Structure and Function of Cartilage
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi in Articular Cartilage, 2017
Fibrocartilage differs from hyaline cartilage by the presence of type I collagen and, to a lesser degree, type II collagen. The GAG content of fibrocartilage is often much lower than that of hyaline cartilage. Chondrocytes in fibrocartilage (fibrochondrocytes) are interspersed among the connective tissue bundles; it is these bundles that help to absorb mechanical loads. Within the body, fibrocartilage is found in the pubic symphysis, the annulus fibrosus of the intervertebral disc, the menisci of the knee (Makris et al. 2011), and the temporomandibular joint disc (Detamore and Athanasiou 2003). Fibrocartilage commonly lacks a perichondrium covering, a feature it shares with hyaline articular cartilage. Fibrocartilage can also form as a repair tissue of damaged articular cartilage (described in more detail in Section 3.2.1), although it lacks adequate biomechanical properties to function as a long-term articular cartilage replacement.
The Anatomy of Joints Related to Function
Verna Wright, Eric L. Radin in Mechanics of Human Joints, 2020
In places, some collagen fibers may be replaced by cartilage or fibrocartilage. This indicates that the stresses acting on the ligament are not merely longitudinal tension but also compression across the fibers, often in association with sliding movements. Ligaments may react in a similar way to tendons, which develop a sesamoid cartilage or bone where they bear upon a bony protuberance. The cartilage, a tissue well able to resist compression, protects the collagen fibers of the tendon from abrasion and provides a low-friction bearing surface. The spring ligament (plantar calcaneonavicular ligament) is almost entirely replaced by fibrocartilage to support the head of the talus, which transmits a significant proportion of body weight directly onto its upper surface. A similar zone of cartilage is also seen on the anterior surface of the transverse ligament of the atlas, where it articulates with the dens of the axis.
Bone Injury, Healing and Grafting
Manoj Ramachandran, Tom Nunn in Basic Orthopaedic Sciences, 2018
The degree of interfragmentary strain appears to govern the cellular response and therefore the type of tissue that forms between the fracture fragments. Each of these tissues is able to tolerate a different amount of strain: Granulation tissue: up to 100%.Fibrous connective tissue: up to 17%.Fibrocartilage: 2–10%.Lamellar bone: 2%.
Time-dependently Appeared Microenvironmental Changes and Mechanism after Cartilage or Joint Damage and the Influences on Cartilage Regeneration
Published in Organogenesis, 2021
Danyang Yue, Lin Du, Bingbing Zhang, Huan Wu, Qiong Yang, Min Wang, Jun Pan
The biocomposite formed by articular cartilage, calcified cartilage (their combination is cartilage) and subchondral bone is called osteochondral unit,1 in which cartilage damage can be caused by several conditions including accidents such as a tear to the anterior cruciate ligament, injury, slow degeneration over time (aging), excessive activity (overuse), excessive weight (obesity), poor alignment of joint, necrosis, and other diseases of osteoarthritis (OA) and rheumatoid arthritis etc. Cartilage has a minimal ability to repair itself in terms of structure, function, and strength for its avascular nature and poor capability for adult chondrocytes to secret extracellular matrix. To be worse, the appeared mesenchymal stromal cells (MSCs) show a changed phenotype, which is susceptible to hypertrophy, matrix metalloproteinase-13 (MMP-13) release and osteogenesis.2 Generally, cartilage damage is healed by fibrocartilage different from normal cartilage, which is difficult to integrate with surrounding tissues, and ultimately degenerated and disintegrated over time. Cartilage damage usually leads to serious medical consequences, in which constant and severe pain, inflammation, and some degree of disability are typical.
Negative effect of zoledronic acid on tendon-to-bone healing
Published in Acta Orthopaedica, 2018
Geir Aasmund Hjorthaug, Endre Søreide, Lars Nordsletten, Jan Erik Madsen, Finn P Reinholt, Sanyalak Niratisairak, Sigbjørn Dimmen
Tendons and ligaments attach to bone through a transitional fibrocartilage tissue, the enthesis. This transitional tissue is complex in composition and organization and is not regenerated during healing of injuries or surgical repair. Tendon and ligament injuries often require surgical repair or reconstruction to regain function, and a favorable outcome depends on solid tendon-to-bone healing (Harryman et al. 1991, Gulotta and Rodeo 2007, Ekdahl et al. 2008). The osteointegration of the graft is the weak link in early tendon-to-bone tunnel healing. In a randomized controlled trial, transient decrease in local bone mineral density (BMD) was observed in the knee region of patients undergoing anterior cruciate ligament (ACL) reconstruction (Lui et al. 2012). Bone loss has also been observed in experimental tendon–bone repair studies and is probably due to increased ostoclastic activity (Galatz et al. 2005, Rodeo et al. 2007). Furthermore, a negative correlation between local bone loss and strength of the tendon–bone interface has been reported (Silva et al. 2002). Bone surfaces with high osteoclastic activity and peri-tunnel bone loss may therefore become a less suitable scaffold for healing of the tendon graft. Thus, prevention of early bone loss could enhance tendon-to-bone healing and improve clinical outcomes.
Recent advances in kartogenin for cartilage regeneration
Published in Journal of Drug Targeting, 2019
Gaorui Cai, Wei Liu, Yong He, Jianghong Huang, Li Duan, Jianyi Xiong, Lijun Liu, Daping Wang
Tendon-bone junction (TBJ) features a characteristic structure composed of a tendon, fibrocartilage zone and bone [17]. Among these parts, fibrocartilage zone is most important as it absorbs shock, reduces stress concentration on the tendon, and protects the tendon from rupture [18]. When damaged, the fibrocartilage of TBJ can hardly recover through self-healing or surgery procedure [19,20]. KGN may possibly enable self-healing of TBJ. Zhang et al. investigated the effects of KGN on rabbit bone marrow stromal cells and patellar tendon stem cells in vitro [18] and observed that after 2 weeks, KGN significantly promoted the growth of both cell types and up-regulated the chondrogenesis genes, including aggrecan, COLII and SOX-9, in a concentration-dependent manner Zhang et al. also created a TBJ injury model of Achilles tendon in rats and injected KGN into the wounded sites at preset intervals. Mature and complete cartilage-like tissue was observed in the experimental group (KGN injection group) after 15 days. By contrast, the results of the control group (saline injection group) were remarkably unsatisfactory. These findings illustrate that KGN plays a critical role in tendon-bone healing.
Related Knowledge Centers
- Cartilage
- Pubic Symphysis
- Symphysis
- Type I Collagen
- Type II Collagen
- Chondrocyte
- Intervertebral Disc
- Extracellular Matrix
- Type II Collagen
- Glenoid Labrum
- Acetabular Labrum