Some 28 types of collagen types have been identified. They differ by how the molecules are assembled, the cell components that are added and where the collagen is used in your body. All collagen fibrils have at least one triple helix structure.
This type makes up 90% of your body’s collagen. Type I is densely packed and used to provide structure to your skin, bones, tendons, and ligaments.
This type is found in elastic cartilage, which provides joint support.
This type is found in muscles, arteries, and organs.
This type is found in the layers of your skin.
This type is found in the cornea of your eyes, some layers of skin, hair, and tissue of the placenta.
Tendon cells are sparsely distributed in a field of aligned collagen fibers in healthy tendon. Tendon cells produce pro-collagen which is formed into triple helix tropocollagen.
During initial tendon formation procollagen synthesis makes up 60% of the total cellular protein production. Tropocollagen is organized into fibrils and fibrils into fibers.
Tendons grow in utero using a growth plate - a region of high density tendon cells with cell density markers triggering cell division and procollagen production (>60% of the cells protein output is procollagen).
As collagen fibers are laid down, cells become more and more disparate (separated by the well organized collagen fibers) and the cell density marker concentration decreases leading to first a loss of cell division and then ultimately the cessation of procollagen production.
During weight-bearing exercise muscles contract and shorten, applying tension to the tendon. The tension applied to the tendon is thought to result in a squeezing of the tendon fibers resulting in a brief extrusion of water from the tendon fibers. Brief removal of water results in a transient spike in cell density marker concentrations, triggering production of more procollagen, resulting in stabilization and growth of the tendon to compensate for the increased muscle strength.
Tendon damage can range from micro-tears in the collagen fibers (strains/sprains) to partial or full width tears. The challenge for healing relates to the natural mechanism of tendon cell growth control:
Non-invasive treatments of tendon damage (rest, physical therapy, massage) typically result in a slow recovery but low re-injury rates.
However, natural tendon healing occurs through immune cell infiltration and collagen re-building by broad-spectrum immune cells rather than tendon cells. The resulting collagen fibers are "tangled" and disorganized. Resulting in a strong "fibro-vascular scar" rather than new tendon. The disorganized collagen scar is brittle and prone to breaking under the stress of normal activities.
A wide range of therapeutic options have been developed including:
None of these interventions have proved effective in shortening recovery time, restoring full function, and preventing/limiting re-tearing of the tendon.
The crucial element lacking in all current therapies is the trigger for coordinated collagen production and alignment.
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