Osteoarthritis (OA) is the most common type of arthritis. Its high prevalence, especially in the elderly, and the high rate of disability related to disease make it a leading cause of disability in the elderly. Because of the aging of Western populations and because obesity, a major risk factor, is increasing in prevalence, the occurrence of osteoarthritis is on the rise. In the United States, osteoarthritis prevalence will increase by 66–100% by 2020.
OA affects certain joints, yet spares others (Fig. 332-1). Commonly affected joints include the cervical and lumbosacral spine, hip, knee, and first metatarsal phalangeal joint (MTP). In the hands, the distal and proximal interphalangeal joints and the base of the thumb are often affected. Usually spared are the wrist, elbow, and ankle. Our joints were designed, in an evolutionary sense, for brachiating apes, animals that still walked on four limbs. We thus develop OA in joints that were ill designed for human tasks such as pincer grip (OA in the thumb base) and walking upright (OA in knees and hips) Some joints, like the ankles, may be spared because their articular cartilage may be uniquely resistant to loading stresses.
Joints affected by osteoarthritis.
OA can be diagnosed based on structural abnormalities or on the symptoms these abnormalities evoke. According to cadaveric studies, by elderly years, structural changes of OA are nearly universal. These include cartilage loss (seen as joint space loss on x-rays) and osteophytes. Many persons with x-ray evidence of OA have no joint symptoms and, while the prevalence of structural abnormalities is of interest in understanding disease pathogenesis, what matters more from a clinical perspective is the prevalence of symptomatic OA. Symptoms, usually joint pain, determine disability, visits to clinicians, and disease costs.
Symptomatic OA of the knee (pain on most days of a recent month in a knee plus x-ray evidence of OA in that knee) occurs in ∼12% of persons age ⩾60 in the United States and 6% of all adults age ⩾30. Symptomatic hip OA is roughly one-third as common as disease in the knee. While radiographically evident hand OA and the appearance of bony enlargement in affected hand joints (Fig. 332-2) are extremely common in older persons, most cases are often not symptomatic. Even so, symptomatic hand OA occurs in ∼10% of elderly individuals and often produces measurable limitation in function.
Severe osteoarthritis of the hands affecting the distal interphalangeal joints (Heberden's nodes) and the proximal interphalangeal joints (Bouchard's nodes). There is no clear bony enlargement of the other common site in the hands, the thumb base.
The prevalence of OA rises strikingly with age. Regardless of how it is defined, OA is uncommon in adults under age 40 and highly prevalent in those over age 60. It is also a disease that, at least in middle-aged and elderly persons, is much more common in women than in men, and sex differences in prevalence increase with age.
X-ray evidence of OA is common in the lower back and neck, but back pain and neck pain have not been tied to findings of OA on x-ray. Thus, back pain and neck pain are treated separately (Chap. 15).
OA is joint failure, a disease in which all structures of the joint have undergone pathologic change, often in concert. The pathologic sine qua non of disease is hyaline articular cartilage loss, present in a focal and, initially, nonuniform manner. This is accompanied by increasing thickness and sclerosis of the subchondral bony plate, by outgrowth of osteophytes at the joint margin, by stretching of the articular capsule, by mild synovitis in many affected joints, and by weakness of muscles bridging the joint. In knees, meniscal degeneration is part of the disease. There are numerous pathways that lead to joint failure, but the initial step is often joint injury in the setting of a failure of protective mechanisms.
Joint protectors include: joint capsule and ligaments, muscle, sensory afferents, and underlying bone. Joint capsule and ligaments serve as joint protectors by providing a limit to excursion, thereby fixing the range of joint motion.
Synovial fluid reduces friction between articulating cartilage surfaces, thereby serving as a major protector against friction-induced cartilage wear. This lubrication function depends on the molecule lubricin, a mucinous glycoprotein secreted by synovial fibroblasts whose concentration diminishes after joint injury and in the face of synovial inflammation.
The ligaments, along with overlying skin and tendons, contain mechanoreceptor sensory afferent nerves. These mechanoreceptors fire at different frequencies throughout a joint's range of motion, providing feedback by way of the spinal cord to muscles and tendons. As a consequence, these muscles and tendons can assume the right tension at appropriate points in joint excursion to act as optimal joint protectors, anticipating joint loading.
Muscles and tendons that bridge the joint are key joint protectors. Their contractions at the appropriate time in joint movement provide the appropriate power and acceleration for the limb to accomplish its tasks. Focal stress across the joint is minimized by muscle contraction that decelerates the joint before impact and assures that when joint impact arrives, it is distributed broadly across the joint surface.
Failure of these joint protectors increases the risk of joint injury and OA. For example, in animals, OA develops rapidly when a sensory nerve to the joint is sectioned and joint injury induced. Similarly, in humans, Charcot arthropathy, a severe and rapidly progressive OA, develops when minor joint injury occurs in the presence of posterior column peripheral neuropathy. Another example of joint protector failure is rupture of ligaments, a well-known cause of ...