Hip pain can be caused by many different factors including labral tears, osteoarthritis, and avascular necrosis.
Labral Tear
The hip joint is a ball and socket joint that contains a fibrocartilaginous structure that outlines the socket, called the acetabular labrum. The labrums main function is to act as a shock absorber, pressure distributor, and provide lubrication for the joint. Tears in the labrum can be caused by trauma, dysplasia, and degeneration. Most tears occur in the anterior portion of the labrum due to a low vascular supply compared to the posterior region. This makes the anterior portion more susceptible to wear and tear without the ability for repair.
Osteoarthritis
Joint inflammation due to joint trauma, mechanical overload, and overuse results in the remodeling of the subchondral bone, upregulation of matrix-degrading enzymes and chondrocyte phenotypic changes which lead to the development and progression of osteoarthritis. The joint injury can cause changes in the periarticular tissues which destabilizes the joint thus causing mechanical stress to the cartilage tissue. These periarticular tissues include subchondral bone, ligaments, tendons, menisci, and synovial membranes. Other factors that influence the disease process are those that can cause joint inflammation or mechanical overload such as aging, genetic predisposition, abnormal biomechanics, obesity, and comorbidities such as cardiovascular disease, metabolic syndrome, and diabetes.
Cartilage Matrix Micro-Cracks and Joint Pain
The earliest change in the development of osteoarthritis is the loss of negatively charged polysaccharide molecules in the cartilage which results in increased water content and swelling of the cartilage matrix. The swelling of the cartilage matrix causes micro-cracks in the superficial zone. As the disease progresses, exfoliation of fragments of cartilage and deep fissures extending into the deeper cartilage layers leads to exposure of the underlying zones of calcified cartilage and subchondral bone. Further mechanical stress and exacerbation of naturally occurring pores in the subchondral bone can also produce micro-cracks that provide conduits for vascular invasion into the calcified zone and enable diffusion of small inflammatory molecules including cytokines and chemokines into the calcified zone.
In addition to cartilage damage, the subchondral bone undergoes remodeling with the additional growth of blood vessels (red) which also contains osteoblasts, osteoclasts, and sensory nerves (green) as well as the diffusion of small inflammatory molecules. Such remodeling induces hypertrophic-like changes in chondrocytes and causes the expansion of the calcified zone. The expansion of the calcified zone leads to loss or thinning of the superficial zones. These hypertrophic-like chondrocytes also produce proangiogenic factors, including VEGF, that promotes further vascular penetration to the calcified zone at the sites of micro-cracks and fissures, accompanied by sensory and sympathetic nerves resulting in joint pain and progressive loss or thinning of the superficial zones.
Cytokine and Enzyme-Mediated Cartilage Destruction
The development of osteoarthritis is highly dependent upon the upregulation of specific matrix-degrading enzymes. The major protagonists of cartilage degradation are the metal-dependent matrix metalloproteinase (MMP), disintegrin, and metalloproteinase with thrombospondin motifs (ADAMTS) families. Damaged cartilage tissue, inflamed synovium, and other injured joint tissues release cytokines, chemokines, alarmins, DAMPs, adipokines, and other mediators into the synovial fluid. These mediators increase chondrocyte production of matrix metalloproteinases (MMPs) which breaks down the cartilage collagen network and weakens the biomechanical function of the articular cartilage. The synovium is also a source of degradative enzymes, including MMPs and aggrecanases that can directly degrade the cartilage matrix causing the degradation of the collagenous and proteoglycan networks. The products of cartilage matrix breakdown along with damage-associated molecular patterns (DAMPs) secreted by chondrocytes also act on the adjacent synovial tissue to induce inflammation and the release of pro-inflammatory products, including cytokines and reactive oxygen species that feedback on the chondrocytes to enhance the catabolic state amplifying a vicious cycle of cartilage break down.
Chondrocyte Hypertrophy and the Bone-on-Bone Condition
Although chondrocytes rarely divide in the healthy tissue and appear relatively ‘quiescent’, they are extremely mechanosensitive. Excessive mechanical loading on the chondrocytes activate the cell-surface mechanosensors and induces hypertrophic-like phenotypic changes in chondrocytes. Hypertrophic chondrocytes trigger extracellular matrix mineralization, blood vessel invasion, and the recruitment of chondroclasts/osteoclasts in the articular cartilage. Chondroclasts/osteoclasts gradually degrade the cartilage matrix, and osteoblasts replace the cartilage scaffold by bone. Eventually, the osteoarthritic joint assumes a bone-on-bone condition. Hypertrophic chondrocytes synthesized uncarboxylated Matrix Gla Proteins which loses the ability to bind calcium and are unable to prevent unwanted calcification leading to the development of bone spur formation, a common complication of late-stage osteoarthritis.
Avascular Necrosis
Avascular necrosis (AVN), otherwise known as osteonecrosis, is the death of bone tissue due to a lack of blood supply. Because bone is living tissue that requires a blood supply, tiny breaks in the bone can occur in the affected area and the bone can eventually collapse. The most common area where AVN occurs is in the hips causing pain on the groin, thigh, or buttock. However, AVN can occur in the shoulders, knees, hands, and feet as well.
The cause of AVN can vary from a dislocation or a fracture, chronic use of corticosteroids, a common anti-inflammatory drug for pain management, excessive alcohol use, damage to the surrounding arteries, or other health conditions such as piriformis syndrome. A dislocation or fracture that leads to AVN is known as trauma-related AVN. This type of injury can affect the blood supply to the bone. All other causes of AVN are known as non-traumatic AVN. Chronic corticosteroid use can interfere with the body’s ability to break down fatty substrates. When these substrates collect in the blood vessels it can make them narrower and therefore reduce the amount of blood supply to that area. Similar to anti-inflammatory drugs or pain killers, excessive alcohol use may also cause fatty substrates to build up in the blood vessels and lead to a reduced blood supply. Blood clots, damage to the arteries and local inflammation can also block blood flow to the bones. The cause of AVN may also lead to the development of hip osteoarthritis. Bone on bone hip osteoarthritis can further aggravate the pain in the hip area making the symptoms of AVN worse.
If osteonecrosis has caused extensive damage to the femur and the bone has begun to collapse causing significant pain in the hip or knee, a total joint replacement may be recommended.
Piriformis syndrome is a condition when the Piriformis muscle contracts and spasms compressing and irritating the sciatic nerve. This causes sciatic pain along the path of the sciatic nerve descending down the lower thigh and into the leg. Piriformis muscle spasms also compress the superior and inferior gluteal nerve and arteries beneath the muscle causing contractions of other muscles in the buttocks and cause symptoms of hip muscle pain, coldness, tightness, tingling, and numbness in the buttocks. Hip muscle contraction and tightening further compress the femoral artery and its branch, the profunnda femoris, the main artery supplying blood to the hip joint capsule and the femur neck, resulting in restricted blood supply and causing hip joint cartilage degeneration, hip osteoarthritis, and femur neck bone death leading to AVN.
The cause of Piriformis syndrome is due to prolonged stress. Our body's fight-or-flight response to a stressor such as a perceived harmful event, attack, or threat to survival involves tightening of the Piriformis muscle which is the most important muscle in the lower body involved in balance, posture and movement. Its contraction moves the body in different directions. Under a prolonged stress condition, the piriformis muscle continually contracts which can eventually lead to Piriformis syndrome. Besides for the Piriformis muscle, the shoulder muscle and the smooth muscle of the stomach also contract in the fight-or-flight response to stress causing reduced blood flow to these areas. It is common for AVN patients to also have shoulder problems and stomach conditions including acid reflux, GERD, poor digestion, or stomach ulcers due to poor blood supply.
