulation tissue deposition was occurring. Hydrocortisone treatment significantly delayed wound healing in wild-type and beta6 integrin-deficient mice in comparison with the untreated controls. However, hydrocortisone treatment in beta6 integrin overexpressing animals did not cause a significant delay in wound healing. The results of this study suggest that alphavbeta6 integrin plays an important role in wound healing in animals compromised by either age or stress mimicked by hydrocortisone.