Osteoarthritis (osteoarthritis) and back pain

Osteoarthritis (syn: degenerative joint disease, osteoarthrosis, hypertrophic osteoarthritis, osteoarthritis) is closely related to neck and back pain. Osteoarthritis is a chronic joint pathology characterized by the destruction and potential loss of articular cartilage in accordance with other joint changes, including bone hypertrophy (osteophyte formation). Symptoms include gradual development of pain that increases or is triggered by activity, stiffness that improves in less than 30 minutes after the start of activity, and rarely, joint swelling. Diagnosis is confirmed by radiography. Treatment includes physical measures (including rehabilitation), medications, and surgery.

Osteoarthritis is the most common joint disease, the symptoms of which appear in the 4th - 5th decade of life and are almost global at the age of 180. Only half of those who have osteoarthritis show symptoms of the disease. Up to 40 years of age, osteoarthritis occurs in men due to injury. Women predominate between the ages of 40 and 70, after which the ratio of men and women equalizes.

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Pathophysiology of osteoarthritis

Normal joints have little friction during movement and do not wear out with normal use, overuse, or injury. Hyaline cartilage has no blood vessels, nerves, or lymphatics. It is 95% water and extracellular matrix and only 5% chondrocytes. Chondrocytes have the longest cell cycle (similar to CNS cells and muscle cells). Cartilage health and function depend on alternating pressure and release during weight bearing and use (pressure forces water out of the cartilage into the joint cavity and into the capillaries and venules, while release allows the cartilage to straighten, take in water, and absorb essential nutrients).

Osteoarthritis begins with tissue damage due to mechanical trauma (eg, meniscus tear), leakage of inflammatory mediators from the synovial fluid into the cartilage, or disruption of cartilage metabolism. Tissue damage stimulates the chondrosteum to repair itself, which increases the synthesis of proteoglycans and collagen. However, the production of enzymes that cause cartilage damage, such as inflammatory cytokines, which are normally present in small amounts, also increases. Inflammatory mediators initiate an inflammatory cycle that further stimulates chondrocytes and lining cells, ultimately leading to cartilage breakdown. Chondrocytes undergo apoptosis. As cartilage is destroyed, the exposed bone becomes hardened and sclerotic.

Osteoarthritis involves all the tissues of the joint. The subchondral bone becomes denser, infarcted, osteoporotic, and subchondral cysts develop. The tendency for bone to regenerate causes subchondral sclerosis and the development of osteophytes along the joint margin. The synovium becomes inflamed, thickened, and produces synovial fluid of lower viscosity and greater volume. Periarticular tendons and ligaments become tense, and tendinitis and contractures develop. As the joint becomes hypomobile, the surrounding muscles weaken and perform a less effective stabilizing function. The menisci crack and may fragment.

Osteoarthritis of the spine may cause marked thickening and proliferation of the posterior longitudinal ligament at the disc level, leading to ventral cord compression; hypertrophy and hyperplasia of the ligamentum flavum often cause posterior cord compression. In contrast, the anterior and posterior spinal root ganglia and the common spinal nerve are relatively well protected in the intervertebral foramen, where they occupy only 25% of the free and well-protected space.

Symptoms of Osteoarthritis

Osteoarthritis begins gradually in one or more joints. Pain is an early symptom, sometimes described as a deep ache. The pain is usually aggravated by body weight (upright position) and relieved by rest, but eventually becomes constant. Stiffness is felt on awakening or after rest, but lasts less than 30 minutes and relieved by movement. As osteoarthritis progresses, joint movement is limited and pain and crepitus or creaking in the joint occur. Proliferation of cartilage, bone, ligaments, tendons, capsule, synovium, combined with varying degrees of joint effusion, eventually lead to the joint enlargement characteristic of osteoarthritis. Flexion contracture may eventually develop. Rarely, acute severe synovitis may develop.

The most commonly affected joints in generalized osteoarthritis are the distal interphalangeal joints, the proximal interphalangeal joints (Heberden's and Bouchard's nodes develop), the first carpometacarpal joint, the intervertebral discs and zygoapophyseal joints of the cervical and lumbar vertebrae, the first metacarpophalangeal joint, the hip and the knee.

Osteoarthritis of the cervical and lumbar spine may result in myelopathy or radiculopathy. The clinical symptoms of myelopathy are usually mild. Radiculopathy may be clinically evident but is uncommon because the nerve roots and ganglia are well protected. Vertebral artery insufficiency, spinal cord infarction, and esophageal compression by osteophytes may occur but are uncommon. Symptoms of osteoarthritis may also originate from the subchondral bone, ligamentous structures, synovium, periarticular bursae, capsules, muscles, tendons, discs, and periosteum, as they all have nociceptors. Increased venous pressure beneath the subchondral bone in the bone marrow may cause pain (sometimes called "bone angina").

Osteoarthritis of the hip causes a gradual decrease in range of motion.

The pain can be felt in the groin area, in the area of the greater trochanter and reflected in the knee. When the cartilage of the knee joint is lost (medial cartilage is lost in 70% of cases), the ligaments become weak and the joint loses stability, local pain arises from the ligaments and tendons.

Tenderness on palpation and pain on passive movements are relatively late symptoms. Muscle spasm and contractures maintain pain. Mechanical blockade due to the presence of loose bodies in the joint cavity or an abnormally located meniscus can lead to blockade (locking) of the joint or its instability. Subluxation and deformations can also develop.

Erosive osteoarthritis of the hand can cause synovitis and cyst formation.

It primarily affects the distal and proximal interphalangeal joints. The first carpopetacarpal joint is involved in 20% of cases of hand osteoarthritis, but the metacarpophalangeal joints and wrist are usually spared.

How is osteoarthritis classified?

Osteoarthritis is classified as primary (idiopathic) or secondary to known causes. Primary osteoarthritis may be localized to a specific joint (e.g., chondromalacia patellae is a mild form of osteoarthritis that occurs in young adults). If primary osteoarthritis involves multiple joints, it is classified as primary generalized osteoarthritis. Primary osteoarthritis is usually subdivided based on the location of the lesion (e.g., hand, foot, knee, hip). Secondary osteoarthritis results from conditions that alter the cartilage microenvironment. These include significant trauma, congenital cartilage abnormalities, metabolic defects (eg, hemochromatosis, Wilson's disease), post-infectious arthritis, endocrinopathies, neuropathic changes, diseases that damage the normal structure and function of hyaline cartilage (eg, rheumatoid arthritis, gout, chondrocalcinosis).

Diagnosis of osteoarthritis

Osteoarthritis should be suspected in patients with gradual onset of symptoms and signs, particularly in adults. When osteoarthritis is suspected, radiographs of the most symptomatic joints should be taken. Radiographs typically show marginal osteophytes, joint space narrowing, increased subchondral bone density, subchondral cysts, bone remodeling, and increased joint fluid. Standing knee radiographs are most sensitive for joint space narrowing.

Laboratory studies are normal in osteoarthritis but may be needed to exclude other disorders (eg, rheumatoid arthritis) or to diagnose disorders that cause secondary osteoarthritis. If synovial fluid is increased in osteoarthritis, its examination may help differentiate osteoarthritis from inflammatory arthritis; in osteoarthritis, synovial fluid is clear, viscous, and contains no more than 2,000 leukocytes per 1 μl. Osteoarthritis that affects joints in unusual locations should raise suspicion of its secondary nature; studies in this situation should be aimed at identifying the primary disorder (eg, endocrine, metabolic, neoplastic, biomechanical).

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Treatment of osteoarthritis

Osteoarthritis usually progresses periodically but occasionally stops or regresses without apparent cause. The goals of treatment are to reduce pain, maintain joint range of motion, and optimize joint and overall function. Primary treatment for osteoarthritis includes physical therapy (facilitation), support devices, strength training, flexibility, and endurance; and modification of daily activity. Adjuvant treatment for osteoarthritis includes NSAIDs (eg, diclofenac, lornoxicam), tizanidine, and surgery.

Rehabilitation treatment of osteoarthritis should be started before signs of disability appear. Exercises (various movements, isometric, isotonic, isokinetic, postural, strength) maintain cartilage health and increase the resistance of tendons and muscles to motor loads. Exercises can sometimes stop or even promote the reverse development of osteoarthritis of the hip and knee. Stretching exercises should be performed daily. Immobilization for a more or less long period of time can contribute to contractures and aggravation of the clinical course. However, some rest (4-6 hours per day) can be useful for maintaining a balance of activity and rest.

Modification of daily activities may be helpful. For example, a patient with osteoarthritis of the lumbar spine, hip, or knee should avoid deep soft chairs and positions associated with postural overload and difficulty in standing. Regular use of a knee pillow promotes the development of contractures and should be avoided. The patient should sit with a straight back without sliding in the chair, sleep on a hard bed and use devices for comfortable adjustment of the driver's seat with a forward tilt, do postural gymnastics, wear comfortable shoes with good foot support or athletic shoes, continue work and physical activity.

Pharmacotherapy is an adjunct to the physical program. Acetaminophen in doses greater than 1 g per day may reduce pain and be safe. However, more powerful analgesic treatment may be required.

NSAIDs may be considered if the patient has refractory pain or signs of inflammation (flushing, local hyperthermia). NSAIDs may be used concomitantly with other analgesics (eg, tizanidine, tramadol, opioids) to achieve better pain and symptom control.

Muscle relaxants (usually in low doses) are rarely helpful in reducing pain from the spasmodic muscles that support the osteoarthritic joint. In older people, however, they may tend to cause more side effects than benefits.

Oral corticosteroids do not play a role. However, intra-articular depot corticosteroids help reduce pain and increase joint range of motion when synovial effusion or inflammation is present. These drugs should not be used more than 4 times a year in any one affected joint.

Synthetic hyaluronidase (an analog of hyaluronic acid, a normal component of the joint) can be injected into the knee joint to reduce pain over a long period of time (over a year). Treatment of osteoarthritis is carried out with a series of 3 to 5 weekly injections.

In osteoarthritis of the spine, knee, or first carpometacarpal joint, various options for pain relief and restoration of function may be used, but maintaining mobility should include specific exercise programs. In erosive osteoarthritis, range-of-motion exercises can be performed in warm water to help avoid contractures. Other pain relief options include acupuncture, transcutaneous electrical nerve stimulation, and local capsaicin therapy. Laminectomy, osteotomy, and total joint replacement should be considered only when nonsurgical treatments fail.

Glucosamine sulfate 1500 mg per day probably reduces pain and joint wear, chondroitin sulfate 1200 mg per day may also reduce pain. Their effectiveness has yet to be proven. Experimental studies are evaluating the possibility of chondrocyte transplantation.