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  2. The “enthesis organ” concept and its relevance to foot and ankle pathology: a literature review.
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Relatedly, in muscle terminology , the insertion is the site of attachment at the end with predominant movement or action opposite of the origin. Thus the words enthesis and insertion [of muscle] are proximal in the semantic field , but insertion in reference to muscle can refer to any relevant aspect of the site i. From Wikipedia, the free encyclopedia. Enthesis Typical Joint. Structural Interfaces and Attachments in Biology.

New York: Springer. Nature Materials. April Journal of Anatomy. Grauer, Anne L.

A Companion to Paleopathology. International Journal of Osteoarchaeology.

The Enthesis Organ Concept and Its Relevance to the Spondyloarthropathies

Ann Search terms: Number papers retrieved: RheumDis. An immunohistochemical study of the dorsal capsule of the lumbar and thoracic facet joints. A portrait of gender in two 19th and 20 th century Portuguese populations: a palaeopathological perspective, Ph. Mechanical regulation of PTHrP expression in entheses.

Paget's disease of bone: a review. Rheumatology International 28 11 Migration of tendinous insertions. Cause and mechanism.


  1. The enthesis organ concept and its relevance to the spondyloarthropathies.!
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  4. Enthesis Organ Concept Its Relevance?
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J Anat a: — Experimental modifications. J Anat b: — Pathology and clinico-pathologic correlations in spondyloarthropathies. Joint Bone Spine. Braun, J. Entheses and enthesitis: a histopathologic review and relevance to spondyloarthritides. Variations in the quality of uncalcified fibrocartilage at the insertions of the extrinsic calf muscles in the foot.

An immunohistochemical study of enthesis development in the medial collateral ligament of the rat 1 Benjamin and McGonagle, a 0 knee joint.

Enthesis Organ Concept Its Relevance

Anat Embryol Berl. Kumai, T. Higashiyama, I. Shinohara, Y. Matsuda, T.

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Repair process after fibrocartilaginous enthesis drilling: pathology AND enthesitis histological study in a rabbit model. Journal of Orthopedic Science 14 1 Anatomy of the subtalar joint and imaging of talo-calcaneal coalition.

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Skeletal Radiol. The developmental morphology of a "periosteal " ligament insertion: growth and maturation of the 21 Benjamin and Bydder ; Benjamin and McGonagle, a; Benjamin and tibial insertion of the rabbit medial collateral ligament. Journal of Orthopedic Research 8 3 Expression of extracellular matrix molecules typical of articular cartilage in the human scapholunate McGonagle, b; Benjamin and Ralphs, ; Benjamin and Ralphs, ; interosseous ligament. Benjamin et al. An immunohistochemical study of the triangular fibrocartilage complex of the wrist: fibrous AND entheses 0 regional variations in cartilage phenotype.

Boszczyk et al. Academic Press: Amsterdam and Benjamin, ; Gao et al. Degenerative diseases of the vertebral column. Radiology 1 Diagnosis of Bone and Joint Disorders. WB Saunders and Co. Adipose tissue at entheses: the innervation and cell composition of the retromalleolar fat pad Table 1. Synovium lines the deep surface of the tendon except in the region of the sesamoid fibrocartilage SF , which, in a flexed finger, is compressed against articular cartilage. Immediately adjacent to its enthesis, the tendon merges with the volar plate VP , in which a sesamoid bone SB is prominent.

This bone is covered on its joint side with articular cartilage that forms a part of the interphalangeal IP joint. However, on its deep surface, the sesamoid bone is covered by thick sesamoid fibrocartilage SF that articulates with a similar but thinner fibrocartilage on the adjacent surface of the tendon. The two are separated by the synovial cavity of the tendon sheath, which is lined by a synovial membrane except over the fibrocartilage.

In each of the 3 examples, a unifying anatomic basis for the SEC complex is that it minimizes the presence of innate immune cells, especially macrophages, at sites of high stressing. Given the extent and complexity of entheses, it is likely that the presence of synovium and synovial fluid in the retrocalcaneal bursa and bursae associated with other attachment sites reflects a physiologic role identical to that in synovial joints Figure 2.

Where a bursa is present adjacent to an enthesis, type A and type B synoviocytes are likely to be involved in maintaining the rheologic properties of synovial fluid, lubricating and nourishing periosteal and sesamoid fibrocartilages Figure 2. The structure and cellular composition of the healthy enthesis and the synovium are diametric opposites. By virtue of respective cellular compositions, the healthy enthesis is generally antiinflammatory and the synovium intrinsically proinflammatory.

Thus, when a mechanically stressed enthesis is injured, any associated inflammatory reaction would be expected to manifest prominently within the juxtaposed synovium. Recently, we showed that extensive microdamage and altered vascularity are present at numerous entheses in elderly individuals, which probably relates to a lifetime of mechanical loading We and others similarly noted that fibrocartilage adjacent to insertions that are closely juxtaposed to synovium are also sites of microdamage 29 , Indeed, Rufai et al suggested that this could trigger retrocalcaneal bursitis The mechanism whereby factors related to SEC microdamage could directly contribute to the initiation of joint inflammation at the molecular level has been elucidated in recent years, as previously stated.

The central tenet of the SEC model is that primary entheseal abnormalities trigger secondary joint synovitis. This is virtually impossible to study in humans, but such study is feasible in animal models of disease.

No animal model exactly mimics human arthritis, and issues such as the relative quantities of fibrocartilage at associated entheses and the extent of microdamage in small animal joints compared with human joints remain unresolved. However, these models provide the researcher with experimental systems for studying specific aspects of the disease process. Investigators in our group previously reported striking similarities between this murine disease and human PsA In addition to observing enthesitis leading to joint ankylosis which presents clinically as arthritis , investigators in our group also recognized dactylitis with extensive subcutaneous edema and onychoperiostitis, both of which are typical of PsA Histomorphologic analysis demonstrated that ankylosis as a result of enthesitis is the hallmark of this murine disease, and that synovitis is not necessary for the appearance of clinical arthritis Two stages can be recognized in this model.

Of particular interest are the foci of intense cell infiltration that are observed adjacent to entheses This acute inflammatory process usually extends into the synovium Figure 4. Synovitis is similarly characterized by cell infiltration without any hyperplasia of the lining layer. In most cases, this acute inflammatory process subsides rapidly, and the second phase of the disease process develops.

This is characterized by endochondral ossification that starts at the enthesis and culminates in joint ankylosis.

Clinical Anatomy of the Ankle and Foot | Reumatología Clínica (English Edition)

In the fused joint, the synovium generally shows little involvement. Mild hyperplasia of the lining layer is rare Figure 4. In late stages of disease, the synovium may disappear in the bridging bony structure between both articular surfaces.

gaysosuldintfur.ml The dual response of the synovium in the inflammatory and remodeling stages provides strong support for the concept of secondary synovial inflammation in the SEC. A , Acute subcutaneous inflammation extending into the entheseal region, with diffuse cell infiltration. B , Details of an inflammatory cell infiltrate.

C , Limited synovial hyperplasia and cell infiltration arrow during progression of endochondral bone formation at the enthesis. D , Joint ankylosis extending into the disappearing synovium in late stages of the disease. When the mice were crossed into a T cell—deficient background, arthritis was milder, with an absence of erosions. However, skin disease remained unchanged. The animal model supports the assertion that innate immune activation within the SEC is critical for the phenotypic expression of PsA, and that adaptive immune responses, as orchestrated by T cells, modify the clinical phenotype.

Both macroscopic and microscopic synovial abnormalities have been described, including less hyperplasia of the lining layer compared with that observed in RA 34 - Two of these studies demonstrated more subsynovial tissue edema and greater vascularity in PsA 34 , 35 , but the other study did not One recent study showed that neutrophilic synovial inflammation was much more common in PsA than in RA Both B cells and T cells have been observed in the synovium of patients with PsA, but specific synovial T cell clonal expansions that might confirm that joint autoantigens drive the immune response have not been shown Furthermore, the assertion that PsA is related to HLA—Cw6 has been challenged by a recent large study that showed a milder spectrum of joint disease in patients carrying this gene There is, therefore, evidence for a distinct pattern of synovitis in PsA but a lack of evidence for autoimmunity.

The notion that synovitis in PsA is unique is also supported by results of macroscopic and microscopic studies showing that the pattern of blood vessels in PsA is disorganized compared with that in RA. This has been interpreted as representing some fundamental angiogenic perturbation that drives synovitis in PsA 40 , However, the question of whether synovial angiogenesis in PsA is abnormal compared with that in RA remains controversial, because this difference in angiogenesis is not supported by some important studies 36 , These differing angiogenic features could be attributable to a relatively slow onset of synovitis in early RA and a more abrupt onset in early PsA and reactive arthritis, in which identical vascular changes have been reported Figure 5.

In RA, synovitis generally develops slowly, as indicated by a subclinical disease phase; this scenario would permit more ordered angiogenesis This is supported by both the demonstration of synovitis during early disease in joints that apparently are not involved and the presence of autoantibodies that predate clinical synovitis by years 43 , The light gray area represents the hitherto poorly understood preclinical disease phases.

The dark gray area represents RA or PsA at the time of clinical presentation with joint swelling and pain.