Porth's Essentials of Pathophysiology, 4e

Disorders of the Skeletal System: Trauma, Infections, Neoplasms, and Childhood Disorders 1093

C h a p t e r 4 3

Local symptoms include pain, immobility, and mus- cle atrophy; joint swelling, mild fever, and leukocytosis also may occur. The most feared complication of spi- nal tuberculosis is neurologic compromise due to spi- nal deformity and epidural abscess formation. Because there are no specific radiographic findings in tubercular osteomyelitis, the diagnosis is usually made by tissue biopsy or culture findings. In spinal tuberculosis, a com- puted tomography (CT)-guided biopsy is often used. The mainstay of treatment for tubercular osteomyelitis remains the appropriate three- or four-drug antimicro- bial therapy based on current guidelines. 35 Conservative treatment is usually as effective as surgery, especially for earlier and milder cases. Osteonecrosis Osteonecrosis, also known as avascular necrosis, is an aseptic destruction of a segment of bone that is due to an interruption in blood flow rather than an infec- tion. 18,19,36,37 It is relatively common and can occur in the medullary cavity of the metaphysis and the subchon- dral region of the epiphysis, especially in the hips, knees, shoulders, and ankles. Destruction of bone frequently is severe enough to require joint replacement surgery. Bone has a rich blood supply that varies from site to site. The flow in the medullary portion of bone originates in nutrient vessels from an interconnecting plexus that supplies the marrow, trabecular bone, and endosteal half of the cortex. The outer cortex receives its blood supply from periosteal, muscular, metaphyseal, and epiphyseal vessels that surround the bone. Some bony sites, such as the head of the femur, have only limited collateral cir- culation so that interruption of the flow, such as with a hip fracture, can cause necrosis and irreversible damage to a substantial portion of medullary and cortical bone. Although bone necrosis results from ischemia, the mechanismsproducing the ischemiaarevariedand include mechanical interruption such as occurs with a fracture; thrombosis and embolism (e.g., sickle cell disease, nitro- gen bubbles caused by inadequate decompression during deep sea diving); vessel injury (e.g., vasculitis, radiation therapy); and increased intraosseous pressure with vas- cular compression. Chart 43-1 lists some of the causes of osteonecrosis. Other than vessel injury and obstruction, the most common known cause is prior corticosteroid therapy. 38,39 Despite numerous studies, the mechanism of steroid-induced osteonecrosis remains unclear. The con- dition may develop after the administration of very high, short-term doses; during long-term treatment; or even from intra-articular injection. Although the risk increases with the dose and duration of treatment, it is difficult to predict who will be affected. Of recent concern is the development of osteonecrosis of the jaw with long-term use of bisphosphonates, drugs that are widely used for the treatment of postmenopausal osteoporosis, Paget disease of the bone, and cancer-related conditions. 40 The pathogenesis of bisphosphonate-associated osteonecro- sis of the jaw remains largely unknown. The complica- tion has mainly been reported in patients receiving the drugs intravenously for treatment of malignancies.

CHART 43-1  Causes of Osteonecrosis

Mechanical disruption of blood vessels Fractures Legg-Calvé-Perthes disease Blount disease Thrombosis and embolism Sickle cell disease Nitrogen bubbles in decompression sickness Vessel injury Vasculitis Connective tissue disease Systemic lupus erythematosus Rheumatoid arthritis Radiation therapy Gaucher disease Corticosteroid therapy Biphosphonate therapy (jaw osteonecrosis)

The pathologic features of bone necrosis are the same, regardless of cause. The site of the lesion is related to the vessels involved. There is necrosis of cancellous bone and marrow. The cortex usually is not involved because of collateral blood flow. In persons with sub- chondral infarcts (i.e., ischemia below the cartilage), a triangular or wedge-shaped segment of tissue that has the subchondral bone plate as its base and the center of the epiphysis as its apex undergoes necrosis (Fig. 43-9). In cases where medullary infarcts occur in fatty marrow, death of bone results in the release of calcium and necro- sis of fat cells results in the release of free fatty acids.

FIGURE 43-9. Osteonecrosis of the head of the femur. A coronal section shows a circumscribed area of subchondral infarction with partial detachment of the overlying articular cartilage and subarticular bone. (From Garcia RA, Klein MJ, Schiller AL. Bones and joints. In: Rubin R, Strayer DS, eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine. 6th ed. Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams &Wilkins; 2012:1217.)