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1 ricin may be a potential biomarker for early joint injury.
2 mation may limit the chronic consequences of joint injury.
3 and is associated with both advanced age and joint injury.
4 itis and has multiple risk factors including joint injury.
5 eniscal repair during arthritis or following joint injury.
6 e niche that regenerate cartilage and repair joint injury.
7 the development of osteoarthritis (OA) after joint injury.
8 ases like osteoarthritis can be initiated by joint injury.
9 inhibitor and studied for 7 or 28 days after joint injury.
10 re protected from cartilage damage following joint injury.
11 , subchondral bone sclerosis, and pain after joint injury.
12 he severity of PTOA and muscle atrophy after joint injury.
13 at is exacerbated two weeks after an induced joint injury.
14 A), female sex, obesity, genetics, and major joint injury.
15 ce of joint hemorrhage and following induced joint injury.
16 graphy enable the diagnosis of simulated MCP joint injuries.
17                                              Joint injury also increased IL-12p70 concentrations in m
18  present evidence on the incongruity between joint injury and experience of OA pain, and review brain
19 d joint injury and the relationships between joint injury and joint degeneration.
20 ividuals, indicating a possible role in knee joint injury and modulation of such by altering muscular
21 lationships between sports participation and joint injury and the relationships between joint injury
22 the relationships among increased joint use, joint injuries, and injury-induced joint degeneration th
23 e of a compression wrap for closed extremity joint injuries; and temporary storage of an avulsed toot
24                                  Obesity and joint injury are primary risk factors for osteoarthritis
25 edominant disease risk factors - obesity and joint injury - are well recognized and modifiable.
26 rticular and systemic inflammation following joint injury, as evidenced by lower gene expression of t
27                                              Joint injury at cohort entry or during follow-up substan
28 ic osteoarthritis (PTOA) are associated with joint injury, biomechanical changes, and synovial bioche
29 e consistent with knee OA being initiated by joint injury, but with progression being a consequence o
30                                    Traumatic joint injury can damage cartilage and release inflammato
31              History of fracture and bone or joint injury (FBJI) and other injury causing limitation.
32 OA) animal models and in naturally occurring joint injuries in humans and animals, with no consensus
33 age transcriptomic response following direct joint injury in a murine model of PTOA is rescued by pha
34 ble model and a whole-joint approach for how joint injury in humans leads to PTOA.
35 n vitro and in vivo in response to cartilage/joint injury in mice.
36 iage could increase the risk of degenerative joint injury in physically active women.
37                                              Joint injury in young adults leads to an increased risk
38 es that orchestrate inflammation following a joint injury; in particular, macrophages are central pro
39                     When OA develops after a joint injury, it is designated as post-traumatic OA (PTO
40 ow-up of 36 years, 141 participants reported joint injuries (knee alone [n = 111], hip alone [n = 16]
41                                    Traumatic joint injury leads to an increased risk of osteoarthriti
42                                              Joint injury leads to cartilage damage, a known determin
43                                        Acute joint injury leads to increased risk for osteoarthritis
44               Existing biomarker data in the joint-injury literature can provide insights into the pa
45                           Furthermore, after joint injury, MRL/MpJ mice had lower gene expression of
46                                    Traumatic joint injuries often result in elevated proinflammatory
47  for the altered composition of the SF after joint injury or during inflammation.
48 cular function, and people with a history of joint injury or mild osteoarthritis should select sports
49  repair or regeneration for the treatment of joint injury or osteoarthritis, as well as for their app
50 bnormal joint anatomy or alignment, previous joint injury or surgery, osteoarthritis, joint instabili
51                             Although various joint injuries result in post-traumatic osteoarthritis (
52 therapeutic intervention, blocking ST2 after joint injury significantly ameliorated joint damage duri
53 d in some samples, indicating that the acute joint injury site can promote osteogenic progression of
54 hritis (PTOA) within 10 years following knee-joint injuries such as anterior cruciate ligament ruptur
55  osteoarthritis (PTOA) develops secondary to joint injury, such as ligament rupture, and there is inc
56 e contribution of synovitis in posttraumatic joint injury, such as meniscal tears, and the protective
57                                  Obesity and joint injury together can alter systemic levels of infla
58  states of macrophages in synovium following joint injury, underpinned by distinct transcriptomic sig
59 ontrolling for adiposity, high fat diet, and joint injury using lipodystrophic (LD) mice.
60                                        Acute joint injury was induced in 4 joints by intraarticular i
61 which mimics a mechanical stimulus for facet joint injury, was measured using an algometer.
62                     Both WD-induced skin and joint injuries were associated with an expansion of IL-1