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Background Subchondral bone changes, which include bone marrow lesion (BML), subchondral bone attrition (SBA) and subchondral bone cyst (SBC) by magnetic resonance imaging (MRI) analysis, are reportedly implicated for knee pain in knee osteoarthritis (OA). However, the relationship between these subchondral bone changes and OA knee pain and the effect of articular cartilage lesion on the pain remain elusive. Methods Elderly subjects (1,145 subjects, 72.9 years old on average) in the Bunkyo Health Study, 71.5% of whom had knee OA with ≥ Kellgren-Lawrence grade 2, were enrolled. Knee pain in daily life over the past few days was measured using Visual Analogue Scale (VAS) in the Japanese Knee Osteoarthritis Measure. The subjects without or with pain were defined if they indicated a pain VAS score of 0 or a pain VAS score of ≥ 1. The association was examined between knee pain and MRI-detected OA structural changes which were determined according to the Whole Organ Magnetic Resonance Imaging Score. Results While 62.2% of the subjects were free from knee pain, 37.8% of the subjects had knee pain. Knee pain was not related with cartilage lesion without subchondral bone changes (odds ratio [OR]: 1.10 [95% confidence interval [CI]: 0.83–1.46]) or BML alone (OR: 1.32 [95% CI: 0.95–1.83]). However, knee pain was significantly associated with BML coexistent with SBA (OR: 2.22 [95% CI: 1.25–3.97]), SBC (OR: 1.79 [95% CI: 1.28–2.51]), or both SBA and SBC (OR: 2.18 [95% CI: 1.35–3.53]). Similar positive relationships between knee pain and coexisted subchondral bone changes were obtained regardless of the presence or absence of cartilage lesion present above the BML region. When BML was not coexistent with either SBA or SBC regardless of cartilage lesion above the subchondral bone changes, BML was not associated with knee pain (OR: 1.26 [95% CI: 0.90–1.77]) or (OR: 2.16 [95% CI: 0.89–5.23]). Conclusions BML coexistent with SBA and/or SBC, but not BML without the coexistence, was associated with knee pain in the elderly with knee OA regardless of the presence or absence of cartilage lesion.

There is emerging awareness that subchondral bone remodeling plays an important role in the development of osteoarthritis (OA). This review presents recent investigations on the cellular and molecular mechanism of subchondral bone remodeling, and summarizes the current interventions and potential therapeutic targets related to OA subchondral bone remodeling. The first part of this review covers key cells and molecular mediators involved in subchondral bone remodeling (osteoclasts, osteoblasts, osteocytes, bone extracellular matrix, vascularization, nerve innervation, and related signaling pathways). The second part of this review describes candidate treatments for OA subchondral bone remodeling, including the use of bone-acting reagents and the application of regenerative therapies. Currently available clinical OA therapies and known responses in subchondral bone remodeling are summarized as a basis for the investigation of potential therapeutic mediators.

This study developed an in vitro method to evaluate fluid ingress into the graft-host interface of osteochondral grafts and mimetic constructs and the risk of graft subsidence, using porcine and ovine tibio-femoral models, to investigate mechanisms associated with cyst development. Distal femurs were implanted with two osteochondral grafts or mimetic constructs. One was implanted axially with the loading direction at the point of initial contact of the femur and tibia (“loaded graft”); another on an unloaded portion of the opposite condyle (“unloaded graft”). During testing under a uniaxial cyclic loading regime, the specimens were housed in a contrast medium. Micro-CT scans taken before and after testing allowed the movement of the contrast fluid to be visualized. Fluid ingress was quantified by comparing the greyscale distribution across line profiles between the μCT scans. Ingress was calculated at six sites of interest: two at each graft site (“graft-host interface”, “graft centre”), one through “loaded host bone”, and one through “unloaded host bone”. Graft presence and loading were key factors to promote fluid ingress (p = 0.001). Fluid ingress at loaded graft-host interfaces relative to the unloaded host bone of porcine-in-porcine was 2.4 ± 8.9 mm, porcine-in-ovine was 9.9 ± 3.1 mm, and mimetic constructs-inporcine was 3.6 ± 3.8 mm. A mismatch in material properties between the graft and host bone promoted ingress, driven by host bone quality. Subchondral bone damage and fluid pooling below grafts was detectable from μCT images. Results indicate host bone quality should be considered when assessing a patient’s suitability for surgery.

The subchondral bone is involved in the pathophysiology of osteoarthritis (OA), both by biochemical and mechanical pathways. Overloaded OA subchondral bone osteoblasts express a pro-angiogenic and pro-inflammatory phenotype which contributes to explain the structural changes (sclerosis and bone marrow lesion) visible in OA subchondral bone. Further, microfractures and conjonctivo-vascular structures constitute exchange routes between bone and the overlying cartilage for mediators produced by osteoblasts. This narrative review describes these physiopathological mechanisms and identifies possible therapeutic targets for pharmacological modalities.

Purpose of Review This review synthesizes recent advancements in understanding subchondral bone (SCB) biomechanics using computed tomography (CT) and micro-computed tomography (micro-CT) imaging in large animal models, particularly horses. Recent Findings Recent studies highlight the complexity of SCB biomechanics, revealing variability in density, microstructure, and biomechanical properties across the depth of SCB from the joint surface, as well as at different joint locations. Early SCB abnormalities have been identified as predictive markers for both osteoarthritis (OA) and stress fractures. The development of standing CT systems has improved the practicality and accuracy of live animal imaging, aiding early diagnosis of SCB pathologies. Summary While imaging advancements have enhanced our understanding of SCB, further research is required to elucidate the underlying mechanisms of joint disease and articular surface failure. Combining imaging with mechanical testing, computational modelling, and artificial intelligence (AI) promises earlier detection and better management of joint disease. Future research should refine these modalities and integrate them into clinical practice to enhance joint health outcomes in veterinary and human medicine.

In the past decades, considerable efforts have been made to propose experimental and clinical treatments for articular cartilage defects. Yet, the problem of cartilage defects extending deep in the underlying subchondral bone has not received adequate attention. A profound understanding of the basic anatomic aspects of this particular site, together with the pathophysiology of diseases affecting the subchondral bone is the key to develop targeted and effective therapeutic strategies to treat osteochondral defects. The subchondral bone consists of the subchondral bone plate and the subarticular spongiosa. It is separated by the cement line from the calcified zone of the articular cartilage. A variable anatomy is characteristic for the subchondral region, reflected in differences in thickness, density, and composition of the subchondral bone plate, contour of the tidemark and cement line, and the number and types of channels penetrating into the calcified cartilage. This review aims at providing insights into the anatomy, morphology, and pathology of the subchondral bone. Individual diseases affecting the subchondral bone, such as traumatic osteochondral defects, osteochondritis dissecans, osteonecrosis, and osteoarthritis are also discussed. A better knowledge of the basic science of the subchondral region, together with additional investigations in animal models and patients may translate into improved therapies for articular cartilage defects that arise from or extend into the subchondral bone.

Osteoarthritis is a whole joint disease characterised by the disappearance of the cartilage associated with subchondral bone sclerosis, formation of osteophytes and a mild inflammation of the synovial membrane. Although all these events have been independently studied, functional interactions between these different joint tissues should exist, especially between subchondral bone and cartilage. Moreover, recent studies show that cartilage and subchondral bone act as a single functional unit. This review highlights this novel concept.

Purpose Magnetic resonance imaging (MRI) findings of subchondral bone marrow edema (SBME) in osteochondral lesions of the talus (OLT) after arthroscopic microfracture are associated with poor clinical outcomes. However, the relationship between SBME volume change and clinical outcomes has not been analyzed. It was hypothesized that clinical outcomes correlated with SBME volume change and extent of cartilage regeneration in patients with OLT. Methods 64 patients who underwent arthroscopic microfracture for OLT were followed up for more than 2 years. SBME volume change was measured by comparing preoperative and 2-year follow-up MRI. Clinical outcomes were assessed using the visual analogue scale (VAS) and the American orthopedic foot and ankle society ankle-hindfoot scale (AOFAS) at the 2-year and final follow-up. To compare clinical outcomes, patients were categorized into two groups: decreased SBME (DSBME) group (cases without SBME on either MRI or with a decreased SBME volume between the MRIs) and increased SBME (ISBME) group (cases with new SBME on postoperative MRI or with an increased SBME volume between the MRIs). Additionally, the effects of age, sex, body mass index, symptom duration, OLT size, OLT location, containment/uncontainment, preoperative subchondral cysts, pre- and postoperative SBME volumes, and MRI observation of cartilage repair tissue score on clinical outcomes were analyzed. Results The DSBME group included 45 patients, whereas the ISBME group included 19. The mean age was 40.1 ± 17.2 years, and mean follow-up period was 35.7 ± 18.3 months. Preoperative SBME volume was significantly higher in the DSBME group, while the ISBME group had higher volumes at the final follow-up. In both groups, the VAS and AOFAS scores significantly improved at the final follow-up ( p  < 0.001, < 0.001). The VAS scores were significantly lower in the DSBME group at the 2-year and final follow-up ( p  = 0.004, 0.011), while the AOFAS scores were significantly higher ( p  = 0.019, 0.028). Other factors including cartilage regeneration did not affect clinical outcomes. Conclusion SBME volume change correlated with clinical outcomes after arthroscopic microfracture for OLT. Clinical outcomes were worse in patients with new postoperative SBME and increased postoperative SBME volume. In patients with an unsatisfactory clinical course that show decreased SBME via postoperative MRI, an extended follow-up in a conservative manner could be considered. Level of evidence Level III.

To determine the diagnostic yield of cone beam computed tomography (CBCT) compared with 3 T magnetic resonance imaging (MRI) for the evaluation of subchondral insufficiency fractures of the knee. Consecutive patients with subchondral insufficiency fractures of the knee examined by 3 T MRI and CBCT of the femoral condyles were reviewed. Two experienced raters graded the lesion severity on 3 T MRI and CBCT images: grade 1: no signs of a subchondral bone lesion; grade 2: subchondral trabecular fracture or cystic changes, but without infraction of the subchondral bone plate; grade 3: collapse of the subchondral bone plate. Ratings were repeated after six weeks to determine reliability. In addition, the bone lesion size was measured as elliptical area (mm 2 ) and compared between CBCT and T1-weighted MRI sequences. Among 30 patients included (43.3% women; mean age: 60.9 ± 12.8 years; body mass index (BMI) 29.0 ± 12.8 kg/m 2 ), the medial femoral condyle was affected in 21/30 patients (70%). The grading of subchondral lesions between MRI and CBCT did not match in 12 cases (40%). Based on MRI images, an underestimation (i.e., undergrading) compared with CBCT was observed in nine cases (30%), whereas overgrading occurred in three cases (10%). Compared to CBCT, routine T1-weighted 3 T sequences significantly overestimated osseus defect zones in sagittal (84.7 ± 68.9 mm 2 vs. 35.9 ± 38.2 mm 2 , p < 0.01, Cohen’s d  = 1.14) and coronal orientation (53.1 ± 24.0 mm 2 vs . 22.0 ± 15.2 mm 2 , p < 0.01, Cohen’s d  = 1.23). The reproducibility of the grading determined by intra- and inter-rater agreement was very high in MRI (intra-class correlation coefficient (ICC) 0.78 and 0.90, respectively) and CBCT (ICC 0.96 and 0.96, respectively). In patients with subchondral insufficiency fractures of the knee, the use of CBCT revealed discrepancies in lesion grading compared with MRI. These findings are clinically relevant, as precise determination of subchondral bone plate integrity may influence the decision about conservative or surgical treatment. CBCT represents our imaging modality of choice for grading the lesion and assessing subchondral bone plate integrity. MRI remains the gold standard modality to detect especially early stages.

Osteoarthritis (OA) is an important subtype of temporomandibular disorders. A simple and reproducible animal model that mimics the histopathologic changes, both in the cartilage and subchondral bone, and clinical symptoms of temporomandibular joint osteoarthritis (TMJOA) would help in our understanding of its process and underlying mechanism. To explore whether injection of monosodium iodoacetate (MIA) into the upper compartment of rat TMJ could induce OA-like lesions. Female rats were injected with varied doses of MIA into the upper compartment and observed for up to 12 weeks. Histologic, radiographic, behavioral, and molecular changes in the TMJ were evaluated by light and electron microscopy, MicroCT scanning, head withdrawal threshold test, real-time PCR, immunohistochemistry, and TUNEL assay. The intermediate zone of the disc loosened by 1 day post-MIA injection and thinned thereafter. Injection of an MIA dose of 0.5 mg or higher induced typical OA-like lesions in the TMJ within 4 weeks. Condylar destruction presented in a time-dependent manner, including chondrocyte apoptosis in the early stages, subsequent cartilage matrix disorganization and subchondral bone erosion, fibrosis, subchondral bone sclerosis, and osteophyte formation in the late stages. Nociceptive responses increased in the early stages, corresponding to severe synovitis. Furthermore, chondrocyte apoptosis and an imbalance between anabolism and catabolism of cartilage and subchondral bone might account for the condylar destruction. Multi-level data demonstrated a reliable and convenient rat model of TMJOA could be induced by MIA injection into the upper compartment. The model might facilitate TMJOA related researches.