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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
12 ctor mediating inflammation in the synovium, enthesis, and bone.
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
17 oading, the biological factors that modulate enthesis development are poorly understood.
18 onstrate that Hh signaling within developing enthesis fibrocartilage cells is required for enthesis f
19 ascular invasion, which occurs along rows of enthesis fibrocartilage cells.
20 nd they form by endochondral ossification of enthesis fibrocartilage.
21                                          The enthesis for many tendons consists of a mineralized grad
22 population of resident lymphoid cells at the enthesis for the first time offers an explanation for th
23 nthesis fibrocartilage cells is required for enthesis formation.
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.
26                                              Enthesis microdamage (fissuring) as well as vascular and
27 esence of inflammatory cells and evidence of enthesis microdamage.
28 maller, with altered bone shape and impaired enthesis morphology, morphometry, and organization.
29                                              Enthesis morphometry, histology, and collagen alignment
30 ry chondrogenesis in the mandibular adductor enthesis of duck versus quail.
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.
33  was to demonstrate the applicability of the enthesis organ concept to other insertion sites.
34                            The concept of an enthesis organ is of general significance in understandi
35 ts there were also inflammatory cells in the enthesis organ itself.
36                  Finally, the concept of an 'enthesis organ' may explain the magnetic resonance imagi
37                   The presence and extent of enthesis organs was evaluated at each site in serial sec
38 ll soft tissue components of the entheses or enthesis organs were examined.
39                                    Articular enthesis organs were found at 14 entheses, including the
40                               Extraarticular enthesis organs were seen at 2 sites, the biceps brachii
41 e to which other insertions form comparable "enthesis organs" has not been established.
42                                       In all enthesis organs, sesamoid and/or periosteal fibrocartila
43                                   The tendon enthesis originates from a specific pool of hedgehog-act
44 evelop when ossification at one point on the enthesis outstrips that on either side.
45  and enthesis altered the differentiation of enthesis progenitor cells, resulting in significantly re
46 d micro-organisms, should be assessed at the enthesis rather than in the synovium.
47         Ion channel inhibition did not alter enthesis secondary cartilage but caused bone to form in
48                 Thus, our study reveals that enthesis secondary cartilage forms through mechanisms th
49 bling that of quail, including an absence of enthesis secondary cartilage.
50         An electron microscopic study of the enthesis site-where the extraocular muscle tendon insert
51 isease patterns in SpA are related to normal enthesis structure and biomechanics.
52 usion, deletion of Scx led to impairments in enthesis structure, which translated into impaired funct
53                                              Enthesis tensile mechanical properties were also assesse
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
58  On MRI, edema within the soft tissue at the enthesis was evident in both groups.
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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