Osteoarthritis¶
Chapter 383 | Harrison's 22e · Part 11 – Rheumatology & Immunology
Detailed clinical reference synthesised from Harrison's Principles of Internal Medicine, 22nd Edition
🔑 Key Clinical Points¶
- See source text for full details
📑 Table of Contents¶
📋 Figures in This Chapter¶
| # | Type | Description |
|---|---|---|
| 1 | 🖼 Figure | Risk factors for osteoarthritis (OA) either contribute to the the joint surface... |
| 2 | 🖼 Figure | X-ray and magnetic resonance imaging (MRI) of knee with medial joint space... |
| 3 | 🖼 Figure | Selected factors involved in the osteoarthritic process including damage-associated molecular pattern (DAMP)... |
| 4 | 🖼 Figure | X-ray and magnetic resonance imaging (MRI) of knee with medial joint space... |
| 5 | 🖼 Figure | are often affected |
| 6 | 🖼 Figure | are often affected |
| 7 | 🖼 Figure | are often affected |
RAW CONTENT¶
[PAGE 2949] Osteoarthritis 2949 CHAPTER 383 383 Osteoarthritis David T. Felson, Tuhina Neogi Osteoarthritis (OA) is the most common type of arthritis. Its high prevalence, especially in the elderly, and its negative impact on physi- cal function 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 OA is on the rise. OA affects certain joints yet spares others (Fig. 383-1). Commonly affected joints include the hip, knee, and first metatarsal phalangeal joint (MTP) and cervical and lumbosacral spine. 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 FIGURE 383-2 Severe osteoarthritis of the hands affecting the distal interphalangeal joints were designed, in an evolutionary sense, for brachiating apes, joints (Heberden’s nodes) and the proximal interphalangeal joints (Bouchard’s animals that still walked on four limbs. We thus develop OA in joints nodes). There is no clear bony enlargement of the other common site in the hands, that were ill designed for human tasks such as pincer grip (OA in the the thumb base. thumb base) and walking upright (OA in knees and hips). Some joints, like the ankles, may be spared because their articular cartilage may be persons, most affected persons have no pain. Even so, painful hand OA uniquely resistant to loading stresses. occurs in ~10% of elderly individuals and often produces measurable OA can be diagnosed based on structural abnormalities or on the limitation in function. symptoms these abnormalities evoke. According to cadaveric studies, The prevalence of OA rises strikingly with age, being uncommon by elderly years, structural changes of OA are nearly universal. These in adults aged 60. It is also a include cartilage loss (seen as joint space loss on x-rays) and osteophytes. disease that, at least in middle-aged and elderly persons, is much more Many persons with x-ray evidence of OA have no joint symptoms, and common in women than in men. although the prevalence of structural abnormalities is of interest in X-ray evidence of OA is common in the lower back and neck, but understanding disease pathogenesis, what matters more from a clinical back pain and neck pain have not been tied to findings of OA on x-ray. perspective is the prevalence of symptomatic OA. Symptoms, usually Thus, back pain and neck pain are treated separately (Chaps. 18 and 19). joint pain, determine disability, visits to clinicians, and disease costs. Symptomatic OA of the knee (pain on most days of a recent month ■ GLOBAL CONSIDERATIONS plus x-ray evidence of OA in that knee) occurs in ~12% of persons age With the aging of the populations, both the prevalence of OA and the ≥60 in the United States and 6% of all adults age ≥30. Symptomatic hip amount of disability worldwide related to OA have been increasing, OA is roughly one-third as common as disease in the knee. Although especially in developed countries where many are living into old age. radiographic hand OA and the appearance of bony enlargement in Hip OA is rare in China and in immigrants from China to the United States. affected hand joints (Fig. 383-2) are extremely common in older Anatomic differences between Chinese and white hips may account for much of the difference in hip OA prevalence, with white hips having a higher prevalence of anatomic predispositions to the development of Distal and proximal First OA. However, OA in the knees is at least as common, if not more so, in interphalangeal carpo- Chinese as in whites from the United States, and knee OA represents a metacarpal major cause of disability in China, especially in rural areas. Cervical DEFINITION vertebrae 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 Lower thickness and sclerosis of the subchondral bony plate, by outgrowth of lumbar osteophytes at the joint margin, by stretching of the articular capsule, vertebrae by variable degrees of synovitis, 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. Hip JOINT PROTECTIVE MECHANISMS AND THEIR FAILURE Joint protectors include joint capsule and ligaments, muscle, sensory Knee 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. First metatarso- phalangeal Synovial fluid reduces friction between articulating cartilage sur- faces, thereby serving as a protector against friction-induced cartilage wear. This lubrication function depends on hyaluronic acid and on lubricin, a mucinous glycoprotein secreted by synovial fibroblasts whose concentration diminishes after joint injury and in the face of synovial FIGURE 383-1 Joints commonly affected by osteoarthritis. inflammation.
[PAGE 2950] 2950 PART 11 Immune-Mediated, Inflammatory, and Rheumatologic Disorders The ligaments, along with overlying skin and tendons, contain increase production of inflammatory cytokines and matrix-degrading mechanoreceptor sensory nerves. These mechanoreceptors fire at enzymes. While chondrocytes synthesize numerous enzymes, matrix different frequencies throughout a joint’s range of motion, provid- metalloproteinases (MMPs; especially collagenases and ADAMTS-5) ing feedback by way of the spinal cord to muscles and tendons. As a are critical enzymes in the breakdown of cartilage matrix. consequence, these muscles and tendons assume the right tension at Local inflammation accelerates the development and progression of appropriate points in joint excursion to act as optimal joint protectors, osteoarthritis and increases the likelihood that an osteoarthritic joint anticipating joint loading. will be painful. Some of this inflammation may be induced by mechan- Muscles and tendons that bridge the joint are key joint protectors. ical stimuli, so called mechanoinflammation. The synovium, carti- Focal stress across the joint is minimized by muscle contraction that lage, and bone all influence disease development through cytokines, decelerates the joint before impact and assures that when joint impact chemokines, and even complement activation (Fig. 383-3). Matrix arrives, it is distributed broadly across the joint surface. fragments released from cartilage stimulate synovium, which releases Failure of these joint protectors increases the risk of joint injury and inflammatory cytokines, and they, in turn, induce chondrocytes to OA. For example, in animals, OA develops rapidly when a sensory nerve synthesize other proinflammatory molecules. Ultimately, the combina- to the joint is sectioned and joint injury induced. Similarly, in humans, tion of effects on chondrocytes triggers matrix degradation. Growth Charcot’s arthropathy, a severe and rapidly progressive OA, develops factors are also part of this complex network, with bone morphogenetic when minor joint injury occurs in the presence of posterior column protein 2 (BMP-2) and transforming growth factor β (TGF-β) playing peripheral neuropathy. Another example of joint protector failure is rup- prominent roles in stimulating the development of osteophytes. Trig- ture of ligaments, a well-known cause of the early development of OA. gered by local vascular endothelial growth factor (VEGF) synthesis, blood vessels invade cartilage and, with them, come nerves that may ■ CARTILAGE AND ITS ROLE IN JOINT FAILURE bring nociceptive innervation. A t
Figures & Illustrations¶
Reproduced from Harrison's 22nd Edition.
Figure 1¶
Caption: FIGURE 383-4 Risk factors for osteoarthritis (OA) either contribute to the the joint surface often causes OA in joints in which the disease is oth- susceptibility of the joint (systemic factors or factors in the local joint environment) erwise rare such as the ankle and the wrist. Avascular necrosis can lead or increase risk by the load they put on the joint. Usually, a combination of loading to collapse of dead bone at the articular surface, producing anatomic and susceptibility factors is required to cause disease or its progression. irregularities and subsequent OA. Tears of ligamentous and fibrocartilaginous structures that protect the joints, such as the anterior cruciate ligament or meniscus in the major acute injury or long-term overloading is necessary to precipitate knee and the labrum in the hip, can lead to premature OA. Meniscal disease (Fig. 383-4). tears increase with age and, when chronic, are often asymptomatic but lead to adjacent cartilage damage and accelerated OA. Even recalled
Figure 2¶
Caption: FIGURE 383-6 X-ray and magnetic resonance imaging (MRI) of knee with medial joint space narrowing of the medial tibiofemoral joint. Coronal intermediate-weighted medial tibiofemoral joint space narrowing. There is diffuse denuded area with no a severe medial meniscus extrusion (arrowhead). Bone marrow lesions, which provide tibial region. Cartilage focal defects are also seen at the lateral weight-bearing femur
Figure 3¶
Caption: FIGURE 383-3 Selected factors involved in the osteoarthritic process including damage-associated molecular pattern (DAMP) molecules, and complement, which molecules (collagen type 2, aggrecan) and the enzymes responsible for the invasion occurs through the calcified cartilage, triggered by vascular endothelial De Roover A et al: Fundamentals of osteoarthritis: Inflammatory mediators in
Figure 4¶
Caption: FIGURE 383-6 X-ray and magnetic resonance imaging (MRI) of knee with medial joint space narrowing of the medial tibiofemoral joint. Coronal intermediate-weighted medial tibiofemoral joint space narrowing. There is diffuse denuded area with no a severe medial meniscus extrusion (arrowhead). Bone marrow lesions, which provide tibial region. Cartilage focal defects are also seen at the lateral weight-bearing femur
Figure 5¶
Caption: are often affected. Usually spared are the wrist, elbow, and ankle. Our FIGURE 383-2 Severe osteoarthritis of the hands affecting the distal interphalangeal joints were designed, in an evolutionary sense, for brachiating apes, joints (Heberden’s nodes) and the proximal interphalangeal joints (Bouchard’s animals that still walked on four limbs. We thus develop OA in joints nodes). There is no clear bony enlargement of the other common site in the hands, that were ill designed for human tasks such as pincer grip (OA in the the thumb base. thumb base) and walking upright (OA in knees and hips). Some joints, like the ankles, may be spared because their articular cartilage may be persons, most affected persons have no pain. Even so, painful hand OA uniquely resistant to loading stresses. occurs in ~10% of elderly individuals and often produces measurable OA can be diagnosed based on structural abnormalities or on the limitation in function. symptoms these abnormalities evoke. According to cadaveric studies,
Figure 6¶
Caption: are often affected. Usually spared are the wrist, elbow, and ankle. Our FIGURE 383-2 Severe osteoarthritis of the hands affecting the distal interphalangeal joints were designed, in an evolutionary sense, for brachiating apes, joints (Heberden’s nodes) and the proximal interphalangeal joints (Bouchard’s animals that still walked on four limbs. We thus develop OA in joints nodes). There is no clear bony enlargement of the other common site in the hands, that were ill designed for human tasks such as pincer grip (OA in the the thumb base. thumb base) and walking upright (OA in knees and hips). Some joints, like the ankles, may be spared because their articular cartilage may be persons, most affected persons have no pain. Even so, painful hand OA uniquely resistant to loading stresses. occurs in ~10% of elderly individuals and often produces measurable OA can be diagnosed based on structural abnormalities or on the limitation in function. symptoms these abnormalities evoke. According to cadaveric studies,
Figure 7¶
Caption: are often affected. Usually spared are the wrist, elbow, and ankle. Our FIGURE 383-2 Severe osteoarthritis of the hands affecting the distal interphalangeal joints were designed, in an evolutionary sense, for brachiating apes, joints (Heberden’s nodes) and the proximal interphalangeal joints (Bouchard’s animals that still walked on four limbs. We thus develop OA in joints nodes). There is no clear bony enlargement of the other common site in the hands, that were ill designed for human tasks such as pincer grip (OA in the the thumb base. thumb base) and walking upright (OA in knees and hips). Some joints, like the ankles, may be spared because their articular cartilage may be persons, most affected persons have no pain. Even so, painful hand OA uniquely resistant to loading stresses. occurs in ~10% of elderly individuals and often produces measurable OA can be diagnosed based on structural abnormalities or on the limitation in function. symptoms these abnormalities evoke. According to cadaveric studies,
Generated from Harrison's Principles of Internal Medicine, 22nd Edition.