Improved Healing of Rabbit Patellar Tendon Defects After an Atelocollagen Injection.

BACKGROUND: Patellar tendinopathy is a common cause of limitations in daily life activities in young and/or active people. The patellar tendon consists of a complex of collagen fibers; therefore, collagen could be used as a scaffold in the treatment of patellar tendinopathy. PURPOSE: To evaluate the healing capacity of injected atelocollagen as a treatment scaffold for patellar tendon defect and, hence, its potential for the treatment of patellar tendinopathy. STUDY DESIGN: Controlled laboratory study. METHODS: After receiving a full-thickness patellar tendon defect, 24 New Zealand White rabbits were divided into a control group (without treatment) and an experimental group that received an atelocollagen injection into the defect. Six rabbits from each group were subsequently used for either histologic scoring or biomechanical testing. The Mann-Whitney U test was used to compare histologic evaluation scores and load to failure between the 2 groups. Statistical significance was set at P < .05. RESULTS: The experimental group showed excellent repair of the damaged patellar tendon and good remodeling of the defective area. In contrast, the control group showed defective healing with loose, irregular matrix fibers and adipose tissue formation. A statistically significant difference was found between the 2 groups in both histologic scores and biomechanical tests at postoperative week 12. CONCLUSION: Injection of atelocollagen significantly improved the regeneration of damaged patellar tendons. CLINICAL RELEVANCE: Atelocollagen gel injections could be used to treat patellar tendinopathy in outpatient clinic settings.

NAMPT enzyme activity regulates catabolic gene expression in gingival fibroblasts during periodontitis.

Periodontal disease is one of the most prevalent chronic disorders worldwide. It is accompanied by inflammation of the gingiva and destruction of periodontal tissues, leading to alveolar bone loss. Here, we focused on the role of adipokines, which are locally expressed by periodontal tissues, in the regulation of catabolic gene expression leading to periodontal inflammation. The expression of the nicotinamide phosphoribosyltransferase (NAMPT) adipokine was dramatically increased in inflamed human and mouse gingival tissues. NAMPT expression was also increased in lipopolysaccharide- and proinflammatory cytokine-stimulated primary cultured human gingival fibroblasts (GF). Adenovirus-mediated NAMPT (Ad-Nampt) overexpression upregulated the expression and activity of COX-2, MMP1 and MMP3 in human GF. The upregulation of IL-1ß- or Ad-Nampt-induced catabolic factors was significantly abrogated by the intracellular NAMPT (iNAMPT) inhibitor, FK866 or by the sirtuin (SIRT) inhibitor, nicotinamide (NIC). Recombinant NAMPT protein or extracellular NAMPT (eNAMPT) inhibition using a blocking antibody did not alter NAMPT target gene expression levels. Moreover, intragingival Ad-Nampt injection mediated periodontitis-like phenotypes including alveolar bone loss in mice. SIRT2, a part of the SIRT family, was positively associated with NAMPT actions in human GF. Furthermore, in vivo inhibition of the NAMPT-NAD+-SIRT axis by NIC injection in mice ameliorated the periodontal inflammation and alveolar bone erosion caused by intragingival injection of Ad-Nampt. Our findings indicate that NAMPT is highly upregulated in human GF, while its enzymatic activity acts as a crucial mediator of periodontal inflammation and alveolar bone destruction via regulation of COX-2, MMP1, and MMP3 levels.