Pathology Ch26 - Bones, Joints, and Soft Tissue Tumors - PARTIAL pp1194-1196
(Osteonecrosis/Osteomyelitis)
Osteonecrosis (Avascular Necrosis)
 Infarction of bone and marrow inside medullary cavity or medulla/cortex
 Vascular insufficiency due to injury to vessels, thromboembolism, pressure on vessels, or venous occlusion
 Conditions associated w/ osteonecrosis:
o Alcohol abuse
o Bisphosphate therapy (esp. jaw bone)
o CT disorders
o Corticosteroid administration***
o Chronic pancreatitis
o Dysbarism (the bends)
o Gaucher disease
o Infection
o Pregnancy
o Radiation therapy
o Sickle cell crisis
o Trauma***
o Tumors
 Morphology: involve trabecular bone and marrow (cortex usually has collateral blood flow)
 Clinical course: symptoms depend on location and extent of infarction
o Subchondral infarcts > pain (initially only w/ activity, progressing to constant)
 Often collapse > severe secondary osteoarthritis
o Medullary infarcts > small and clinically silent
Osteomyelitis
 Inflammation of bone and marrow, almost always secondary to infection
o Can be produced by viruses, parasites, fungi, and bacteria
 Pyogenic Osteomyelitis
o Always caused by bacterial infections (Staphylococcus aureus responsible for 80-90%)
o Organisms reach bone via (1) hematogenous spread, (2) extension from contiguous site, (3) direct implantation
o Location of infection depends on circulation
 Neonates = metaphyseal vessels > infection of metaphysis and/or epiphysis
 Children = localized to metaphysis
 Adults = metaphyseal vessels reunite w/ epiphyseal > infection of epiphyses and/or subcondral
o Morphology: depends on stage and location of infection
 Acute phase = neutrophillic inflammatory reaction > necrosis within first 48hrs
 Dead bone = "sequestrum"
 Chronic (after 1 week) = cytokines released > stimulate osteoclast bone resorption + fibrous deposition
 Newly deposited bone shell = "involucrum"
 Brodie abscess = small intraosseous abscess of cortex
 Sclerosing osteomyelitis of Garre = develops in jaw, associated w/ extensive new bone formation
o Clinical course:
 Hematogenous osteomyelitis > acute systemic illness (malaise, fever, leukocytosis, throbbing pain)
 Diagnosed: lytic focus of bone destruction surrounded by zone of sclerosis
 Treatment: antibiotics and surgical drainage
 Chronic infections may persist if not caught early, treatment not sufficient, or extensive necrosis develops
 Acute flare-ups (may occur after years of dormancy)
 May result in pathologic fracture, secondary amyloidosis, endocarditis, sepsis, carcinoma in
draining sinus tracts, sarcoma in infected bone
 Mycobacterial Osteomyelitis
o Organisms blood borne, originating from active visceral disease during its initial stages
o Bone infection may persist for years before being recognized
o Symptoms: localized pain, low-grade fever, weight loss
o Tend to be more destructive and resistant to control vs pyogenic osteomyelitis
o Tuberuclous spondylitis (Pott disease) especially destructive > involves spine in 40% of cases

Skeletal Syphilis
o Syphilis (Treponema pallidum) and yaws (Treponema pertenue) can involve bone
o Congenital syphilis = bone lesions develop ~5mo gestation > fully developed by birth
o Spirochetes localize in areas of active enchondral ossification (osteochondritis) and in periosteum (periostitis)
o Saber shin = massive reactive periosteal bone deposition on medial/anterior tibia
o Morphology: edemantous granulation tissue w/ numerous plasma cells and necrotic bone