The pathophysiology of Hypermobility Syndrome is not completely understood, but it appears to be related to a systemic collagen abnormality. This abnormality affects the structure and function of connective tissues throughout the body.
Understanding the Collagen Connection
The core problem in Hypermobility Syndrome seems to be a defect in collagen, the main structural protein in connective tissues. Connective tissues provide support and elasticity to joints, ligaments, tendons, skin, and blood vessels. The reference states that the ratio of collagen (type I, II and III) is decreased in the skin. This impacts the integrity of these tissues, leading to increased joint mobility and other related symptoms.
Collagen Types and Hypermobility
Collagen comes in several types, each with a specific role. While the exact types involved in Hypermobility Syndrome and their specific defects are still under investigation, research suggests that issues with collagen type I, III, and V are more common:
| Collagen Type | Role | Potential Impact in Hypermobility Syndrome |
|---|---|---|
| Type I | Most abundant, found in skin, bone, tendons | Reduced tensile strength, leading to joint instability, skin laxity, and increased risk of tendon and ligament injuries. |
| Type II | Predominantly in cartilage | Although decreased in skin, as per reference, role not well established. |
| Type III | Found in skin, blood vessels, and internal organs | Reduced support in vascular tissues, potentially contributing to easy bruising, and weakness in organ support structures. |
Consequences of Abnormal Collagen
The collagen abnormality contributes to:
- Joint Hypermobility: Increased range of motion due to weakened ligaments and joint capsules.
- Skin Laxity: Skin may be unusually stretchy or fragile.
- Tissue Fragility: Increased risk of bruising, scarring, and other tissue-related problems.
Further Research
Research is ongoing to identify the specific genes and molecular mechanisms that lead to these collagen abnormalities in Hypermobility Syndrome. Understanding these mechanisms could pave the way for more targeted therapies and better management strategies.
