Factors associated with upper leg muscle strength in knee osteoarthritis: A scoping review

Zwart, A.H. de; Dekker, Joost; Lems, Willem F.; Roorda, Leo D.; Esch, M. van der; Leeden, M. van der

doi:10.2340/16501977-2284

Cited by 29 publications

(25 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies have shown that expression of mTOR is increased in peripheral blood mononuclear cells of OA patients, and is related to disease activity, 31 and that pharmacological inhibition or genetic deletion of mTOR in chondrocyte decreases the severity of OA in an animal model. 16,32 However, whether or not mTORC1 is activated in subchondral bone, and its role in OA has not been reported. Western blot analysis of subchondral bone tissues from collected tibial plateau specimens showed an enhanced phosphorylation of S6 (S235/236) (p-S6, a target and marker of mTORC1 activation) in OA patients compared to that of control (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…12 Indeed, homeostasis and integrity of articular cartilage rely on its biochemical and biomechanical interplay with subchondral bone and other joint tissues, 13 and treatment targeting articular cartilage alone in OA has proven to be insufficient to halt disease progression. In a situation of instability, such as occurring with ligament injury, 14 excessive body weight, 15 or weakening muscles related to aging, 16 the mechanical loading on weight-bearing joints is dramatically increased, and changes in the subchondral bone microarchitecture may precede articular cartilage damage. Thus, changes in the subchondral bone have been suggested to predict the severity of cartilage damage in OA.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Activation of mTORC1 in subchondral bone preosteoblasts promotes osteoarthritis by stimulating bone sclerosis and secretion of CXCL12

et al. 2019

View full text Add to dashboard Cite

Increasing evidences show that aberrant subchondral bone remodeling plays an important role in the development of osteoarthritis (OA). However, how subchondral bone formation is activated and the mechanism by which increased subchondral bone turnover promotes cartilage degeneration during OA remains unclear. Here, we show that the mechanistic target of rapamycin complex 1 (mTORC1) pathway is activated in subchondral bone preosteoblasts (Osterix+) from OA patients and mice. Constitutive activation of mTORC1 in preosteoblasts by deletion of the mTORC1 upstream inhibitor, tuberous sclerosis 1, induced aberrant subchondral bone formation, and sclerosis with little-to-no effects on articular cartilage integrity, but accelerated post-traumatic OA development in mice. In contrast, inhibition of mTORC1 in preosteoblasts by disruption of Raptor (mTORC1-specific component) reduced subchondral bone formation and cartilage degeneration, and attenuated post-traumatic OA in mice. Mechanistically, mTORC1 activation promoted preosteoblast expansion and Cxcl12 secretion, which induced subchondral bone remodeling and cartilage degeneration during OA. A Cxcl12-neutralizing antibody reduced cartilage degeneration and alleviated OA in mice. Altogether, these findings demonstrate that mTORC1 activation in subchondral preosteoblasts is not sufficient to induce OA, but can induce aberrant subchondral bone formation and secrete of Cxcl12 to accelerate disease progression following surgical destabilization of the joint. Pharmaceutical inhibition of the pathway presents a promising therapeutic approach for OA treatment.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activation of mTORC1 in subchondral bone preosteoblasts promotes osteoarthritis by stimulating bone sclerosis and secretion of CXCL12

et al. 2019

View full text Add to dashboard Cite

show abstract

“…This is in contrast to measures of maximal force or strength measured using instruments such as dynamometers, where there is unlimited time for recruitment of motor units and optimal engagement of muscle filaments, which may therefore not detect slowing of these components. This slowing is well documented with regards to aging [21], and there is growing evidence of similar processes occurring in osteoarthritis [3]. This reinforces the importance of measures of muscle power which include velocity, to detect early changes in neuromuscular function.…”

Section: Discussionmentioning

confidence: 67%

“…Muscle weakness is a recognised feature of osteoarthritis, with reports of 20-40% weaker quadriceps in knee osteoarthritis patients compared with age-matched controls [3]. Proposed mechanisms behind this relationship include the role of these muscles in stabilising the joint and as shock absorbers, to reduce joint loading and muscle weakness is also associated with worsening pain and physical function [4].…”

Section: Introductionmentioning

confidence: 99%

Jumping Joints: The Complex Relationship Between Osteoarthritis and Jumping Mechanography

et al. 2019

View full text Add to dashboard Cite

We investigated the relationship between lower limb osteoarthritis (OA) and muscle strength and power (assessed by jumping mechanography) in UK community-dwelling older adults. We recruited 249 older adults (144 males, 105 females). OA was assessed clinically at the knee according to ACR criteria and radiographically, at the knee and hip, using Kellgren and Lawrence grading. Two-footed jumping tests were performed using a Leonardo Mechanography Ground Reaction Force Platform to assess maximum muscle force, power and Esslinger Fitness Index. Linear regression was used to assess the relationship between OA and jumping outcomes. Results are presented as β (95% confidence interval). The mean age of participants was 75.2 years (SD 2.6). Males had a significantly higher maximum relative power during lift off (mean 25.7 W/kg vs. 19.9 W/kg) and maximum total force during lift off (mean 21.0 N/kg vs. 19.1 N/kg) than females. In adjusted models, we found significant associations in males between clinical knee OA and maximum relative power [− 6.00 (CI − 9.10, − 2.94)] and Esslinger Fitness Index [− 19.3 (− 29.0, − 9.7)]. In females, radiographic knee OA was associated with total maximum power [− 2.0 (− 3.9, − 0.1)] and Esslinger Fitness Index [− 8.2 (− 15.9, − 0.4)]. No significant associations were observed for maximum total force. We observed significant negative associations between maximum relative power and Esslinger Fitness Index and clinical knee OA in males and radiographic knee OA in females. We have used novel methodology to demonstrate relationships between muscle function and OA in older adults.

show abstract

“…OA patients have pain related to joint degeneration, inflammation and joint stiffness that reduce range of motion [4][5][6][7]. These disabilities can combine with depressive states and expose them to a negative spiral of accumulation of negative effects due to sedentary lifestyle [8][9][10][11]. Such disuse atrophy of muscle is associated with ectopic adipogenesis and loss of knee muscle strength with limited flexion range [4].…”

Section: Introductionmentioning

confidence: 99%

Hypergravity as a gravitational therapy mitigates the effects of knee osteoarthritis on the musculoskeletal system in a murine model

Dechaumet¹,

Cleret²,

Linossier³

et al. 2020

PLoS ONE

View full text Add to dashboard Cite

Insights into the effects of osteoarthritis (OA) and physical interventions on the musculoskeletal system are limited. Our goal was to analyze musculoskeletal changes in OA mice and test the efficacy of 8-week exposure to hypergravity, as a replacement of physical activity. 16-week-old male (C57BL/6J) mice allocated to sham control and OA groups not centrifuged (Ctrl 1g and OA 1g, respectively) or centrifuged at 2g acceleration (Ctrl 2g and OA 2g). OA 1g displayed decreased trabecular bone in the proximal tibia metaphysis and increased osteoclastic activity and local TNFα gene expression, all entirely prevented by 2g gravitational therapy. However, while cortical bone of tibia midshaft was preserved in OA 1g (vs. ctrl), it is thinner in OA 2g (vs. OA 1g). In the hind limb, OA at 1g increased fibers with lipid droplets by 48% in the tibialis anterior, a fact fully prevented by 2g. In Ctrl, 2g increased soleus, tibialis anterior and gastrocnemius masses. In the soleus of both Ctrl and OA, 2g induced larger fibers and a switch from type-II to type-I fiber. Catabolic (myostatin and its receptor activin RIIb and visfatine) and anabolic (FNDC5) genes dramatically increased in Ctrl 2g and OA 2g (p<0.01 vs 1g). Nevertheless, the overexpression of FNDC5 (and follistatine) was smaller in OA 2g than in Ctrl 2g. Thus, hypergravity in OA mice produced positive effects for trabecular bone and muscle typology, similar to resistance exercises, but negative effects for cortical bone.

show abstract

Factors associated with upper leg muscle strength in knee osteoarthritis: A scoping review

Cited by 29 publications

References 84 publications

Activation of mTORC1 in subchondral bone preosteoblasts promotes osteoarthritis by stimulating bone sclerosis and secretion of CXCL12

Activation of mTORC1 in subchondral bone preosteoblasts promotes osteoarthritis by stimulating bone sclerosis and secretion of CXCL12

Jumping Joints: The Complex Relationship Between Osteoarthritis and Jumping Mechanography

Hypergravity as a gravitational therapy mitigates the effects of knee osteoarthritis on the musculoskeletal system in a murine model

Contact Info

Product

Resources

About