Additional morphologic findings may help in the differential diagnosis between synovial effusion and synovial thickening, such as the presence of scalloping or truncation of the prefemoral fat pad, defects of Hoffa’s fat pad and the non-visualization or irregular margins of the quadriceps fat pad, that have been described as signs of synovial proliferation. During the subacute stage of the pathology, in case of repeated stress, synovial thickening becomes more prominent and so more detectable from the synovial fluid. Synovial thickening or proliferation can be challenging to detect in the presence of a joint effusion since both reveal themselves as an increased signal intensity on fluid-sensitive (T2-weighted) images. Due to the release of pluripotent cells (mainly fibroblasts), the synovial membrane undergoes to hyperplasia and/or hypertrophy that can be less or more fibrous, depending on the kind and the time lasting of the stress. So, effusion can be considered a sensitive indicator of joint pathology, but it may occur in either the presence or absence of proliferative synovitis. However, this is a nonspecific finding as it can be associated with traumatic, degenerative, overload, inflammatory and neoplastic pathology ( 21). Visualization of the synovium, in facts, suggests the presence of underlying pathologic changes. The normal synovium is barely perceptible at MR imaging. Synovial effusion is defined as the increase of the normal quantity of fluid on the articular cavity: its distribution is specific for each joint and follows the capsule anatomy. Diagnostic imaging modalities, uniquely if integrated, are reliable support to diagnosis by demonstrating the type of anatomic alteration, approaching - in most cases - the final pathologic diagnosis, and being a noninvasive follow-up tool ( 4- 20).

In the chronic phases, fibrotic changes may also occur ( 2, 3).Īs in most anatomical districts, although the first step of the approach to synovial pathology is clinical evaluation, this can often have low sensitivity and specificity. The process proceeds inducing synovial proliferation accompanied by mononuclear infiltration this leads to synovial hyperplasia that encroaches upon the articular surface. The initial fast response is characterized by the increase of blood flow that causes edema, alteration of the synovial matrix, and intra-articular effusion. Synovial tissue reacts to the numerous kinds of stresses it may be subjected in a fast but stereotypical manner, and the pathogenesis of the majority of the synovial disorders routes into a final and common anatomopathological pathway. Synovial membrane roles are the production of synovial fluid, the removal of articular debris, and the facilitation of the sliding between the articular surfaces ( 1).

The subsynovium is characterized by the presence of a vascular and lymphatic network through this capillary network, fluid enters into the joint cavity as an ultrafiltrate of blood plasma. The synovial intima is formed by a layer of loosely connected synovial cells, while the subsynovial tissue widely varies in the structure based on its location, and it may be mainly fibrous, areolar, or adipose. Normal synovium is made up of two layers, the synovial intima, and subsynovial tissue. Synovial anatomy, physiology, and pathophysiology

Synovial fluid inflammation