Condylar Cartilage Research Articles

HMGB2 promotes chondrocyte proliferation under negative pressure through the phosphorylation of AKT

Cells in articular cartilage are zonal arranged. Cells in superficial zone cartilage are generally small and proliferative. Appropriate negative pressure stimulation is beneficial to cell survival and tissue repair. Whether negative pressure has promotive impact on the proliferation activity of the superficial zone chondrocytes is of interest. In this study, we isolated superficial chondrocytes from the mandibular condylar cartilage of rats. After negative pressure treatment, the cells were collected for RNA-sequencing, quantitative real-time PCR and western blotting assays, aiming to detect the proliferative responses of chondrocytes to negative pressure and explore the potential molecular mechanisms. Data from RNA-sequencing analysis indicated that the superficial chondrocytes responded to the 4 h −10 kPa treatment by a significant increase in proliferation. In addition, the expression of high-mobility group box 2 (HMGB2) and the phosphorylation of AKT were obviously promoted. Knockdown of HMGB2 decreased AKT phosphorylation and diminished the negative pressure-induced proliferation of chondrocytes, as shown by decreased expression of Ki67 and cyclin-dependent kinase 6 (CDK6). In contrast, overexpression of HMGB2 enhanced AKT phosphorylation and further promoted proliferative activity. Moreover, LY294002, an AKT inhibitor, suppressed the proliferative activity of chondrocytes under negative pressure, while SC79, an activator of AKT phosphorylation, enhanced the proliferation of chondrocytes. Our data demonstrated that HMGB2 exhibits a promotion impact on chondrocyte proliferation under negative pressure via the phosphorylation of AKT. These results provide a new perspective for superficial zone chondrocytes proliferation under negative pressure, which should be benefit for cartilage regeneration.

Type V collagen regulates the structure and biomechanics of TMJ condylar cartilage: A fibrous-hyaline hybrid

This study queried the role of type V collagen in the post-natal growth of temporomandibular joint (TMJ) condylar cartilage, a hybrid tissue with a fibrocartilage layer covering a secondary hyaline cartilage layer. Integrating outcomes from histology, immunofluorescence imaging, electron microscopy and atomic force microscopy-based nanomechanical tests, we elucidated the impact of type V collagen reduction on TMJ condylar cartilage growth in the type V collagen haploinsufficiency and inducible knockout mice. Reduction of type V collagen led to significantly thickened collagen fibrils, decreased tissue modulus, reduced cell density and aberrant cell clustering in both the fibrous and hyaline layers. Post-natal growth of condylar cartilage involves the chondrogenesis of progenitor cells residing in the fibrous layer, which gives rise to the secondary hyaline layer. Loss of type V collagen resulted in reduced proliferation of these cells, suggesting a possible role of type V collagen in mediating the progenitor cell niche. When the knockout of type V collagen was induced in post-weaning mice after the start of physiologic TMJ loading, the hyaline layer exhibited pronounced thinning, supporting an interplay between type V collagen and occlusal loading in condylar cartilage growth. The phenotype in hyaline layer can thus be attributed to the impact of type V collagen on the mechanically regulated progenitor cell activities. In contrast, knee cartilage does not contain the progenitor cell population at post-natal stages, and develops normal structure and biomechanical properties with the loss of type V collagen. Therefore, in the TMJ, in addition to its established role in regulating the assembly of collagen I fibrils, type V collagen also impacts the mechanoregulation of progenitor cell activities in the fibrous layer. We expect such knowledge to establish a foundation for understanding condylar cartilage matrix development and regeneration, and to yield new insights into the TMJ symptoms in patients with classic Ehlers-Danlos syndrome, a genetic disease due to autosomal mutation of type V collagen.

Temporomandibular joint and orthodontics –A contemporary review

The Temporomandibular joint is an atypical synovial joint that is dynamic in structure. A delicate balance between the musculature, the condylar cartilage and the bony structures is maintained for harmonious functioning of the joint. Over the years the role of occlusion in temporomandibular disorders (TMD) has been extensively debated, leading to many opinions and much controversy. The changes in the joint caused in response to orthodontic therapy as well the adverse reactions caused have been studied. The present article is a review on the effects of Orthodontic appliance therapy on the joint and the present modalities opted to treat the joint disorders.

Evaluation of Changes in Condylar Cartilage Thickness Using MRI and Ultrasound Imaging in Patients Treated by Mandibular Advancement With Myofunctional Appliance: An In-Vivo Pilot Study.

IntroductionThe changes occurring due to growth modulation of the condylar cartilage act as an important mechanism for mandibular advancement using myofunctional appliance therapy. So this study aims to evaluate the condylar cartilage thickness by using MRI and USG in patients undergoing myofunctional appliance therapy for mandibular advancement with the null hypothesis being that there are no changes seen in the thickness of condylar cartilage in growing children.Materials and methodsA prospective evaluation of samples having skeletal Class-II malocclusion ranging between cervical vertebral maturation index (CVMI) stage II and III, requiring twin block functional therapy was performed. Ten patients were selected randomly who underwent MRI and USG in the open and close positions for the evaluation of condylar cartilage thickness and the dimensional changes in the width of the right and left condyle in mm at T0 and T1.ResultThere was no statistically significant difference between the values interpreted by MRI or USG imaging when compared at T0 and T1 and in the open and closed mouth on the left and right sides. At T0, the mean thickness noted was 0.49 mm and 0.48 mm during opening and closing on the left side and 0.52 mm in both positions on the right side. At T1, the mean thickness noted was 0.8 and 0.79mm during opening and closing on the left side, whereas it was 0.81 mm in both positions on the right side.ConclusionThe condylar cartilage thickness increases significantly after twin block therapy suggestive of mandibular growth in skeletal class II malocclusion. It can be inferred that both MRI and USG carry equal diagnostic interpretation, as there was no statistically significant difference between the two imaging modalities.

The Antioxidant Resveratrol Protects against Chondrocyte Apoptosis by Regulating the COX-2/NF-κB Pathway in Created Temporomandibular Osteoarthritis.

Temporomandibular joint osteoarthritis (TMJOA) is characterized by chronic inflammatory degradation of mandibular condylar cartilage (MCC). Studies have found a positive correlation between inflammation and cyclooxygenase- (COX-) 2 in OA pathology. NF-κB is a crucial transcription factor of inflammatory and immune responses in the cause of TMJOA pathology. Resveratrol (RES) plays a critical role in antioxidation and anti-inflammation. But, studies on the effects of RES on TMJOA are very limited. So, the purpose of this study is to investigate the antioxidant and protective effects of RES against MCC degradation through downregulating COX-2/NF-κB expression. In vitro studies, the MCC cells were divided into three groups: the NC group, OA group, and RES group. The optimum dose of RES (10 μM) was determined. The TMJOA model of mice was created by injection of collagenase. And mice were injected with RES (100 μg/10 μl) 3 times one week for 4 weeks in the RES group. The expressions of COX-2, P65, MMP1, MMP13, COL2, and ACAN were measured by RT-PCR. Morphological changes of MCC were studied with HE staining. The results showed that inflammation could induce MCC degradation in vitro and vivo, while RES could reverse the degradation. Meanwhile, RES could downregulate COX-2/NF-κB/MMP expression and increase cartilage markers in vitro and vivo studies. The results indicated that RES treatment had antioxidant effects against chondrocyte apoptosis by downregulating the COX-2/NF-κB pathway in created TMJOA.

Parathyroid hormone promotes cartilage healing after free reduction of mandibular condylar fractures by upregulating Sox9.

After high fractures of the mandibular condyle, the insufficient blood supply to the condyle often leads to poor bone and cartilage repair ability and poor clinical outcome. Parathyroid hormone (PTH) can promote the bone formation and mineralization of mandibular fracture, but its effects on cartilage healing after the free reduction and internal fixation of high fractures of the mandibular condyle are unknown. In this study, a rabbit model of free reduction and internal fixation of high fractures of the mandibular condyle was established, and the effects and mechanisms of PTH on condylar cartilage healing were explored. Forty-eight specific-pathogen-free (SPF) grade rabbits were randomly divided into two groups. In the experimental group, PTH was injected subcutaneously at 20 µg/kg (PTH (1-34)) every other day, and in the control group, PTH was replaced with 1 ml saline. The healing cartilages were assessed at postoperative days 7, 14, 21, and 28. Observation of gross specimens, hematoxylin eosin staining and Safranin O/fast green staining found that every-other-day subcutaneous injection of PTH at 20 µg/kg promoted healing of condylar cartilage and subchondral osteogenesis in the fracture site. Immunohistochemistry and polymerase chain reaction showed that PTH significantly upregulated the chondrogenic genes Sox9 and Col2a1 in the cartilage fracture site within 7-21 postoperative days in the experimental group than those in the control group, while it downregulated the cartilage inflammation gene matrix metalloproteinase-13 and chondrocyte terminal differentiation gene ColX. In summary, exogenous PTH can stimulate the formation of cartilage matrix by triggering Sox9 expression at the early stage of cartilage healing, and it provides a potential therapeutic protocol for high fractures of the mandibular condyle.

A Non-Invasive Method for Generating the Cyclic Loading-Induced Intra-Articular Cartilage Lesion Model of the Rat Knee

Here, we present the cyclic loading-induced intra-articular cartilage lesion model of the rat knee, generated by 60 cyclic compressions over 20 N, resulting in damage to the femoral condylar cartilage in rats.

The effect induced by alternated mechanical loading on Notch-1 in mandibular condylar cartilage of growing rabbits.

AimsThe aim of our study is to investigate the effect induced by alternated mechanical loading on Notch-1 in mandibular condylar cartilage (MCC) of growing rabbits.MethodsA total of 64 ten-day-old rabbits were randomly divided into two groups according to dietary hardness: normal diet group (pellet) and soft diet group (powder). In each group, the rabbits were further divided into four subgroups by feeding time: two weeks, four weeks, six weeks, and eight weeks. Animals would be injected 5-bromo-2′-deoxyuridine (BrdU) every day for one week before sacrificing. Histomorphometric analysis of MCC thickness was performed through haematoxylin and eosin (HE) staining. Immunochemical analysis was done to test BrdU and Notch-1. The quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were used to measure expression of Notch-1, Jagged-1, and Delta-like 1 (Dll-1).ResultsThe thickness of MCC in the soft diet group was thinner than the one in normal diet group. Notch-1 was restricted in fibrous layer, proliferative layer, and hypertrophic layer. The expression of Notch-1 increased from two weeks to six weeks and then fell down. Notch-1 in normal diet group was higher than that in soft diet group in anterior part of MCC. The statistical differences of Notch-1 were shown at two, four, and six weeks (p < 0.05). The result of western blot and quantitative real-time PCR (qRT-PCR) showed the expression of Dll-1 and Jagged-1 rose from two to four weeks and started to decrease at four weeks. BrdU distributed in all layers of cartilage and subchondral bone. The number of BrdU-positive cells, which were less in soft diet group, was decreasing along with the experiment period. The significant difference was found at four, six, and eight weeks in anterior and posterior parts (p < 0.05).ConclusionThe structure and proliferation of MCC in rabbits were sensitive to dietary loading changes. The proper mechanical loading was essential for transduction of Notch signalling pathway and development of mandibular condylar cartilage.Cite this article: Bone Joint Res 2021;10(7):437–444.

Cell depleted areas do not repopulate after diphtheria toxin-induced killing of mandibular cartilage chondrocytes

Growth of mandibular condylar cartilage (MCC) is associated with cell proliferation within the polymorphic cell layer and subsequent differentiation into chondrocytes that reside along the condylar surface and along the cartilage/subchondral bone interface. We examined whether cells in the polymorphic layer would proliferate and repopulate toxin-induced cell-depleted areas in MCCs of adult mice. We induced diphtheria toxin (DTA) expression (ROSA26l-s-lDTA) to cell-autonomously kill large fractions of MCC chondrocytes throughout the cartilage or along the articular cartilage surface with Aggrecan-CreERt2 (AcanCreERt2) or Lubricin-CreERt2 (Prg4CreERt2) Cre-recombinase-inducible mice, respectively. We examined MCCs from these mice shortly after cell killing or several months later with histology and confocal microscopy for evidence of chondrocyte proliferation and repopulation. AcanCreERt2-induced DTA expression killed an average of 53% MCC chondrocytes in adult mice after 1 week (39-66%, 95% confidence interval (CI)). Twelve weeks later, surviving chondrocytes had proliferated but not migrated to cell depleted areas. Prg4CreERt2-induced DTA expression killed an average of 24% surface chondrocytes in mice after 5 weeks (14-34% CI). After thirteen weeks there was 34% fewer surface chondrocytes (4-63% CI) in Prg4CreERt2 DTA-induced mice compared to controls. In adult mice, after diphtheria toxin-mediated chondrocyte killing, cell depleted areas within MCC cartilage are not repopulated by new cells.

Mineral deposition intervention through reduction of phosphorus intake suppresses osteoarthritic lesions in temporomandibular joint

To explore the suppressing impact of low phosphorus intake on osteoarthritic temporomandibular joint and the possible mechanisms of nuclear acid injury in the insulted chondrocytes. Chondrocytes were loaded with fluid flow shear stress (FFSS) with or without low phosphorus medium. Seventy-two mice (sampled at 3-, 7- and 11-wk, n=6) and forty-eight rats (sampled at 12-wks for different testing purpose, n=6) were applied with unilateral anterior crossbite (UAC) with or without low phosphorus diet. In the FFSS model, the Ca and P content, molecules related to nucleic acid degradation and the mineral-producing responses in chondrocytes were detected. The effect of culture dish stiffness on chondrocytes osteogenic differentiation was measured. In the UAC model, the content of Ca and P in serum were tested. The condylar cartilage ossification and stiffness were detected using micro-CT, scanning electron microscope and atomic force microscope. FFSS induced nucleic acid degradation, Pi accumulation and mineral-producing responses in the cultured chondrocytes, all were alleviated by low P medium. Stiffer dish bottoms promoted the osteogenic differentiation of the cultured chondrocytes. UAC stimulated cartilage degeneration and chondrocytes nucleic acid damage, increased PARP 1 and serum P content, and enhanced ossification and stiffening of the cartilage, all were suppressed by low phosphorus diet (all, P<0.05). Nucleic acid damage takes a role in phosphorus production in osteoarthritic cartilage, contributing to the enhanced mineralization and stiffness of the cartilage that in turn promotes cartilage degradation, which can be alleviated by low phosphorus intake.

Senolytics alleviate the degenerative disorders of temporomandibular joint in old age.

Aging is one of the major risk factors for degenerative joint disorders, including those involving the temporomandibular joint (TMJ). TMJ degeneration occurs primarily in the population over 65, significantly increasing the risk of joint discomfort, restricted joint mobility, and reduced quality of life. Unfortunately, there is currently no effective mechanism‐based treatment available in the clinic to alleviate TMJ degeneration with aging. We now demonstrate that intermittent administration of senolytics, drugs which can selectively clear senescent cells, preserved mandibular condylar cartilage thickness, improved subchondral bone volume and turnover, and reduced Osteoarthritis Research Society International (OARSI) histopathological score in both 23‐ to 24‐month‐old male and female mice. Senolytics had little effect on 4 months old young mice, indicating age‐specific benefits. Our study provides proof‐of‐concept evidence that age‐related TMJ degeneration can be alleviated by pharmaceutical intervention targeting cellular senescence. Since the senolytics used in this study have been proven relatively safe in recent human studies, our findings may help justify future clinical trials addressing TMJ degeneration in old age.

Long‐term effect of bilateral anterior elevation of occlusion on the temporomandibular joints

Incisors tubed prosthesis with bilateral anterior elevation (BAE) relation had been reported to stimulate the proliferative response in the mandibular condylar cartilage of mice, thus the prosthetic occlusion elevation had been proposed to treat cartilage degeneration. Currently, we aimed to detect the long-term effect of BAE on temporomandibular joints (TMJs). Twelve 6-week-old female mice were assigned to age-matched control and BAE groups (n=6). Micro-CT images and the macro- and micro-morphology of the mandibular condyles were analyzed at 29weeks. Compared with the age-matched controls, in BAE group, there were loss of subchondral cortical bone and heavy loss of the subchondral trabecular bone at the superior sites of the TMJ condyles, but hyperostosis at the inferior sites as revealed by micro-CT images and histological slices. In BAE group, cartilage thickness and matrix area were increased with upregulated expression of type II, type X collagen, and Ki67, but the expression of cleaved caspase-3 was downregulated (all, p<0.05). In addition to cartilage thickening, long-term BAE induces loss of the subchondral cortical bone and heavy loss of the underneath subchondral trabecular bone, but hyperostosis further underneath. Using BAE as a treatment remains double-edged.

Overloading stress-induced progressive degeneration and self-repair in condylar cartilage.

Overloading stress-induced condylar cartilage degeneration acts as the main pathologic change in temporomandibular joint osteoarthritis (TMJ-OA). However, the progression of degeneration and the ability for self-repair remain poorly understood. Here, we explored the progression of cartilage degeneration by dividing pathological stages using a steady mouth-opening mouse model. Then, we observed changes of cartilage by removing the loading at different stages to test the potential self-repair after degeneration induced. Three-dimensional confocal microscopy combined with histology and micro-CT scanning was applied to examine TMJ at different stages of degeneration before and after self-repair. We found the cartilage underwent progressive and thorough degeneration as the overloading stress developed. During the initial adaptation stage, robust proliferation of posteromedial cartilage began at the area of direct loading. Subsequently, widespread chondrocyte apoptosis was found, followed by new chondrocyte proliferation in aggregates with matrix degradation and subchondral bone catabolism. Finally, with cartilage surface damage, the degeneration reached a point where the lesion could not be reversed by self-repair. While the cartilage nearly returned to normal when the interference was removed within 5 days. These results suggested overloading force induces a pathological process of successive degeneration in TMJ cartilage, which can be reversed by self-repair at early stages.

Effect of Losartan on Patellar Cartilage Volume Among Patients With Knee Osteoarthritis

Purpose Losartan previously in murine Osteoarthritis (OA) model displaying the heterozygous chondroplasia gene (cho/+), a col11a1 mutation shown reduced cartilage loss in temporomandibular joint (TMJ) condylar and knee joint articular cartilage (Osteoarthritis and Cartilage, 2019, 27; 676-686). Losartan is an angiotensin receptor blocker and an inhibitor of TGF-beta. This cross sectional study explores the effect of losartan on patellar cartilage volume in patients with knee osteoarthritis using publicly available database. Methods Using data from Osteoarthritis Initiative (OAI), we compared patellar cartilage volume in patients with and without losartan. A total of 4796 men and women aged 45-79 years were enrolled into the study primarily consisting of those with knee OA and those at high risk for developing knee OA. Our study focused on the progression sub cohort, which consisted of 1390 subjects with knee OA. This study used three measurement periods; baseline, 12 months and 24 months. Patients with missing data for entire series or part missing data and patients who were taking other angiotensin receptor blocker drugs excluded from analysis. Patients data then divided into losartan group and control group (patients without losartan). Specific data sets for the analysis included of demographics such age, sex, race (Clinical_FNOH, Enrollees), patient drug usage (MIF00), Magnetic Resonance Imaging (MRI) data sets on cartilage volume were used from KMRI_FNIH_Qcart_Biomediq00 (baseline), KMRI_FNIH_Qcart_Biomediq01 (12 months), and KMRI_FNIH_Qcart_Biomediq03 (24 months). The patellar cartilage volume variables were V00PatellarCartilage (baseline), V01PatellarCartilage (12 months) and V03PatellarCartilage (24 months). Additional protocol details are published and available on the internet (https://oai.epi-ucsf.org/datarelease/docs/StudyDesignProtocol.pdf). Results Our analysis of the progression sub cohort included a total of 85 (44 %) were men and 108 (56 %) women with symptomatic knee OA (Total n=193). Average age of the participants was 59.6 years (SD, 8.7 years; range, 45–78 years). The majority of the participants were Caucasian (n=142; 73.6 %) and African American (n=42; 21.8 %) (Table 1). Of the 193 patients included in analysis, 30 patients were taking losartan and remaining 163 patients were placed into control group. Mean cartilage volume for losartan and control groups at baseline, 12 months and 24 months are shown in figure 1. Over the period of two years, there was a progressive decline in cartilage volume in both groups. Our analysis show that there was no significant loss of cartilage volume with patients on losartan over baseline at 12 months (5 %) and 24 months (8 %) post enrollment. Patients without losartan showed significantly higher cartilage loss at 24 months post enrollment over baseline (~15 %, p≤ 0.05, Student's t-test assuming unequal variances). Conclusion This study suggests that losartan reduces loss of patellar cartilage in patients with knee osteoarthritis. Further analysis is needed to ascertain association of losartan and reduced loss of cartilage volume and beneficial effects of losartan in osteoarthritis.

Fibrocartilage Stem Cells in the Temporomandibular Joint: Insights From Animal and Human Studies.

Temporomandibular disorders (TMD) are diseases involving the temporomandibular joint (TMJ), masticatory muscles, and osseous components. TMD has a high prevalence, with an estimated 4.8% of the U.S. population experiencing signs and symptoms, and represents a financial burden to both individuals and society. During TMD progression, the most frequently affected site is the condylar cartilage. Comprising both fibrous and cartilaginous tissues, condylar cartilage has restricted cell numbers but lacks a vascular supply and has limited regenerative properties. In 2016, a novel stem cell niche containing a reservoir of fibrocartilage stem cells (FCSCs) was discovered in the condylar cartilage of rats. Subsequently, FCSCs were identified in mouse, rabbit, and human condylar cartilage. Unlike mesenchymal stem cells or other tissue-specific stem/progenitor cells, FCSCs play a unique role in the development and regeneration of fibrocartilage. More importantly, engraftment treatment of FCSCs has been successfully applied in animal models of TMD. In this context, FCSCs play a major role in the regeneration of newly formed cartilage. Furthermore, FCSCs participate in the regeneration of intramembranous bone by interacting with endothelial cells in bone defects. This evidence highlights the potential of FCSCs as an ideal stem cell source for the regeneration of oral maxillofacial tissue. This review is intended to detail the current knowledge of the characteristics and function of FCSCs in the TMJ, as well as the potential therapeutic applications of FCSCs. A deep understanding of the properties of FCSCs can thus inform the development of promising, biologically based strategies for TMD in the future.

Are Stem Cells Useful in the Regeneration and Repair of Cartilage Defects in the TMJ Condyle? An In Vivo Study

Temporomandibular Joint (TMJ) disorders affect up to 10-40% of the population and if left untreated, may eventually lead to Osteoarthritis (OA) of the TMJ. In vivo TMJ repair and regeneration has received significant attention and represents a promising approach for the treatment of degenerative TMJ disorders. The aim of this study was to present a pre-clinical mouse model of TMJ articular cartilage defect and evaluate the utility of a potential tissue engineered TMJ therapy utilizing Mesenchymal Stem Cells (MSCs) derived from mice condyle, hydrogel, and biosilica. C57BL/6 mice (n=30) were equally divided into the following groups: sham group (S-group); control group, condylar cartilage defect only (CD-group); experimental group, condylar cartilage defect + direct administration of MSCs+hydrogel+biosilica (H-group). Mice were euthanized at 4 (n=15) and 8 (n=15) weeks and TMJ joint specimens were harvested for analysis. H&amp;E and Safranin O stained sections showed intact articular surfaces on the condyle and glenoid fossa at both time points, maturation and distribution of chondrocytes along the condyle for the H-group compared to the CD-group. Data from this preliminary study shows that MSCs+hydrogel+biosilica may represent an experimental therapeutic compound for TMJ condylar cartilage regeneration.

The partial femoral condyle focal resurfacing (HemiCAP-UniCAP) for treatment of full-thickness cartilage defects, systematic review and meta-analysis

Knee osteochondral defects are a common problem among people, especially young and active patients. So effective joint preserving surgeries is essential to prevent or even delay the onset of osteoarthritis for these group of patients. This study aims to critically appraise and evaluate the evidence for the results and effectiveness of femoral condyle resurfacing (HemiCAP/ UniCAP) in treatment of patients with focal femoral condyle cartilage defect. Using the search terms : HemiCAP, UniCAP, Episurf, focal, femoral, condyle, inlay and resur-facing, we reviewed the PubMed and EMBASE and the Cochrane Database of Systematic Reviews (CDSR) to find any articles published up to March 2020. The short term follow-up of the HemiCAP shows (6.74 %) revision rate. However, 29.13 % loss of follow up let us consider these results with caution especially if the revision rate progressively increased with time to 19.3 % in 5-7 years with no enough evidence for the long term results except the data from the Australian Joint Registry 2018, where the cumulative revision rate was 40.6 % (33.5, 48.4) at ten years. The UniCAP that used for defect more than 4 cm 2 has a high revision rate (53.66 %) which is considered unacceptable revision rate in com-parison to another similar prosthesis such as Uni-Knee Arthroplasty (UKA). The evidence from published studies and our meta- analysis suggests that partial resurfacing of the femoral condyle (HemiCAP) doesn't support its usage as a tool to treat the focal cartilage defect in middle- aged patients. The UniCAP as femoral condyle resurfacing has very high revision rate at 5-7 years (53.66 %) which make us recommend against its usage.

Concentrated growth factors in the repair of a full-thickness condylar cartilage defect in a rabbit

Concentrated growth factors in the repair of a full-thickness condylar cartilage defect in a rabbit

3D-Printed Polycaprolactone Reinforced Hydrogel as an Artificial TMJ Disc

The replacement of a damaged temporomandibular joint (TMJ) disc remains a long-standing challenge in clinical settings. No study has reported a material with comprehensively excellent properties similar to a natural TMJ disc. In this work, we designed a novel artificial TMJ disc using polyvinyl alcohol (PVA) hydrogel crosslinked by cyclic freeze-thaw and reinforced by 3D-printed polycaprolactone (PCL) implants. The mechanical properties and surface morphologies of the artificial TMJ disc and the natural goat TMJ disc were tested and compared via compression, tensile, cyclic compression/tensile, creep, friction, scanning electron microscopy, and atomic force microscopy. The fibroblasts and chondrocytes were cultured on the artificial TMJ disc for 1, 3, and 5 d for cytotoxicity testing. Importantly, the artificial discs were placed into the TMJs of goats in an innovative way to induce disc defect repair for 12 wk. The PVA + PCL artificial disc demonstrated mechanical strength similar to that of natural disc, as well as 1) better fatigue resistance, viscoelasticity, and hydrophilicity; 2) less creep; and 3) low friction, cytotoxicity, and cell adhesion. By repairing the defects of the TMJ disc in goats, the artificial disc demonstrated the ability to maintain joint stability and protect condylar cartilage and bone from damage. These promising results indicate the feasibility of using a PVA + PCL artificial TMJ disc in a clinical context.

Early changes in osteochondral tissues in a rabbit model of post-traumatic osteoarthritis.

Concurrent osteoarthritic (OA) manifestations in bone and cartilage are poorly known. To shed light on this issue, this study aims to investigate changes in subchondral bone and articular cartilage at two time points after anterior cruciate ligament transection (ACLT) in a rabbit model. 2 (N = 16) and 8 (N = 10) weeks after ACLT, the subchondral bone structure, cartilage thickness, Osteoarthritis Research Society International (OARSI) score, fixed charged density (FCD), and collagen orientation angle were analyzed. OA related changes were evaluated by comparing the ACLT to the contralateral (C-L) and control knees. Already 2 weeks after ACLT, higher trabecular number in the medial femoral condyle and femoral groove, greater OARSI score in the femoral condyles, and thinner trabeculae in the lateral tibial plateau and femoral groove were observed in ACLT compared to C-L knees. Only minor changes of cartilage collagen orientation in the femoral condyles and femoral groove and smaller FCD in the femoral condyles, medial tibial plateau, femoral groove and patella were observed. 8 weeks post-ACLT, the surgical knees had thinner subchondral plate and trabeculae, and smaller trabecular bone volume fraction in most of the knee locations. OARSI score was greater in the femoral condyle and lateral tibial plateau cartilage. FCD loss was progressive only in the femoral condyle, femoral groove, and patellar cartilage, and minor changes of cartilage collagen orientation angle were present in the femoral condyles, femoral groove, and lateral tibial plateau. We conclude that ACLT induces progressive subchondral bone loss, during which proteoglycan loss occurs followed by their partly recovery, as indicated by FCD results.