Knee Flexion Contractures in Patients with Osteoarthritis: Clinical Features and Histologic Characterization of the Posterior Capsule

Campbell, Thomas M.; Trudel, Guy; Laneuville, Odette

doi:10.1016/j.pmrj.2014.12.001

Cited by 45 publications

(43 citation statements)

References 31 publications

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“…Michelson and Hunneyball observed the development of inflammation in the immobilized joint capsules of rabbits, and found that subsequent remobilization further aggravated the synovitis. In general, joint inflammation can lead to arthrofibrosis, which is characterized by collagen deposition in joint components and results in loss of ROM . Based on these reports, we speculate that inflammation and subsequent arthrofibrosis observed early during remobilization may be a primary mechanism responsible for the progression of arthrogenic contracture.…”

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confidence: 76%

Development of arthrogenic joint contracture as a result of pathological changes in remobilized rat knees

et al. 2017

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This study aimed to elucidate how rats recover from immobilization-induced knee joint contracture. Rats' right knees were immobilized by an external fixator at a flexion of 140° for 3 weeks. After removal of the fixator, the joints were allowed to move freely (remobilization) for 0, 1, 3, 7, or 14 days (n = 5 each). To distinguish myogenic and arthrogenic contractures, the passive extension range of motion was measured before and after myotomy of the knee flexors. Knee joints were histologically analyzed and the expression of genes encoding inflammatory or fibrosis-related mediators, interleukin-1β (1L-1β), fibrosis-related transforming growth factor-β1 (TGF-β1), and collagen type I (COL1A1) and III (COL3A1), were examined in the knee joint posterior capsules using real-time PCR. Both myogenic and arthrogenic contractures were established within 3 weeks of immobilization. During remobilization, the myogenic contracture decreased over time. In contrast, the arthrogenic contracture developed further during the remobilization period. On day 1 of remobilization, inflammatory changes characterized by edema, inflammatory cell infiltration, and upregulation of IL-1β gene started in the knee joint posterior capsule. In addition, collagen deposition accompanied by fibroblast proliferation, with upregulation of TGF-β1, COL1A1, and COL3A1 genes, appeared in the joint capsule between days 7 and 14. These results suggest the progression of arthrogenic contracture following remobilization, which is characterized by fibrosis development, is possibly triggered by inflammation in the joint capsule. It is therefore necessary to focus on developing new treatment strategies for immobilization-induced joint contracture. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1414-1423, 2017.

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confidence: 76%

Development of arthrogenic joint contracture as a result of pathological changes in remobilized rat knees

et al. 2017

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“…After immobilization, arthrogenic joint ROM restriction was significantly aggravated by AGE accumulation. Many investigators have focused on the joint capsule as a key factor in arthrogenic contracture . Previous studies have shown that flexion contracture induced by joint immobilization is attributable to the posterior joint capsule .…”

Section: Discussionmentioning

confidence: 99%

“…Many investigators have focused on the joint capsule as a key factor in arthrogenic contracture. [13][14][15][16][17][18][19][20][21] Previous studies have shown that flexion contracture Expression of the TGF-b1 gene was affected by neither joint than in nonimmobilized joints in the ribose group, but not in the saline group. In the immobilized joints, ribose injection caused COL1A1 expression to increase relative to saline injection.…”

Section: Role Of the Progression Of Contracturementioning

confidence: 99%

“…In posttraumatic contracture, there is a consensus that collagen proteins and fibrosis‐related genes are increased in the joint capsule in rats and rabbits . In immobilization‐induced contracture, however, collagen expression patterns in joint capsules are inconsistent among studies . These findings suggest that arthrogenic joint contracture is a result of multifactorial etiopathogenesis.…”

mentioning

confidence: 99%

“…16,17 In immobilization-induced contracture, however, collagen expression patterns in joint capsules are inconsistent among studies. [18][19][20][21] These findings suggest that arthrogenic joint contracture is a result of multifactorial etiopathogenesis.…”

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confidence: 99%

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Accumulation of advanced‐glycation end products (AGEs) accelerates arthrogenic joint contracture in immobilized rat knee

Ozawa

Kaneguchi

Minamimoto

et al. 2017

Journal Orthopaedic Research

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Joint mobility decreases in the elderly and in diabetics, this process is thought to be caused by accumulation of advanced-glycation end products (AGEs). Here, we aimed to elucidate the role of AGEs in joint contracture formation in rat knees. Rats were injected with ribose or saline into the knees twice weekly for 8 weeks. Pentosidine (AGE) levels were measured in the knee-joint tissues. After serial injections, rats were subjected to unilateral knee-joint immobilization in a flexion position for various periods. At day 21, the passive knee ranges of motions (ROMs) were measured. Knee joint histopathology were assessed, and the expression of fibrotic genes in the posterior joint capsules was examined using real-time PCR. Ribose injection induced a 7.0-fold increase in pentosidine levels relative to saline injection. Joint immobilization resulted in equal myogenic ROM restriction in both groups. Arthrogenic ROM restriction was greater with ribose injection in the immobilized joints (p < 0.05), but was not affected in nonimmobilized joints. Type-I (COL1A1) and type-III (COL3A1) collagen gene expression increased significantly in immobilized joints relative to nonimmobilized joints in the ribose group, but was not affected in the saline group. Ribose injection increased COL1A1 expression slightly and COL3A1 expression significantly in immobilized joints. Histologically, inflammatory changes appeared at day 3 of immobilization and peaked at day 7. These responses trended to be more severe and prolonged in the ribose group than in the saline group. Our data provide evidence for a causal relationship between AGEs and joint contracture formation following immobilization. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:854-863, 2018.

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Inferior patellar mobility before and after knee arthroplasty: A comparison with healthy knees

Lachowski,

Prill,

Salzmann

et al. 2024

Knee surg. sports traumatol. arthrosc.

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PurposeThe aim of this study was to evaluate patellar mobility in patients before and after knee arthroplasty (KA) and compare it with that of healthy subjects. It was hypothesised that patellar mobility is diminished in patients with osteoarthritis (OA) and remains unchanged after KA.MethodsA total of 101 patients (59 females and 42 males) with a mean age of 70.9 ± 9.9 years underwent KA and were compared with 25 healthy individuals (seven females and 18 males) with a mean age of 32.3 ± 9.3 years. Mediolateral patellar displacement was measured by applying a force of 10 N, and the medial and lateral patellar shifts were recorded separately using a validated novel patellostabilometer. Patients were examined preoperatively and at 3 months postoperatively, assessing the range of knee motion and the clinical and functional status based on the Oxford Knee Score (OKS), Kujala Score, subjective Knee Society Score (sKSS), Forgotten Joint Score (FJS) and Western Ontario and McMaster Universities Arthritis Index (WOMAC).ResultsTotal patellar displacement was 42.1 ± 6 mm for healthy subjects, 31 ± 6 mm before surgery and 32.8 ± 7.8 mm after surgery in osteoarthritic patients (p < 0.01). The mean lateral patellar shift differed significantly between healthy individuals (17.9 ± 4 mm) and osteoarthritic patients (15.1 ± 6 mm) (p < 0.01). The mean medial patellar mobility of healthy individuals (24.2 ± 7 mm) was significantly greater than that of osteoarthritic patients (15.8 ± 4.8 mm) (p < 0.01). All scores improved significantly postoperatively. No correlation was found between patellar mobility and OKS, Kujala Score, sKSS, FJS and WOMAC (r = −0.11). Improvement in patellar mobility also showed no correlation with clinical outcomes according to OKS, Kujala Score, sKSS, FJS and WOMAC (r = 0.08).ConclusionThis study has demonstrated reduced patellar mobility in patients with OA. While patellar mobility significantly improved after KA, it may not hold clinical significance (p = 0.04). No impact on clinical outcome can be expected when the presurgical patella mobility is preserved in KA.Level of EvidenceLevel IV.

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Knee Flexion Contractures in Patients with Osteoarthritis: Clinical Features and Histologic Characterization of the Posterior Capsule

Cited by 45 publications

References 31 publications

Development of arthrogenic joint contracture as a result of pathological changes in remobilized rat knees

Development of arthrogenic joint contracture as a result of pathological changes in remobilized rat knees

Accumulation of advanced‐glycation end products (AGEs) accelerates arthrogenic joint contracture in immobilized rat knee

Inferior patellar mobility before and after knee arthroplasty: A comparison with healthy knees

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