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1 (11 of 20 patients; P < 0.001 versus distal enthesis).
2 maturation of the tendon-to-bone attachment (enthesis).
3 bone across a specialized tissue called the enthesis.
4 utero eventually populate the entire mature enthesis.
5 synovial invasion (pannus formation) of the enthesis.
6 were present on the soft tissue side of the enthesis.
7 t the presence of small blood vessels at the enthesis.
8 e periodontal ligament (PDL) functions as an enthesis, a connective tissue attachment that dissipates
9 eness to Ihh, from the developing tendon and enthesis altered the differentiation of enthesis progeni
10 sites: the proximal and distal halves of the enthesis and the adjacent calcaneal superior tuberosity.
11 nt inflammatory changes in ligament, tendon, enthesis, and adjacent bone in the DIP joint disease of
13 bined ultrasonography of the Achilles tendon enthesis at different stages of spondylarthritis (SpA) w
14 t in general, especially the hypothesis that enthesis-bone architecture may be important in disease i
15 presence of activated hedgehog signaling in enthesis cells early in the healing process may enhance
16 sed the number of Hh-responsive cells in the enthesis, demonstrating that responsiveness to Hh is mod
18 onstrate that Hh signaling within developing enthesis fibrocartilage cells is required for enthesis f
22 population of resident lymphoid cells at the enthesis for the first time offers an explanation for th
24 ent of Gli1+ cells and hedgehog signaling in enthesis healing, Gli1 expression was examined via linea
25 n the healing process may enhance healing of enthesis injuries by mimicking developmental processes.
31 secondary cartilage at the insertion (i.e., enthesis) of the mandibular adductor muscles on the lowe
32 ns unclear whether IL-23 acts locally at the enthesis or distally on circulating cell populations.
45 and enthesis altered the differentiation of enthesis progenitor cells, resulting in significantly re
52 usion, deletion of Scx led to impairments in enthesis structure, which translated into impaired funct
54 Hh-responsive cells in the developing murine enthesis that were distinct from tendon fibroblasts and
55 cause of the relative inaccessibility of the enthesis, the inflammatory, microbiologic, and immunolog
56 were noted on the soft tissue side of every enthesis; the most common changes were cell clustering a
57 he cortical shell is an integral part of the enthesis, transferring load to an extensive skeletal reg
59 ere present almost exclusively at the distal enthesis, were evident in patients with early SpA and in
60 ration of proinflammatory mediators from the enthesis, whereas the synovitis of rheumatoid arthritis
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