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Osteomyelitis & Osteonecrosis

Name: Osteomyelitis & Osteonecrosis
Creator: Veli Bakalov, MD

Infected bone versus starved bone: routes, organisms, pathology and imaging clues

Musculoskeletal, Skin & Connective Tissue·Bone & Soft Tissue·6 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Hematogenous osteomyelitis seeds the metaphysis of long bones in children (slow looping capillaries) and the vertebral body and disc in adults (IV drug use, dialysis, endocarditis).
S. aureus is the most common cause overall; coagulase-negative staphylococci infect hardware, GBS and E. coli infect neonates, Kingella infects children under 4.
Salmonella in sickle cell disease, Pseudomonas after a nail through a sneaker or in IV drug users, Pasteurella after cat or dog bites, polymicrobial flora in diabetic foot ulcers.
Pott disease: tuberculosis of adjacent anterior thoracolumbar vertebrae with gibbus deformity and psoas cold abscess; caseating granulomas on biopsy.
Sequestrum is dead bone, involucrum is new periosteal bone around it, and a Brodie abscess is a walled-off subacute abscess; chronic sinus tracts can become squamous cell carcinoma (Marjolin ulcer).
MRI is the most sensitive imaging test for osteomyelitis and osteonecrosis; bone biopsy with culture is definitive; radiographs lag about 2 weeks; ESR and CRP track response.
Osteonecrosis causes: glucocorticoids (most common nontraumatic), alcohol, sickle cell disease, SLE, Gaucher disease, decompression sickness, radiation, and femoral neck, scaphoid and talar neck fractures.
Crescent sign = subchondral fracture that precedes femoral head collapse; histology shows empty osteocyte lacunae.
Legg-Calvé-Perthes is idiopathic femoral head osteonecrosis in boys aged 4–10; bisphosphonates and denosumab cause jaw osteonecrosis, especially high-dose IV therapy plus tooth extraction.

Routes and sites of osteomyelitis

Three routes. Bacteria reach bone by hematogenous seeding, by contiguous spread from adjacent soft tissue (diabetic foot ulcers, sacral pressure ulcers), or by direct inoculation (open fractures, surgery and hardware, bites and puncture wounds). Hematogenous infection is usually caused by a single organism, whereas contiguous and inoculation infections are often polymicrobial.

Children: the metaphysis. In growing long bones, metaphyseal capillaries loop back on themselves, blood flow slows and phagocytes are sparse, so circulating bacteria settle there; the distal femur and proximal tibia are favorite sites. The child has fever, point tenderness and a limp or refuses to bear weight. In infants under about 18 months, vessels still cross the physis, so infection can extend into the epiphysis and joint, producing concurrent septic arthritis.

Adults: the spine. Hematogenous osteomyelitis in adults favors the vertebral bodies and the adjacent disc (spondylodiscitis), lumbar more than thoracic. Classic hosts are people who inject drugs, patients on hemodialysis, and those with bacteremia from endocarditis or urinary tract infection. Back pain with fever and a raised ESR is the usual picture; an epidural abscess can compress the cord.

Contiguous and direct infection. Neuropathy and vascular disease let diabetic foot ulcers deepen until they reach bone, and pressure ulcers do the same over the sacrum; a sterile probe that touches bone through an ulcer strongly suggests osteomyelitis.

Organisms by host and exposure

Clinical clue → classic organism

Setting	Organism	Why or clue
Any age (default)	Staphylococcus aureus	Collagen-binding adhesins; biofilm on hardware
Prosthetic joint or hardware	Coagulase-negative staphylococci, S. aureus	Biofilm on foreign material
Neonate	Group B streptococcus, E. coli, S. aureus	Often multifocal; spreads into joints
Child under 4 years	Kingella kingae	Fastidious; easily missed on culture
Sickle cell disease	Salmonella (S. aureus also common)	Functional asplenia, gut microinfarcts, infarcted bone
Nail puncture through a sneaker	Pseudomonas aeruginosa	Grows in moist foam soles
Injection drug use	S. aureus, Pseudomonas, Candida	Vertebral involvement common
Cat or dog bite	Pasteurella multocida	Sharp cat teeth reach periosteum
Diabetic foot or pressure ulcer	Polymicrobial, including anaerobes	Contiguous spread
Spine, weight loss, endemic exposure	Mycobacterium tuberculosis	Pott disease

Sickle cell disease. Functional asplenia weakens clearance of bacteremia, bowel microinfarcts let enteric organisms such as Salmonella (a non–lactose-fermenting, H2S-producing gram-negative rod) into the blood, and infarcted bone gives them a foothold. Infection is often multifocal. Because vaso-occlusive bone infarction mimics osteomyelitis, persistent fever, rising inflammatory markers and a focal collection favor infection.

Pott disease. Hematogenous M. tuberculosis seeds the anterior vertebral bodies of the lower thoracic and upper lumbar spine and spreads beneath the anterior longitudinal ligament to adjacent levels. Collapse produces anterior wedging and a gibbus (angular kyphotic) deformity. A cold abscess may track along the psoas to present as a groin or thigh mass, and cord compression causes paraplegia. Biopsy shows caseating granulomas with acid-fast bacilli.

Pyogenic spondylodiscitis destroys the disc early; tuberculosis relatively spares it early while tunneling under the ligament to neighboring vertebrae.

Pathology and diagnosis

Bacteria settleMetaphyseal capillary loops or vertebral endplates
Pus under pressureNeutrophils raise intraosseous pressure and strip the periosteum
IschemiaCompressed vessels leave fragments of dead bone
SequestrumNecrotic bone that antibiotics cannot reach, a haven for bacteria
Involucrum and sinus tractThe lifted periosteum lays down a shell of new bone; pus drains to the skin

From bacteremia to chronic osteomyelitis

Brodie abscess. A walled-off subacute intraosseous abscess with a sclerotic rim, usually in a long-bone metaphysis (often the tibia) and caused by S. aureus.

Complications. Chronic draining sinuses can undergo malignant change to squamous cell carcinoma (Marjolin ulcer), presenting as a heaped-up, bleeding, nonhealing ulcer at the sinus opening. Others are pathologic fracture, growth disturbance when the physis is damaged, spread to the adjacent joint, and secondary (AA) amyloidosis from years of inflammation.

Diagnosis. Radiographs lag about 2 weeks behind infection before showing periosteal reaction and lytic foci. MRI is the most sensitive and specific imaging test, showing marrow edema within days. Bone biopsy with culture and histology is the definitive test and identifies the organism; blood cultures may do so in hematogenous cases. ESR and CRP are elevated and are followed to judge response. Treatment combines weeks of targeted antibiotics with surgical removal of dead bone.

Osteonecrosis (avascular necrosis)

Mechanism. When blood supply is interrupted, osteocytes and marrow die; histology shows trabeculae with empty lacunae. The dead trabeculae keep their shape at first, but as repair (creeping substitution) resorbs them, the subchondral bone weakens, fractures and collapses. The femoral head is most often affected because its supply, mainly the medial circumflex femoral artery, has little collateral flow; the humeral head, femoral condyles, talus, scaphoid and lunate are other sites.

Causes of osteonecrosis by mechanism

Mechanism	Examples
Vessel disruption	Displaced femoral neck fracture, scaphoid waist fracture, talar neck fracture, hip dislocation
Intravascular occlusion	Sickle cell disease, decompression sickness (nitrogen bubbles), fat emboli, thrombosis with antiphospholipid antibodies
Marrow expansion or infiltration	Glucocorticoids (most common nontraumatic cause) and alcohol (swollen marrow fat); Gaucher cells
Mixed or other	SLE (steroids, vasculitis, antiphospholipid antibodies), radiation, pancreatitis; idiopathic in Legg-Calvé-Perthes disease

Traumatic sites. Displaced femoral neck fractures tear the retinacular branches of the medial circumflex femoral artery. The scaphoid is supplied retrograde from distal branches of the radial artery, so a waist fracture starves the proximal pole. Talar neck fractures devascularize the talar body.

Anatomic snuffbox tenderness with a normal first radiograph is treated as a scaphoid fracture: thumb spica immobilization, then repeat imaging or MRI.

Imaging course. Early disease is invisible on radiographs; MRI is the most sensitive test and may show a double-line sign. Later films show sclerosis and cysts, then the crescent sign, a subchondral radiolucent line marking a subchondral fracture. Collapse of the articular surface and secondary osteoarthritis follow.

Legg-Calvé-Perthes disease and jaw osteonecrosis

Legg-Calvé-Perthes disease. Idiopathic osteonecrosis of the femoral head in children aged 4–10, boys about four times as often as girls, usually unilateral. The child has a painless or mildly painful limp, pain referred to the knee, and limited abduction and internal rotation. Radiographs show a small, dense, flattened epiphysis that fragments and then reossifies over years. Slipped capital femoral epiphysis, by contrast, affects obese adolescents, and transient synovitis resolves within days.

Medication-related osteonecrosis of the jaw. Exposed maxillofacial bone for more than 8 weeks in a patient taking bisphosphonates, denosumab or antiangiogenic drugs, with no history of jaw radiation (which would suggest osteoradionecrosis). Suppressed osteoclastic remodeling, reduced angiogenesis and oral bacteria prevent injured bone from repairing. Risk is highest with high-dose IV regimens for cancer, such as zoledronic acid, and after tooth extraction; the mandible is affected more often than the maxilla.

Complete invasive dental work before high-dose antiresorptive therapy begins; at osteoporosis doses the risk is very low.