The degeneration of articular cartilage underscores the clinical pathology of temporomandibular joint osteoarthritis (TMJ-OA) and is promoted through dysfunctional biochemical or biophysical signaling. Transduction of these signals has a multifaceted regulation that includes important cell-matrix derived interactions. The matrix encapsulating the cells of the mandibular condylar cartilage (MCC) is rich in type VI collagen. Neuron/glia antigen 2 (NG2) is a type I transmembrane proteoglycan that binds with type VI collagen. This study defines the temporospatial dynamics of NG2-type VI collagen interactions during the progression of TMJ-OA. Membrane-bound NG2 is found to colocalize with pericellular type VI collagen in superficial layer cells in the MCC perichondrium but is present at high levels in the cytosol of chondroblastic and hypertrophic cells. When TMJ -OA is induced using a surgical instability model, localized disruptions of pericellular type VI collagen are observed on the central and medial MCC and are associated with significantly higher levels of cytosolic NG2. NG2 localized within the cytosol is found to be transported through clathrin and dynamin mediated endocytic pathways. These findings are consistent with NG2 behavior in other injury models and underscore the potential of NG2 as an entirely novel molecular mechanism of chondrocyte function contextually linked with TMJ-OA.
The purpose of the present study was to determine the relationship between crosssectional design and fracture load using a static load bearing test in yttria-stabilized tetragonal zirconia polycrystal ceramic frameworks on a molar fixed partial denture. The test framework was designed as a 3-unit bridge with two abutment teeth at the second premolar and second molar of the mandible. The cross-sectional area of the connector was 9.0, 7.0, or 5.0 mm 2 . In terms of shape, the cross-section was either circular or oval, with a height/width ratio of 1:1, 3:4, or 2:3. For each of the 9 combinations of crosssectional area and shape, 5 frameworks were prepared (45 in total). Frameworks were cemented to a metallic test model with adhesive resin cement. After fracture load was measured, the percentage of fracture sites was determined and the fracture surfaces observed. In terms of cross-sectional area, there was a statistically significant difference in fracture load between 9.0, 7.0, and 5.0 mm 2 . No significant difference in fracture load was observed between any two shapes of connector (pϾ0.05). The fracture load of all frameworks with a cross-sectional area of 9.0 or 7.0 mm 2 was over 880 N, which was recognized as parafunctional occlusal force. Fracture occurred at the distal connector in 82.2% of all frameworks on average. Fracture load decreased as cross-sectional area of the connector became smaller. The cross-sectional shape used in the present study was less influential on fracture load. It appears to be clinical possible to apply a connector with a crosssectional area of 7.0 mm 2 . Fracture often occurred at the distal connector between the pontic and the abutment, corresponding to the second molar.
Initial attachment of human oral keratinocytes cultured on yttria-stabilized tetragonal zirconia polycrystal (TZP) surfaces that were subjected to UV or oxygen plasma (O2-plasma) treatment was investigated. The viability of the attached cells, mRNA expression of laminin γ2 and integrin β4, distribution of laminin γ2 and integrin β4, cell area, and cell morphology were assessed. The results showed that no differences in the viability of attached cells were recognized among the conditions. However, expression of laminin γ2 and integrin β4 as well as cell morphology were promoted only in O2-plasma specimens even though superhydrophilicity was obtained in both the UV and O2-plasma specimens compared with the untreated control specimen. The photocatalytic activity was believed to be closely involved in the above-mentioned differences. The results of this study suggest that TZP surface treated with oxygen plasma promotes the initial attachment capability of human oral keratinocytes with enhancing the extracellular matrix such as laminin γ2.
End stage temporomandibular joint osteoarthritis (TMJ-OA) is characterized by fibrillations, fissures, clefts, and erosion of the mandibular condylar cartilage. The goal of this study was to define changes in pericellular and interterritorial delineations of the extracellular matrix (ECM) that occur preceding and concurrent with the development of this end stage degeneration in a murine surgical instability model. Two-photon fluorescence (TPF) and second harmonic generation (SHG) microscopy was used to evaluate TMJ-OA mediated changes in the ECM. We illustrate that TPF/SHG microscopy reconstructs the three-dimensional network of key fibrillar and micro-fibrillar collagens altered during the progression of TMJ-OA. This method not only generates spatially distinct pericellular and interterritorial delineations of the ECM but distinguishes early and end stage TMJ-OA by signal organization, orientation, and composition. Early stage TMJ-OA at 4- and 8-weeks post-injury is characterized by two structurally distinct regions containing dense, large fiber collagens and superficial, small fiber collagens rich in types I, III, and VI collagen oriented along the mesiodistal axis of the condyle. At 8-weeks post-injury, type VI collagen is locally diminished on the central and medial condyle, but the type I/III rich superficial layer is still present. Twelve- and 16-weeks post-injury mandibular cartilage is characteristic of end-stage disease, with hypocellularity and fibrillations, fissures, and clefts in the articular layer that propagate along the mediolateral axis of the MCC. We hypothesize that the localized depletion of interterritorial and pericellular type VI collagen may signify an early marker for the transition from early to end stage TMJ-OA, influence the injury response of the tissue, and underlie patterns of degeneration that follow attritional modes of failure.
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