Structure and Function of Cartilage
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi in Articular Cartilage, 2017
Type II collagen is the predominant collagen type (∼90%) in articular cartilage, comprising more than half the dry weight of the tissue (Deshmukh and Nimni 1973) and complexes with type IX and XI collagens. Type II collagen forms an extracellular framework to resist both imparted tensile forces from articulation and the swelling pressures due to proteoglycans. This collagen serves as a marker for articular cartilage differentiation because it is only localized to the hyaline and fibrous cartilages and the vitreous humor of the eye. The presence of type I collagen with type II helps to distinguish between hyaline and fibrocartilages. Except for small amounts of collagen type I in its superficial zone, collagen type I is not found in hyaline articular cartilage. Since the expression of type I collagen increases with monolayer culture-induced dedifferentiation of chondrocytes, the ratio of type I to type II cartilage is further used to track chondrocyte differentiation.
Molecular Structure and Functions of Collagen
Marcel E. Nimni in Collagen, 1988
The collagen in cartilage, as discussed earlier, consists almost entirely of type II collagen, a collagen with unique characteristics. X-ray diffraction studies of collagen from human intervertebral discs revealed differences in the intermolecular spacing of the collagen molecules within the fibers. Whereas the molecules in type I collagen are laterally separated by a distance of 14 Å, collagen type II molecules are separated by a distance of 16 to 17 Å. No differences were noted after the specimens were dried.342 The intermolecular volume of fully hydrated collaged fibrils from a number of mineralized and nonmineralized tissues of adult rats has been determined by an exclusion technique and by monitoring specific X-ray diffraction parameters.343 Measurements made on a wet rat tail tendon show that 55% of the volume of a fibril is occupied by collagen molecules and 45% by water.344
Autologous Stem Cell Transplantation in Relapsing Polychondritis
Richard K. Burt, Alberto M. Marmont in Stem Cell Therapy for Autoimmune Disease, 2019
Although the etiology and pathogenesis of relapsing polychondritis are still unknown, several findings suggest that both humoral and cell-mediated immune responses are involved. Cartilage contains large quantities of type II collagen. Serum autoantibodies to native collagen II as well as to collagen IX and XI were found during acute attacks.2-5 Granular deposits of immunoglobulins and complement were detected at the chondrofibrous junction of affected cartilage by immunofluorescence.6,7 A predominance of HLA-DR positive cells and significant quantities of CD4+ T lymphocytes in cellular infiltrates were found by immunohistology. Susceptibility to relapsing polychondritis is significantly associated with HLA-DR4, and the extent of organ involvement is negatively associated with HLA-DR6.8,9 Experimental immunization of rats with type II collagen can induce auricular chondritis and arthritis. As in humans, the murine lesions were characterized by severe chondritis, positive immunofluorescence reactions to IgG and C3, and circulating IgG that reacted with native type II collagen.10,11
Severe osteoporosis in a premenopausal woman
Published in Scandinavian Journal of Rheumatology, 2019
Type II collagen provides strength to the structure and integrity of connective tissues such as muscles, joints, and skin. Collagen type II mutations are expressed in clinical syndromes called collagenopathies, which include achondrogenesis, spondyloepiphyseal dysplasia, Kniest dysplasia, and Stickler’s syndrome. Apart from severe osteoporosis and vertebral fractures, our patient did not express other characteristics of the above syndromes, such as facial deformities, short stature, deformed arms and legs, barrel-shaped chest, or hearing or visual losses. Given that the patient’s father had a history of severe osteoporosis and spontaneous fractures without an identifiable underlying cause, it is suspected that the patient’s pathology may be due to a genetic collagen defect transmitted from her father with an autosomal dominant trait. This phenotype of the collagen II mutation has not been previously correlated with only severe osteoporosis or osteogenesis imperfecta. We present this case to alert the medical community to the association of a collagen II mutation with severe osteoporosis in a young woman, without underlying causes such as alcoholism, heavy smoking, or endocrine, metabolic, or malabsorption disorders. The patient was placed on bisphosphonates (alendronate 35 mg/week), along with calcium and cholecalciferol supplementation to treat the severe osteoporosis.
Coll2-1 and Coll2-1NO2 as exemplars of collagen extracellular matrix turnover – biomarkers to facilitate the treatment of osteoarthritis?
Published in Expert Review of Molecular Diagnostics, 2019
Ali Mobasheri, Cecile Lambert, Yves Henrotin
Type II collagen is the major structural protein in cartilage. It makes up approximately 50% of the ECM [19]. This is one of the most obvious reasons why many biomarker researchers and biomarker development companies have focused their efforts on type II collagen breakdown products as biomarkers [20] for cartilage degradation in degenerative diseases such as OA [21] and RA [22]. Type II collagen breakdown products are also biomarkers of intervertebral disk degeneration [23]. Interestingly, some of the collagen breakdown products also possess inflammatory and immunomodulatory properties that are poorly understood and understudied. Furthermore, there is evidence that portions of some collagen molecules also possess anti-angiogenic properties when released from the parent protein by degradative extracellular enzymes. For example, the NH2-propeptide of type IIB collagen possesses anti-angiogenic and anti-tumor properties.
Reconstructive rhinoplasty using cadaver cartilage in relapsing polychondritis
Published in Baylor University Medical Center Proceedings, 2023
Rishabh Shah, Eugene L. Alford
Accumulating data strongly suggest that both humoral and cell-mediated immunity play a role in the pathogenesis of relapsing polychondritis. Antibodies to type II collagen, matrilin-1, and immune complexes are detected in the serum of patients. The possibility that an immune response to type II collagen may be important in the pathogenesis has been supported in animal studies. Humoral responses to type IX and type XI collagen, matrilin-1 (noncollagenous protein present in the extracellular matrix in cartilage), and cartilage oligomeric matrix protein have been demonstrated in some patients. One study showed that rats immunized with matrilin-1 were found to develop severe inspiratory stridor and swelling of the nasal septum. The rats had severe inflammation with erosions of the involved cartilage, which was characterized by increased numbers of CD4+ and CD8+ T cells in the lesions. All had IgG antibodies to matrilin-1. A subsequent study demonstrated serum anti-matrillin-1 antibodies in ∼13% of patients with relapsing polychondritis. Cell-mediated immunity may also be operative in causing tissue injury, since lymphocyte transformation can be demonstrated when lymphocytes of patients are exposed to cartilage extracts. T cells specific for type II collagen have been found in some patients, and CD4+ T cells have been observed at sites of cartilage inflammation.2
Related Knowledge Centers
- Cartilage
- Collagen
- Homotrimer
- Hyaline Cartilage
- Proteoglycan
- Type I Collagen
- Collagen, Type Iii, Alpha 1