SummaryCollagen degradation by phagocytosis is essential for physiological collagen turnover and connective tissue homeostasis. The rate limiting step of phagocytosis is the binding of specific adhesion receptors, which include the integrins and discoidin domain receptors (DDR), to fibrillar collagen. While previous data suggest that these two receptors interact, the functional nature of these interactions is not defined. In mouse and human fibroblasts we examined the effects of DDR1 knockdown and over-expression on β1 integrin subunit function. DDR1 expression levels were positively associated with enhanced contraction of floating and attached collagen gels, increased collagen binding and increased collagen remodeling. In DDR1 over-expressing cells compared with control cells, there were increased numbers, area and length of focal adhesions immunostained for talin, paxillin, vinculin and activated β1 integrin. After treatment with the integrin-cleaving protease jararhagin, in comparison to controls, DDR1 over-expressing cells exhibited increased β1 integrin cleavage at the cell membrane, indicating that DDR1 over-expression affected the access and susceptibility of cell-surface β1 integrin to the protease. DDR1 over-expression was associated with increased glycosylation of the β1 integrin subunit, which when blocked by deoxymannojirimycin, reduced collagen binding. Collectively these data indicate that DDR1 regulates β1 integrin interactions with fibrillar collagen, which positively impacts the binding step of collagen phagocytosis and collagen remodeling.

No abstract

Introduction Loss of the interdental papilla, leading to the formation of black triangular spaces just below the contact area of adjacent teeth, is one of the most challenging periodontal conditions to treat and often requires an interdisciplinary approach by the periodontist, restorative dentist, and orthodontist. Although these “black triangles” may appear quite small from a clinician's standpoint, they can have a significant impact on oral health satisfaction for patients. This case series illustrates a novel minimally invasive approach to restore interdental papilla deficiencies. Case Presentation Four interdental papilla defects were treated in three females. No patients were lost to follow‐up over 6 months. The surgery consisted of a horizontal incision placed apical to the area of papillary loss in the alveolar mucosa just beyond the mucogingival junction. An interdental subperiosteal tissue space was then created by tunneling toward and under the dental papilla. Once adequate release was achieved, dermal filler was administered into and underneath the deficient papilla. The papillary margins were then sealed with cyanoacrylate and additional dermal filler was injected as needed to achieve ideal papillary fill. Six months after treatment there was an improvement in patient‐satisfaction regarding papilla fill demonstrated by a mean increase in visual analogue scale (VAS) measurements of 62.46%. Mean papilla fill was 1.75 mm. Conclusion This surgical technique demonstrates the restoration of deficient interdental papillae between teeth and implants, and perhaps as importantly, a considerable improvement in patient‐based outcomes quantified through VASs.