Two-photon fluorescence and second harmonic generation characterization of extracellular matrix remodeling in post-injury murine temporomandibular joint osteoarthritis.

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.

Seeking treatment for temporomandibular disorders: What patients can expect from non-dental health care providers.

The dental profession has long been the primary source for clinical management of patients with temporomandibular disorders (TMDs). However, patients with a facial pain problem may seek diagnosis and/or treatment from other health care providers. These providers may be physicians or other professional-level practitioners, or they could be members of various allied groups, such as physical therapists or occupational therapists. However, little has been written about what patients might experience if they seek care outside of the dental profession. This article reports the results of an Internet survey of non-dental professionaland allied health care professionals to learn what they might offer to patients who may be seeking treatment for TMDs. The official organizational websites for all groups, as well as the websites of individual practitioners in each group, were reviewed. Most of the official websites had little or no information about TMDs, but some members of every group surveyed were offering to treat TMDs in their offices. The variety of treatments being offered went far beyond the boundaries of appropriate TMD management in the 21st century. These results are presented with a critical discussion of each concept or practice, as well as advice for both dentists and patients to deal with this situation.

Neuron/Glial Antigen 2-Type VI Collagen Interactions During Murine Temporomandibular Joint Osteoarthritis.

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.