Cartilage is a highly specialized connective tissue that plays a mechanical role in the body, primarily by covering the ends of bones within a joint. Hyaline cartilage, or articular cartilage, is a smooth, slick material that provides an exceptionally low-friction surface for bones to glide over one another. Fibrocartilage is stiffer and acts as a tough shock absorber in areas like the knee menisci and spinal discs. Damage to either form of cartilage disrupts the joint’s ability to absorb shock and move freely, leading to pain and restricted motion.
Acute Traumatic Injuries
Cartilage damage can occur instantly from a single, high-energy impact that overwhelms the tissue’s structural integrity. This acute traumatic injury is common in sports or falls, where a sudden force is applied directly to the joint. The mechanism involves immediate mechanical failure, resulting in specific tears or fractures of the tissue.
A forceful twist or impact can cause a chondral fracture, where a piece of the articular cartilage breaks off the bone surface. Meniscal tears, affecting the fibrocartilage shock absorbers in the knee, are another common example of acute failure due to sudden, high-magnitude loading. This damage involves a focal, immediate disruption of the tissue’s structure.
The sudden compression or shear force can lead to the death of chondrocytes, the cells that maintain the cartilage matrix. Since cartilage lacks a direct blood supply, its capacity for self-repair is extremely limited following mechanical destruction. The resulting defect often fails to heal with the original, resilient tissue, leaving the joint vulnerable to further breakdown.
Chronic Degenerative Conditions
The most frequent cause of cartilage deterioration is the slow, progressive breakdown associated with Osteoarthritis (OA). This condition involves cumulative micro-trauma and biological changes that occur over decades, representing a structural failure of the joint’s components. The initial stage often involves the gradual loss of proteoglycans, particularly aggrecan, from the cartilage matrix.
Proteoglycans are large molecules that give cartilage its ability to resist compressive forces. Their depletion leads to a decrease in the tissue’s stiffness and an increase in its water content, causing the cartilage to soften and swell. This softening, called chondromalacia, makes the tissue less able to withstand normal mechanical stress.
As the process continues, the collagen fiber network, primarily Type II collagen, begins to fray and fragment. This network provides the tissue’s tensile strength. This leads to surface irregularities, pitting, and eventual thinning of the cartilage layer. The structural breakdown progresses until the cartilage is completely worn away, exposing the underlying, pain-sensitive bone.
Autoimmune and Inflammatory Disease Mechanisms
Cartilage can be damaged by processes driven by the body’s own immune system or chronic inflammation, rather than purely mechanical stress. Rheumatoid Arthritis (RA) is a prime example, where the immune system mistakenly attacks the synovium, the joint lining. The inflamed synovium then thickens and forms an invasive tissue called pannus.
This hyperactive tissue releases high concentrations of destructive inflammatory signaling molecules, known as cytokines, such as Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-1 (IL-1). These cytokines trigger the production of matrix metalloproteases (MMPs), which are enzymes that directly erode the cartilage matrix. The resulting damage is chemical and biological, causing widespread destruction across the joint surface.
Other inflammatory conditions can lead to cartilage loss through similar enzyme-mediated mechanisms. Gout, characterized by the deposition of urate crystals in the joint, causes intense inflammation that releases tissue-degrading enzymes. Septic arthritis, a bacterial infection within the joint, results in a severe inflammatory response that rapidly destroys cartilage tissue if not quickly treated.
Contributing Biomechanical and Lifestyle Factors
External conditions and pre-existing joint issues can accelerate the rate at which cartilage damage occurs, particularly in chronic degenerative processes. Increased body weight, or obesity, is a major factor because it dramatically increases the load transmitted across weight-bearing joints like the knees and hips. This excessive pressure leads to accelerated wear and tear of the cartilage.
Beyond mechanical load, adipose tissue secretes pro-inflammatory hormones called adipokines, which contribute to low-grade systemic inflammation. This biological factor can interfere with the cartilage’s ability to maintain its matrix, creating a combined mechanical and biochemical burden.
Joint instability or misalignment, often resulting from a previous ligament injury or congenital abnormality, contributes to damage by causing uneven stress distribution. When a joint is unstable or positioned incorrectly, the force is concentrated on smaller, non-ideal areas of the cartilage surface. This focused, repetitive overloading can quickly initiate the degenerative process, accelerating the progression toward cartilage failure.