The subintima layer has few macrophages and lymphocytes, fat cells, and blood vessels, which provide nutrients to the SM and the adjacent avascular cartilage [ 9 — 11 ]. Cells from the SM intimal layer secrete the SF, which provides articular cartilage lubrication, chondrocyte activity, and nutrition.
The synovial intima is composed of two different cell types: type A and B synoviocytes [ 12 ]. Type A and B synoviocytes present cell surface markers that identify them as coming from macrophage and fibroblast lineages, respectively [ 13 ]. Type A synoviocytes synovial macrophages stand round the upper part of synovial lining, whose surface is covered by microvilli and microplicae, like typical macrophage structures [ 12 ].
These cells proliferate in inflammatory conditions. Macrophages are not only in the intimal but also in the subintimal layers of SM, deriving from circulating monocytes originated from the BM [ 9 ].
Synovial intimal fibroblasts express the surface marker CD55, which is used to distinguish them from synovial macrophages [ 9 ]. Type B synoviocytes synovial fibroblasts , which are fibroblast-like cells, express the class II major histocompatibility molecule, which confers a key role in antigen presentation in early phases of immune responses in the SM.
Type B synoviocytes are found further from the synovial lining and produce mainly the glycosaminoglycan hyaluronic acid HA , one of the main constituents of cartilage extracellular matrix, involved with cell signaling by binding to cell receptor CD44 [ 11 ].
In addition, these SM cells produce lubricin, which is responsible for protecting the surface of articular cartilage [ 12 ]. Lubricin helps in joint lubrication, thus reducing pathologic deposition of proteins over the articular cartilage surface [ 12 , 16 , 17 ], and small molecules such as growth factors and cytokines instead easily diffuse in the SF [ 12 ].
These results showed that SM also acts as a semipermeable membrane that controls molecules traffic and the composition of the SF [ 2 , 12 ]. MSCs have been defined following the studies by Friedenstein and colleagues [ 18 ] and Pittenger and colleagues [ 19 ] as BM cell components of non-hematopoietic origin. In this regard, BM spindle-shaped adherent cells with heterogeneous appearance were described.
In the s, other investigators established that those cells were multipotent, able to differentiate in osteoblasts, chondroblasts, adipocytes, and, in certain conditions, myoblasts [ 17 , 20 ]. MSCs were also identified in several organs as cells that have the function of replacing local cells lost in physiological turnover or repairing and regenerating injured tissues [ 21 ]. Microscopic analysis revealed cell aggregates entrapped in fibrin, typical of inflammatory SF.
Intact pieces of synovium have been documented, but synovial cells were not well characterized in vitro. Some findings demonstrated the presence of clonogenic and multipotent MSCs in the SF of both young animals and human joints not affected by arthritis.
Since these fragments are significantly hyperplastic, they seem to be a result of avulsion from weakened synovium because of a lack of nutrients [ 3 ]. According to the International Society for Cytotherapy, MSCs must be able to adhere to plastic material and expand when cultured in vitro.
Moreover, MSCs must show the ability to differentiate into three lineages of mesenchymal cells: osteoblasts, chondroblasts, and adipocytes [ 22 ].
Mesenchymal stem cell markers for cells derived from synovial membrane, cartilage, fat pad, bone marrow, and synovial fluid. During synovial joint development, prior to cavitation, CD44 is expressed in the interzone and the articular surfaces. Conversely, UDPG activity is increased in the articular surfaces but is lowered in the interzone. HA free and bound are found at this time in the interzone. After cavitation, synovium and articular surfaces bind CD44 to HA.
This process facilitates tissue separation and helps create a functional joint cavity [ 33 ]. In cultures enriched with CD90 cells, levels of chondrogenesis were higher than in culture fractions depleted of CD90 [ 26 ].
The CD90 receptor was demonstrated to interact with integrins, tyrosine kinases, growth factors, and cytokines, promoting downstream cellular events such as adhesion, apoptosis, proliferation, and migration. However, the heterogeneity of synovial cells has not been well described [ 26 ]. Another study revealed that intra-articular bleeding soon after anterior cruciate ligament rupture leads to a shift of SF MSCs by expression of cytokines and chemokines that recruit MSCs from elsewhere.
Synovial inflammation is present in early OA and is possibly the trigger of the cascades leading to articular destruction but may also be the focus of repairing responses from progenitor cells [ 32 ]. In patients with OA, there is a decrease on the cartilage extracellular matrix components type II collagen fibers and aggrecan proteoglycan, the latter of which is formed by HA associated with distinct sulfated glycosaminoglycans, the main one of which is chondroitin sulfate.
This condition leads to a reduction in the absorption of mechanical forces [ 16 ]. Moreover, SF lubricin decreases in OA, contributing to lower articular cartilage lubrication [ 37 ]. In addition, higher levels of vascular endothelial growth factor were demonstrated in SF of patients with OA versus rheumatoid arthritis, indicating that angiogenesis might play a role in cartilage degeneration.
Also, the activation of pro-inflammatory cytokines, such as IL-6, IL-8, interferon-gamma, and monocyte chemoattractant protein-1, of human chondrocytes by OA patient SF supports the pro-inflammatory process in the development of OA [ 38 ].
Moreover, elevated IL levels are found in the synovium of patients with early knee OA, providing evidence of activation of innate immunity within SM [ 39 ].
Immature articular cartilage contains a population of progenitor cells responsible for its appositional growth. Notch 1 is present in the chondrocytes of the surface zone articular cartilage, determining the proliferation of these cells.
Thus, Notch-1 signaling has been associated with healthy cartilage progenitors [ 32 , 40 ]. Overexpression of Notch-1, Notch-2, RbpJ, and Hes1 has been observed in chondrocyte differentiation [ 41 ]. Besides, Notchpositive cells were found in greater numbers in cartilage clusters from patients with OA than in control experiments [ 32 ]. Cartilage clusters are a typical phenotype of OA and may result from dedifferentiation and proliferation of resident chondrocytes, although migration of progenitor cells cannot be discarded [ 32 ].
SM has an intrinsic ability of regeneration given its recovery after sinovectomy [ 35 ], suggesting that SM could act as a cell source for cartilage repair [ 25 ]. Synovial chondromatosis is a rare proliferative condition of unknown etiology. It evoked a possible role of SM MSCs in the production of multiple intrasynovial cartilaginous nodules [ 42 ].
The presence of MSCs in the synovial lining leads to questions on their origin. They could have been recruited from blood that penetrates synovial tissue or originated from BM that connects to intra-articular space. The possible role of MSCs in synovial lining is related to healing potential of tissues originated from the mesoderm. Furthermore, their cells may be involved in early stages of osteoarticular diseases. SM MSCs have high self-renewal ability and multipotentiality inherent to single cells.
Single cell-derived MSCs become heterogenous during expression. Non-clonal plastic adherent synovial MSCs consist of a uniform cell population [ 46 ]. Koga and colleagues [ 47 ] demonstrated that transplanted synovium-derived MSCs were altered according to the microenvironments in rabbits. Cells derived from human synovium were shown to have the greatest chondrogenesis potential among the mesenchymal tissue-derived cells, representing a possible source for cartilage repair.
In addition, MSCs derived from BM, synovium, or periosteum were shown to be superior in osteogenesis [ 29 ].
Studies revealed that synovial MSCs precultured with autologous human serum were able to differentiate into chondrocytes in vitro but that their chondrogenic potential was lower than that of the cells maintained with fetal bovine serum [ 48 ]. In addition, synovial cells derived from older human osteoarthritic donors could be reprogrammed to pluripotent cells in alginate culture by stimulation of BMP-2 or BMP-7 in dexamethasone- and serum-free conditions [ 49 ].
These results showed that SM has a therapeutic potential for treatment of chondral defects using in vitro experiments, since human autologous serum increased the proliferative potential of SM MSCs through platelet-derived growth factors signaling activation [ 48 ]. The problem remains in the complexity of the signaling pathways involved in chondrogenesis stimulated by cell-to-cell contact [ 23 ].
The chemokine profile of healthy and arthritic SF could contribute to the recruitment of human mesenchymal progenitor from the subchondral bone [ 51 ]. The number of MSCs recruited by SF from rheumatoid arthritis patients is lower than from OA or normal donors, suggesting that the chemotactic factors contribute to the attraction of progenitors [ 50 ]. We have observed distinct morphological aspects of cells derived from SF of healthy persons and OA patients Figure 1. SF MSCs probably participate in homeostasis, remodeling, and tissue repair through the replacement of cells.
We can speculate that these cells are liable to re-establish the imbalance between OA catabolism and joint anabolism. Secreted mucous traps the pathogens in the body, preventing any further progression of microbes. Most mucous membranes contain stratified squamous or simple columnar epithelial tissue. The epithelial tissue sheet lies directly over the layer of loose connective tissue called lamina propria.
In some mucosa, the lamina propria rests on a deeper, third layer of smooth muscle. The submucosa is the tissue that connects the mucosa to the muscle outside the tube. Submucosal glands consist of exocrine glands that secrete mucus. The submucosal glands are a companion to unicellular goblet cells, which also produce mucus, and are found lining the same tubes. General organization of the gastrointestinial tract : Illustration of mucosa in relation to other lining components.
A synovial membrane is the soft tissue found between the articular capsule joint capsule and the joint cavity of synovial joints. Membranes are thin sheets of tissue found within the body which can line cover tissues or line cavities. Connective tissue membranes do not contain an epithelial cell layer and there are two forms found in the body; synovial and meninges membranes. The synovial membrane or synovium is the connective tissue which lines the inner surface of the capsule of a synovial joint and secretes synovial fluid which serves a lubricating function, allowing joint surfaces to smoothly move across each other.
The morphology of synovial membranes may vary, but it often consists of two layers. The outer layer, or subintima, is a thicker and fibrous protecting the single cell initma layer which is composed of synoviocytes. The intimal cells are termed synoviocytes and are of two types: fibroblastic type B and macrophagic type A. It is the lack of epithelial cells within the initma which defines the synovial membrane as connective rather than epithelial.
The type B synoviocytes manufacture a long-chain sugar polymer called hyaluronan, which makes the synovial fluid together with a molecule called lubricin, which lubricates the joint surfaces. The water component of synovial fluid is effectively trapped in the joint space by the hyaluronan, due to its large, highly negatively charged moeties.
The type A synoviocytes are responsible for the removal of undesirable substances from the synovial fluid. Synovial Membrane : A synovial joint showing the location of the synovial membrane.
The surface of synovium may be flat or may be covered with finger-like projections villi , to allow the soft tissue to change shape as the joint surfaces move on one another. Just beneath the intima, most synovium has a dense net of small blood vessels that provide nutrients, not only for synovium, but also for the avascular cartilage. The synovial fluid is the clear, viscid fluid that functions by lubricating the articulating joints, supplying nutrients and oxygen, and removing metabolic wastes.
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