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Wednesday, November 11, 2020 | History

2 edition of Neurogenic modulation of articular cartilage degeneration. found in the catalog.

Neurogenic modulation of articular cartilage degeneration.

Alex Dart Ming Chan

Neurogenic modulation of articular cartilage degeneration.

  • 216 Want to read
  • 17 Currently reading

Published .
Written in English


The Physical Object
Pagination207 leaves.
Number of Pages207
ID Numbers
Open LibraryOL20655132M
ISBN 100612411230

The fact that joint diseases affect the soft tissues primarily (above all the synovial lining, articular cartilage, and tendons) and the bones secondarily is common to all joint disorders. Anatomy of the Synovial Joints. A synovial joint consists of (Fig. ): epiphysis (articular end of the bone), articular cartilage, joint capsule, joint fluid. Degenerative changes in the glenoid process and extensive degenerative and/or genuine cyst formation. a, b Already tangential (a, arrow) and axial (b, arrow) radiographic views of the glenoid process show multiple cysts in the glenoid process and subchondral sclerosis and articular irregularities of the glenoid fossa.


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Neurogenic modulation of articular cartilage degeneration. by Alex Dart Ming Chan Download PDF EPUB FB2

However, it was not elucidated if the degenerative consequences on cartilage were triggered by an inflammatory event or if they were also directly mediated by neurogenic processes.

In a previous work, we developed an experimental approach to study early effects on distant articular cartilage of a nonsystemic local inflammatory event Cited by: 7.

This study was designed to investigate the pathways involved in neurogenic-mediated articular cartilage damage triggered by a nonsystemic distant subcutaneous or intra-articular Cited by: 7.

Abstract. The glassy translucent material found at the ends of bones, within synovial joints, is termed articular cartilage. While healthy, it provides a low-friction bearing surface, preventing bone-to-bone contact, and to an extent, absorb shock during vigorous by: 1.

BibTeX @MISC{Modulation_acquisitionsand, author = {Neurogenic Modulation and Of Articular and Cartilage Degeneration and Alex Dart and Ming Chan and On Ottawaon and Ka On and Alex Dart and Ming Chan}, title = {Acquisitions and Acquisitions et Bibliographie Services services.

Poole et al. 4 have suggested that an imbalance between degeneration and repair might help to explain, in part, the differences among joints in susceptibility to OA. There have been almost no studies that have compared the cartilages from different adult human joints in an attempt to identify features within joints that might either retard or stimulate cartilage by: Key words: Knee, Ankle, Cartilage, Degeneration, Repair.

Introduction Osteoarthritis (OA) is a degenerative joint disease that involves not only articular cartilage but also synovium, joint capsule and bone.

OA is a common joint disease of the elderly; however, it does not affect all joints equally1,2, even in those individuals with generalized OA.

Aging is a major risk factor of osteoarthritis, which is characterized by the degeneration of articular cartilage. Neurogenic modulation of articular cartilage degeneration.

book CCN3, a member of the CCN family, is expressed in cartilage and has various physiological functions during chondrocyte development, differentiation, and regeneration.

Here, we examine the role of CCN3 in cartilage maintenance. During aging, the expression of Ccn3 mRNA in mouse. Schematic representation of the contribution of mast cells and microglia to degenerative joint diseases and neuroinflammation.

At the articular level, mast cells are located mainly in the synovial. Damaged cartilage rarely heals spontaneously, and its subsequent degeneration in association with degeneration of other articular tissues may lead to knee osteoarthritis, which is both a cartilaginous and a whole-organ disease.

In recent decades, magnetic resonance (MR) imaging has become the most important modality for assessment of. Articular cartilage degeneration is considered as the primary pathological change at the tissue level related to OA symptoms and disability. In healthy joints, collagen and proteoglycan are two major matrix components of articular cartilage, which function to cushion and distribute mechanical load uniformly to the whole joint (Sophia Fox et al.

Osteoarthritis (OA) is a major cause of disability and socioeconomic loss worldwide. However, the current pharmacological approaches used to treat OA.

Osteoarthritis is a degenerative disease affecting the TMJ. It is the most common TMJ disorder and shows a higher prevalence in women and older people. TMJ osteoarthritis (TMJ-OA) is characterized by variable degrees of inflammation, destruction of the articular cartilage, and sub-chondral bone resorption.

In this context, diverse pro-inflammatory cytokines, chemokines, enzymes, and bone. John T. Cavanaugh MEd, PT/ATC, Nicholas A. Sgaglione MD, in Postsurgical Orthopedic Sports Rehabilitation, ASSESSMENT. Diagnosis of articular cartilage pathology can now be more precise through the use of noninvasive cartilage-specific MRI.

Potter and co-workers 19 have shown a significant degree of accuracy using high-resolution modified echo time fast spin sequence techniques. x Osteoarthritis (OA) is a degenerative joint disease inducing the degradation of the articular cartilage. Syndecan-4 (Sdc4) is a heparan sulfate proteoglycan, expressed under inflammatory conditions and by chondrocytes during OA.

Little is known about Sdc4 shedding and its regulation in OA. Therefore, we investigated the regulation of Sdc4. In articular cartilage, primary cilia are required for chondrocyte mechanotransduction and the development of healthy tissue.

Loss of primary cilia in Col2aCre;ift88 fl/fl transgenic mice results in up-regulation of osteoarthritic (OA) markers and development of OA like cartilage with greater thickness and reduced mechanical stiffness.

Hypertrophy of articular cartilage, chondrocyte cloning, fibrillation, and changes in tangential zone chondrocytes were less prominent in the OA knee when electrocautery and irrigation were used. The in vitro and in vivo evidence is reviewed concerning the potential of the modulation of PRP on normal articular cartilage and OA progression.

PRP modulates the repair and regeneration of damaged articular cartilage in the joints and delays the degeneration of cartilage by stimulation of mesenchymal stem cell migration, proliferation, and.

Background Full-thickness defects of articular cartilage in the knee have a poor capacity for repair. They may progress to osteoarthritis and require total knee replacement. We performed autologous. Arthritis pain affects millions of people worldwide yet we still have only a limited understanding of what makes our joints ache.

This review examines the sensory innervation of diarthroidal joints and discusses the neurophysiological processes that lead to the generation of painful sensation.

During inflammation, joint nerves become sensitized to mechanical stimuli through the. Structurally, as early as 1 day after MIA injection, alterations to the surrounding synovium and articular cartilage have been described (Bove et al., ; Guzman et al., ; Orita et al., ).

Chondrocytes are shrunken with fragmented nuclei, and some areas of chondrocyte degeneration are present 1 to 3 days post-injection. Summary. The remarkable ability of articular cartilage to provide a low-friction gliding surface and to simultaneously distribute loads across synovial joints makes possible the rapid, smooth, painless movements necessary for participation in sports.

Unfortunately, with increasing age, the prevalence of articular cartilage degenerative changes increases and for many individuals these changes. OA, a common degenerative disease in the hip joint, is characterized by cartilage degeneration, chondrocyte hyper-plasia, subchondral sclerosis, inflammation and osteophyte formation (14).

Among these effects, the primary feature of OA is articular cartilage degradation. In normal cartilage, the chondrocyte is embedded in ECM, of which. Inflammation of the synovial membrane may arise secondary to degenerative processes in articular cartilage (AC), or may be a primary occurrence in OA pathogenesis.

However, synovial inflammation plays a key role in the pathogenesis and disease progression of OA through the production of pro-inflammatory mediators, and is associated with. The results of the current study are the first to demonstrate that articular cartilage degeneration occurring after DMM surgery correlates with increased in mTOR expression, and consequently local intra-articular injection of rapamycin reduced mTOR expression, which delayed articular cartilage.

IL-1β has been reported to reduce collagen type 2 expression and GAG content of human nasal and articular chondrocytes cultured on a type 1 collagen scaffold, 98 and both IL-1β and TNF-α have been shown to impact the integration of engineered cartilage with native tissue.

99 Additionally, these pro-inflammatory cytokines have been shown to. Abstract. Osteoarthritis (OA) is a disease characterized by a degeneration of articular cartilage.

Although the etiology of OA is not yet known and is likely multifactorial, this disease process involves a disturbance in the normal balance of degradation and repair in articular cartilage (1).The breakdown of the cartilage matrix leads to the development of fibrillation, fissures, the.

of cartilage could be one of the chief reasons for this tis-sue’s degeneration [10, 14, 15, 25]. Autoradiographic and tracer studies in animals have indicated that while imma-ture articular cartilage can be nourished via both synovial and subchondral routes, articular cartilage in mature ani.

Articular Cartilage Degeneration by Inhibition of Tgf-β1 Signaling in a Mouse Model of Osteoarthritis The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Chen, Rebecca Y.

Attenuation of the Progression of Articular. Introduction. Progressive degeneration of articular cartilage is typical in osteoarthritis (OA) (1, 2).At the early stage of the disease cartilage macromolecules are affected, the amount of proteoglycans (PG) decreases, water content of the cartilage increases and collagen fibril network is disrupted (1, 2).Also the mechanical properties of cartilage are compromised.

INCREASED ARTICULAR CARTILAGE THICKNESS IN ACROMEGALY. One of the major problems in osteoarthritis care today is traditional medicine’s inability to promote effective cartilage regeneration in the presence of adult chondromalacia (cartilage degeneration).

Yet such regeneration is consistently present in acromegalics. Acromegaly is a condition whereby the pituitary gland secretes too much. Articular cartilage (AC) covers the diarthrodial joints and is responsible for the mechanical distribution of loads across the joints. The majority of its structure and function is controlled by chondrocytes that regulate Extracellular Matrix (ECM) turnover and maintain tissue homeostasis.

Imbalance in their function leads to degenerative diseases like Osteoarthritis (OA). Introduction. Osteoarthritis (OA), the most common form of arthritis in middle aged and older individuals, is characterized by the progressive degeneration of articular cartilage, joint space narrowing, subchondral bone sclerosis, and the formation of bony outgrowths at the joint margins.1 During the development of OA, the articular chondrocytes undergo distinct phenotypic changes, including.

Osteoarthritis is a degenerative joint disease which primarily affects the articular cartilage and subchondral bones. Since there is an underlying localized inflammatory component in the pathogenesis of osteoarthritis, compounds like tocotrienol with anti-inflammatory properties may be able to retard its progression.

This study aimed to determine the effects of oral tocotrienol supplementation. Intra-articular NGF injection. Rats were given a single 50 µL intra-articular injection into their left knees of NGF in sterile % normal saline, pHor saline control.

Initial dose–response studies in normal rats used 10 µg, 1 µg or ng of NGF. Additionally, the mechanically demanding environment in which articular cartilage exists may cause degeneration of repair tissue that is mechanically inferior to healthy native cartilage [8,9].

Articular cartilage tissue. Articular cartilage was obtained under the ethics committee approval held by the Sheffield Musculoskeletal Biobank (STH, SMB).All patients provided written, informed consent before participation.

Cartilage blocks were taken from waste tissue within each anatomic compartment of the knee (medial and lateral tibio-femoral and patello-femoral compartments) during. Also, at the junction of the articular hyaline cartilage and adjacent subchondral bone, there is evidence of vascular invasion and advancement in the zone of calcified cartilage in the region of the so‐called tidemark that further contributes to a decrease in articular cartilage thickness (Lane et al., ; Burr and Schaffler, ).

Articular cartilage degeneration was classified into four grades. Result Articular cartilage degeneration grade of each section was as follows: patella: 9 knees in grade 0, knees in grade 1, knee in grade 2, 89 knees in grade 3, average grade was (r ), patella.

Osteoarthritic joints are characterized by degradation of the articular cartilage, which provides the cushioning between bones, and by bony protrusions called osteophytes, which interfere with. Articular cartilage has limited potential for repair due to a lack of vascularity and limited cellularity.

6,7 As a consequence, cartilage injuries can result in chronic disability, 6,7 the development of osteoarthritis with significant physical limitations and decreased quality of life. A novel cartilage degeneration algorithm can predict the progression of osteoarthritis in individual patients, according to new research.

The new algorithm could greatly facilitate clinical. A comparative study of articular cartilage thickness in the stifle of animal species used in human pre-clinical studies compared to articular cartilage thickness in the human knee.

Vet Comp Orthop TraumaCrossref, Medline, Google Scholar;   The disc collagen demonstrates evidence of proteolytic collagenase action, which accumulates and eventually contributes to the weakening mechanical properties of the disc. 9, 57, 63 It is significant that the triple helix structure of disc collagen is more denatured and damaged than that of the collagen in articular cartilage, which may.