Tissue engineering potentially offers new treatments for disorders of the temporomandibular joint which frequently afflict patients. Damage or disease in this area adversely affects masticatory function and speaking, reducing patients' quality of life. Effective treatment options for patients suffering from severe temporomandibular joint disorders are in high demand because surgical options are restricted to removal of damaged tissue or complete replacement of the joint with prosthetics. Tissue engineering approaches for the temporomandibular joint are a promising alternative to the limited clinical treatment options. However, tissue engineering is still a developing field and only in its formative years for the temporomandibular joint. This review outlines the anatomical and physiological characteristics of the temporomandibular joint, clinical management of temporomandibular joint disorder, and current perspectives in the tissue engineering approach for the temporomandibular joint disorder. The tissue engineering perspectives have been categorized according to the primary structures of the temporomandibular joint: the disc, the mandibular condyle, and the glenoid fossa. In each section, contemporary approaches in cellularization, growth factor selection, and scaffold fabrication strategies are reviewed in detail along with their achievements and challenges.

Serious meniscus injuries seldom heal and increase the risk for knee osteoarthritis; thus, there is a need to develop new reparative therapies. In that regard, stimulating tissue regeneration by autologous stem/progenitor cells has emerged as a promising new strategy. We showed previously that migratory chondrogenic progenitor cells (CPCs) were recruited to injured cartilage, where they showed a capability in situ tissue repair. Here, we tested the hypothesis that the meniscus contains a similar population of regenerative cells. Explant studies revealed that migrating cells were mainly confined to the red zone in normal menisci: However, these cells were capable of repopulating defects made in the white zone. In vivo, migrating cell numbers increased dramatically in damaged meniscus. Relative to non-migrating meniscus cells, migrating cells were more clonogenic, overexpressed progenitor cell markers, and included a larger side population. Gene expression profiling showed that the migrating population was more similar to CPCs than other meniscus cells. Finally, migrating cells equaled CPCs in chondrogenic potential, indicating a capacity for repair of the cartilaginous white zone of the meniscus. These findings demonstrate that, much as in articular cartilage, injuries to the meniscus mobilize an intrinsic progenitor cell population with strong reparative potential. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1966-1972, 2017.

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Axial compressive loads whose direction changes along the spinal curvature (so called compressive follower loads (CFLs)) was postulated as a normal physiological load in the lumbar spine in the literature. Computational analyses were conducted in this study using finite element and optimization models of the spinal system incorporating 244 fascicles of back muscles. It was feasible to find optimum solutions for spinal muscle forces generating CFLs in the lumbar spine in 3-D postures of neutral standing, flexion 40°, extension 10°, axial rotation 10°, or lateral bending 30°. FE analyses demonstrated that the lumbar spine can be in a stable condition not under all CFL generating muscle forces but under those producing CFLs along a curve parallel to the spinal curvature located in the vicinity of the base spinal curve constructed by connecting the geometrical centers of the vertebral bodies. It was also possible to estimate the stable range of the relative location of such CFL curve to the base spinal curve. These results suggest that the lumbar spine in various 3-D postures can be stabilized by spinal muscles that generate CFLs in the spine, which at least in part supports the hypothesis of CFLs as a physiological load in the lumbar spine. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.