Abstract Temporomandibular joint (TMJ) diseases such as osteoarthritis and disc displacement have no permanent treatment options, but lubrication therapies, used in other joints, could be an effective alternative. However, the healthy TMJ contains fibrocartilage, not hyaline cartilage as is found in other joints. As such, the effect of lubrication therapies in the TMJ is unknown. Additionally, only a few studies have characterized the friction coefficient of the healthy TMJ. Like other cartilaginous tissues, the mandibular condyles and discs are subject to changes in friction coefficient due to fluid pressurization. In addition, the friction coefficients of the inferior joint space of the TMJ are affected by the sliding direction and anatomic location. However, these previous findings have not been able to identify how all three of these parameters (anatomic location, sliding direction, and fluid pressurization) influence changes in friction coefficient. This study used Stribeck curves to identify differences in the friction coefficients of mandibular condyles and discs based on anatomic location, sliding direction, and amount of fluid pressurization (friction mode). Friction coefficients were measured using a cartilage on glass tribometer. Both mandibular condyle and disc friction coefficients were well described by Stribeck curves (R2 range 0.87–0.97; p < 0.0001). These curves changed based on anatomic location (Δμ ∼ 0.05), but very few differences in friction coefficients were observed based on sliding direction. Mandibular condyles had similar boundary mode and elastoviscous mode friction coefficients to the TMJ disc (μmin ∼ 0.009 to 0.19) and both were lower than hyaline cartilage in other joints (e.g., knee, ankle, etc.). The observed differences here indicate that the surface characteristics of each anatomic region cause differences in friction coefficients.
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Degradation alters the lubrication of articular cartilage by high viscosity, hyaluronic acid‐based lubricants
Hyaluronic acid (HA) is widely injected as a viscosupplement in the treatment of osteoarthritis. Despite its extensive use, it is not currently known if cartilage degradation alters how HA‐based solutions lubricate the articular surface. In this study we utilized a model of cartilage degradation by IL‐1β along with a recently developed framework to study role of cartilage degradation on lubrication by clinically‐approved HA‐based lubricants with high viscosities. Cartilage explants were cultured up to 8 days with 10 ng/ml IL‐1β. After culture, samples were examined histologically, immunohistochemically, biochemically, mechanically, topographically, and tribologically. The tribological testing analyzed both boundary and mixed lubrication modes to assess individual effects of viscosity and boundary lubricating ability. Friction testing was carried out using PBS and two clinically approved HA‐based viscosupplements in a cartilage‐glass configuration. After culture with IL‐1β, boundary mode friction was elevated after both 4 and 8 days. Additionally, friction in mixed mode lubrication, where HA is most effective as a lubricant, was significantly elevated after 8 days of culture. As cartilage became rougher, softer, and more permeable after culture, the boundary mode plateau was extended, and as a result, significantly increased lubricant viscosities or sliding speeds were necessary to achieve effective mixed lubrication. Overall, this study revealed that lubrication of cartilage by HA is degradation‐dependent and coincides with changes in mechanics and roughness. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1456–1464, 2018.
- NSF-PAR ID:
- 10047705
- Publisher / Repository:
- Wiley Blackwell (John Wiley & Sons)
- Date Published:
- Journal Name:
- Journal of Orthopaedic Research
- Volume:
- 36
- Issue:
- 5
- ISSN:
- 0736-0266
- Page Range / eLocation ID:
- p. 1456-1464
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Objective To elucidate the role of decorin, a small leucine‐rich proteoglycan, in the degradation of cartilage matrix during the progression of post‐traumatic osteoarthritis (
OA ).Methods Three‐month–old decorin‐null (Dcn−/−) and inducible decorin‐knockout (Dcni
KO ) mice were subjected to surgical destabilization of the medial meniscus (DMM ) to induce post‐traumaticOA . TheOA phenotype that resulted was evaluated by assessing joint morphology and sulfated glycosaminoglycan (sGAG ) staining via histological analysis (n = 6 mice per group), surface collagen fibril nanostructure via scanning electron microscopy (n = 4 mice per group), tissue modulus via atomic force microscopy–nanoindentation (n = 5 or more mice per group) and subchondral bone structure via micro–computed tomography (n = 5 mice per group). Femoral head cartilage explants from wild‐type and Dcn−/−mice were stimulated with the inflammatory cytokine interleukin‐1β (IL ‐1β) in vitro (n = 6 mice per group). The resulting chondrocyte response toIL ‐1β and release ofsGAG s were quantified.Results In both Dcn−/−and Dcni
KO mice, the absence of decorin resulted in acceleratedsGAG loss and formation of highly aligned collagen fibrils on the cartilage surface relative to the control (P < 0.05). Also, Dcn−/−mice developed more salient osteophytes, illustrating more severeOA . In cartilage explants treated withIL ‐1β, loss of decorin did not alter the expression of either anabolic or catabolic genes. However, a greater proportion ofsGAG s was released to the media from Dcn−/−mouse explants, in both live and devitalized conditions (P < 0.05).Conclusion In post‐traumatic
OA , decorin delays the loss of fragmented aggrecan and fibrillation of cartilage surface, and thus, plays a protective role in ameliorating cartilage degeneration. -
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Abstract Lubricin is an important boundary lubricant and chondroprotective glycoprotein in synovial fluid. Both increased and decreased synovial fluid lubricin concentrations have been reported in experimental post-traumatic osteoarthritis (PTOA) animal models and in naturally occurring joint injuries in humans and animals, with no consensus about how lubricin is altered in different species or injury types. Increased synovial fluid lubricin has been observed following intra-articular fracture in humans and horses and in human late-stage osteoarthritis; however, it is unknown how synovial lubricin is affected by knee-destabilizing injuries in large animals. Spontaneous rupture of cranial cruciate ligament (RCCL), the anterior cruciate ligament equivalent in quadrupeds, is a common injury in dogs often accompanied by OA. Here, clinical records, radiographs, and synovial fluid samples from 30 dogs that sustained RCCL and 9 clinically healthy dogs were analyzed. Synovial fluid lubricin concentrations were nearly 16-fold greater in RCCL joints as compared to control joints, while IL-2, IL-6, IL-8, and TNF-α concentrations did not differ between groups. Synovial fluid lubricin concentrations were correlated with the presence of radiographic OA and were elevated in three animals sustaining RCCL injury prior to the radiographic manifestation of OA, indicating that lubricin may be a potential biomarker for early joint injury.
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Interactions between molecules in the synovial fluid and the cartilage surface may play a vital role in the formation of adsorbed films that contribute to the low friction of cartilage boundary lubrication. Osteoarthritis (OA) is the most common degenerative joint disease. Previous studies have shown that in OA-diseased joints, hyaluronan (HA) not only breaks down resulting in a much lower molecular weight (MW), but also its concentration is reduced ten times. Here, we have investigated the structural changes of lipid-HA complexes as a function of HA concentration and MW to simulate the physiologically relevant conditions that exist in healthy and diseased joints. Small angle neutron scattering and dynamic light scattering were used to determine the structure of HA-lipid vesicles in bulk solution, while a combination of atomic force microscopy and quartz crystal microbalance was applied to study their assembly on a gold surface. We infer a significant influence of both MW and HA concentrations on the structure of HA-lipid complexes in bulk and assembled on a gold surface. Our results suggest that low MW HA cannot form an amorphous layer on the gold surface, which is expected to negatively impact the mechanical integrity and longevity of the boundary layer and could contribute to the increased wear of the cartilage that has been reported in joints diseased with OA.more » « less
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Background Ultra‐high field magnetic resonance imaging (MRI) has obvious advantages in acquiring high‐resolution images. 7 T MRI has been clinically approved and 21.1 T MRI has also been tested on rodents.
Purpose To examine the effects of ultra‐high field on mice behavior and neuron activity.
Study Type Prospective, animal model.
Animal Model Ninety‐eight healthy C57BL/6 mice and 18 depression model mice.
Field Strength 11.1–33.0 T
SMF (static magnetic field) for 1 hour and 7 T for 8 hours. Gradients were not on and no imaging sequence was used.Assessment Open field test, elevated plus maze, three‐chambered social test, Morris water maze, tail suspension test, sucrose preference test, blood routine, biochemistry examinations, enzyme‐linked immunosorbent assay, immunofluorescent assay.
Statistical Tests The normality of the data was assessed by Shapiro–Wilk test, followed by Student's
t test or the Mann–WhitneyU test for statistical significance. The statistical cut‐off line isP < 0.05.Results Compared to the sham group, healthy C57/6 mice spent more time in the center area (35.12 ± 4.034, increased by 47.19%) in open field test and improved novel index (0.6201 ± 0.02522, increased by 16.76%) in three‐chambered social test a few weeks after 1 hour 11.1–33.0 T SMF exposure. 7 T SMF exposure for 8 hours alleviated the depression state of depression mice, including less immobile time in tail suspension test (58.32% reduction) and higher sucrose preference (increased by 8.80%). Brain tissue analysis shows that 11.1–33.0 T and 7 T SMFs can increase oxytocin by 164.65% and 36.03%, respectively. Moreover, the c‐Fos level in hippocampus region was increased by 14.79%.
Data Conclusion 11.1–33.0 T
SMFs exposure for 1 hour or 7 TSMF exposure for 8 hours did not have detrimental effects on healthy or depressed mice. Instead, these ultra‐high fieldSMFs have anti‐depressive potentials.Evidence Level 1
Technical Efficacy Stage 1
