C h a p t e r 4 3
Disorders of the Skeletal System: Trauma, Infections, Neoplasms, and Childhood Disorders
1093
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.
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.
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)
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.)
