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Backgrounds <p>Osteoporosis (OP) and osteoarthritis (OA) of the knee are common and serious human health problems. However, the relationship between knee OP and the progression of OA, and the potential association between knee OP and adipose tissue within the knee, is not well understood. This study aims to characterize differences in IPFP morphology and lipid metabolism markers, bone metabolism profiles between patients with isolated knee OA and those with concurrent OA and OP, to explore potential mechanisms linking adipose tissue dysfunction to OA-OP comorbidity.</p> Methods <p>This study enrolled 402 participants (89 healthy volunteers, 100 knee OA patients, 108 OP patients, and 105 OA + OP patients) from September 2011 to January 2023. Synovial inflammation markers (effusion grading: 0–3; IPFP abnormalities: 0–3; synovial proliferation: 0–2) and structural knee abnormalities (Whole-Organ Magnetic Resonance Imaging Score [WORMS]: cartilage, bone marrow edema, meniscus sub-scores) were assessed via MRI. Pathological analysis of IPFP tissue (fibrosis: 0–3; vascularization: 0–2) was performed by two blinded pathologists in OA patients undergoing arthroplasty. Clinical outcomes (WOMAC, Oxford Knee Score, Anterior Knee Pain Score) were evaluated preoperatively and at 1-year follow-up. Risk factors (triglycerides, hip BMD, IPFP abnormalities) were analyzed using LASSO regression with 10-fold cross-validation.</p> Results <p>The OA + OP group exhibited higher grades of synovial effusion (mean ± SD: 2.1 ± 0.7 vs. 1.3 ± 0.5, <i>p</i> &lt; 0.01), IPFP abnormalities (2.4 ± 0.6 vs. 1.8 ± 0.4), and synovial proliferation scores (1.9 ± 0.5 vs. 1.2 ± 0.3) compared to the OA group. Total WORMS scores were significantly elevated in OA + OP (32.5 ± 8.2 vs. 24.1 ± 6.5, <i>p</i> &lt; 0.001), driven by higher cartilage degradation, increase of bone marrow edema, and meniscus damage sub-scores. Pathological analysis confirmed increased fibrosis (2.7 ± 0.4 vs. 1.9 ± 0.3) and vascularization (1.8 ± 0.5 vs. 1.1 ± 0.2) in OA + OP. At 1-year follow-up, OA + OP patients had worse WOMAC (45.2 ± 10.1 vs. 33.5 ± 8.7) and OKS (22.1 ± 5.3 vs. 28.4 ± 4.9). LASSO regression identified TG, total hip BMD, and IPFP abnormalities as key risk factors.</p> Conclusion <p>Our results identify a pathophysiological triad of (1) IPFP fibrosis/hypervascularization, (2) systemic hypertriglyceridemia, and (3) low BMD that collectively accelerates structural degeneration and symptom progression in knee OA. While genetic and biomechanical factors initiate OA pathogenesis, these acquired metabolic-inflammatory mechanisms represent tractable therapeutic targets for modifying disease evolution in established OA, particularly with OP comorbidity.</p>

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The role of the infrapatellar fat pad in osteoporotic knee osteoarthritis: bone-fat crosstalk: cross-sectional studies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月7日

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  • Qin Yin,
  • Yu Liu,
  • Fei Yin,
  • Wenyu Xiao,
  • Zhiyuan Guan,
  • Jun Gu

摘要

Backgrounds

Osteoporosis (OP) and osteoarthritis (OA) of the knee are common and serious human health problems. However, the relationship between knee OP and the progression of OA, and the potential association between knee OP and adipose tissue within the knee, is not well understood. This study aims to characterize differences in IPFP morphology and lipid metabolism markers, bone metabolism profiles between patients with isolated knee OA and those with concurrent OA and OP, to explore potential mechanisms linking adipose tissue dysfunction to OA-OP comorbidity.

Methods

This study enrolled 402 participants (89 healthy volunteers, 100 knee OA patients, 108 OP patients, and 105 OA + OP patients) from September 2011 to January 2023. Synovial inflammation markers (effusion grading: 0–3; IPFP abnormalities: 0–3; synovial proliferation: 0–2) and structural knee abnormalities (Whole-Organ Magnetic Resonance Imaging Score [WORMS]: cartilage, bone marrow edema, meniscus sub-scores) were assessed via MRI. Pathological analysis of IPFP tissue (fibrosis: 0–3; vascularization: 0–2) was performed by two blinded pathologists in OA patients undergoing arthroplasty. Clinical outcomes (WOMAC, Oxford Knee Score, Anterior Knee Pain Score) were evaluated preoperatively and at 1-year follow-up. Risk factors (triglycerides, hip BMD, IPFP abnormalities) were analyzed using LASSO regression with 10-fold cross-validation.

Results

The OA + OP group exhibited higher grades of synovial effusion (mean ± SD: 2.1 ± 0.7 vs. 1.3 ± 0.5, p < 0.01), IPFP abnormalities (2.4 ± 0.6 vs. 1.8 ± 0.4), and synovial proliferation scores (1.9 ± 0.5 vs. 1.2 ± 0.3) compared to the OA group. Total WORMS scores were significantly elevated in OA + OP (32.5 ± 8.2 vs. 24.1 ± 6.5, p < 0.001), driven by higher cartilage degradation, increase of bone marrow edema, and meniscus damage sub-scores. Pathological analysis confirmed increased fibrosis (2.7 ± 0.4 vs. 1.9 ± 0.3) and vascularization (1.8 ± 0.5 vs. 1.1 ± 0.2) in OA + OP. At 1-year follow-up, OA + OP patients had worse WOMAC (45.2 ± 10.1 vs. 33.5 ± 8.7) and OKS (22.1 ± 5.3 vs. 28.4 ± 4.9). LASSO regression identified TG, total hip BMD, and IPFP abnormalities as key risk factors.

Conclusion

Our results identify a pathophysiological triad of (1) IPFP fibrosis/hypervascularization, (2) systemic hypertriglyceridemia, and (3) low BMD that collectively accelerates structural degeneration and symptom progression in knee OA. While genetic and biomechanical factors initiate OA pathogenesis, these acquired metabolic-inflammatory mechanisms represent tractable therapeutic targets for modifying disease evolution in established OA, particularly with OP comorbidity.