ObjectiveMatrix-associated chondrocyte transplantation is routinely used in joints of the extremities but not in the temporomandibular joint (TMJ).Study DesignWe report the first case series in 7 patients of a tissue engineering approach to regenerate severely degraded articulating surfaces in the TMJ by simultaneously completely resurfacing both the mandibular condyle and the articular eminence/glenoid fossa with a commercially available collagen sponge seeded with autologous cells stabilized within a fibrin matrix. To facilitate healing, we temporarily employed a silicone membrane to protect the engineered tissues. The indications for surgery were posttraumatic fibro-osseous ankylosis, ankylosing osteoarthritis, or late-stage osteoarthritis.ResultsSix of the patients were recalled for follow-up after 3 years 6 months to 12 years 1 month. The maximum incisal opening was 18.2 ± 9.2 mm (range, 9-33 mm) before and 31.2 ± 13.6 mm (range, 12-47 mm) at the latest follow-up. Histologic specimens taken at 4 months showed beginning differentiation of fibrocytes into chondrocytes, whereas at 3 and 11 years, mature hyaline cartilage—not typical for the TMJ—was present.ConclusionsWe conclude that the reconstruction of TMJ surfaces by matrix-associated chondrocyte transplantation may become a routine method for cartilage regeneration in the TMJ in the future.

Purpose: We and others have previously shown that periostin expression is dramatically elevated in human OA cartilage and in three surgical models of OA (medial menisectomy and anterior crucial ligament, partial meniscectomy) in rodents. In vitro periostin promotes collagen and proteoglycan degradation in human chondrocytes via activation of MMP-13 and ADAMTS4 expression. Therefore, we hypothesized that periostin-deficient mice may be protected from surgically-induced posttraumatic OA. Periostin has been shown to control gene expression in bone cells by interacting with avb3 integrin. However, the nature of periostin receptor(s) in chondrocytes is unknown. DDR1, a receptor tyrosine kinase, is highly expressed in chondrocytes and controls MMP-13 expression during chondrogenesis. Therefore, we hypothesized that the effect of periostin on chondrocytes is mediated by DDR1. Methods: Periostin (Postn) knockout (PostnÀ/À) mice were purchased from Jackson Laboratory (B6;129-Postntm1Jmol/J Stock No: 009067). We subjected 3-months old littermates (Postnþ/þ, Postnþ/À and PostnÀ/À) to partial medial menisectomy (PMX) or sham surgery, and harvested the knee joints 8 week post-surgery for histological assessment of OA progression. Human OA cartilage explant cultures were incubated in the presence or absence of the DDR1 inhibitor DDR1-IN-1 dihydrochloridein (100e500 nM) for 2 h before addition of periostin (1 mg/ml) or control vehicle to the culture medium. MMP-13 levels were determined by ELISA-24 h post stimulation. Results: PostnÀ/À deficient mice showed reduced PMX-induced cartilage degeneration and osteophyte formation relative to Postnþ/þ mice. We also observed reduced subchondral bone thickening in both Postnþ/À and PostnÀ/À mice relative to Postnþ/þ controls. In ex vivo studies, pre-incubation of human cartilage explants with the DDR1 inhibitor, DDR1-IN-1 dihydrochloridein, inhibited both constitutive and periostin-induced MMP-13 expression in a dose-dependent manner ( Fig. 1). In contrast, neutralizing antibody to avb3 integrin had no effect on periostin-induced MMP-13 expression. Conclusions: PostnÀ/À mice are protected from surgically-induced post-traumatic OA showing that periostin promotes cartilage degeneration.. DDR1 mediates the stimulatory effect of periostin on MMP-13 expression. Further studies are in progress to investigate the potential of periostin as a druggable target for the treatment of OA.Purpose: The aim of this study was to identify the expression of Latexin of chondrocytes from the three zones of the cartilage and their possible role during the OA pathogenesis in an animal model. Methods: We conducted a proteomic study of osteoarthritic cartilage during the early stages of OA using an experimental rat model. Then, we identify and evaluated the presence of Latexin (Lxn) in the three zones of the cartilage during OA pathogenesis. Results: In this work, we performed a proteomic study of osteoarthritic cartilage during the early stages of an experimental OA rat model. Ten proteins were differentially e...

Background Reducing the necessary time to restore primary teeth improves the cooperation of paediatric patients. This study aimed to investigate the marginal integrity of restorations prepared with a bulk-fill resin-based composite (RBC) containing additional fragmentation chain transfer (AFCT) compared to a conventional RBC when light cured with a rapid high-irradiance (3 s) and a regular (10 s) curing mode. Methods Forty class-II cavities were prepared in 40 primary molars. The molars were randomly divided into four groups based on the applied light-curing modes (regular: 10 s @ 1200 mW/cm2 or high-irradiance: 3 s @ 3000 mW/cm2) and the used restorative material (AFCT-containing bulk-fill RBC “Power Fill” or AFCT-free conventional RBC “Prime”). After thermo-mechanical loading, the marginal integrity was analysed using scanning electron microscopy. A beta regression model and pairwise comparisons were used to statistically analyse the data. Results The mean marginal integrity (% ± SD) of the restorations for each group was as follows: Power Fill (10 s: 79.7 ± 15.6) (3 s: 77.6 ± 11.3), Prime (10 s: 69.7 ± 11.1) (3 s: 75.0 ± 9.7). The difference between the RBCs for the same light-curing mode was statistically significant (p ≤ 0.05). The difference between the light-curing modes for the same RBC was not statistically significant (p ˃ 0.5). Conclusions AFCT-containing bulk-fill RBC “Power Fill” achieves similar marginal integrity when light-cured with either high-irradiance or regular light-curing modes. “Power Fill” achieves better marginal integrity than the conventional RBC “Prime” regardless of the applied light-curing mode.