Pathology Key Points:

Bone:
Type of connective tissue.
Type 1 collagen
Normally undergoes mineralization
Unmineralized bone osteoid
Biochemically inorganic calcium
- organic bone cells, protein
Osteoprogenitor cells osteoblasts- mineralization
Osteoprogenitor cells- ostecytes- nutrition
Monocyte- macrophage system- osteoclasts- remodelling
Woven bone- immature, irregular collagen
Lamellar bone- mature, regular collagen
Bone diseases:
I .Congenital Diseases :
Osteogenesis Imperfecta ("brittle bone disease)
Achrondroplasia (cause of dwarfism )
Osteopetrosis (literally "stone bone")
II. Inflammation Infections
III. Tumours
IV. Metabolic / Degenerative diseases
Osteomyelitis:
Designates inflammation of the bone and marrow cavity
Always implies infection
Although any microorganism can cause osteomyelitis, the most common etiologic agents are
pyogenic bacteria and Mycobacterium tuberculosis.
Types : Acute ;
Chronic Non-specific,
Specific e.g. Tuberculosis
Pyogenic Osteomyelitis:
Caused by pyogenic bacteria
Routes of spread
organism may reach the bone by
Hematogenous spread septic focus, trivial infection
Extension from a contiguous site gangrene foot, tooth to mandible
Direct implantation surgery, fractures
Aetiology of pyogenic osteomyelitis:
1 Bacteria : Staphylococci most common (80 90%)
E.coli, Klebseilla,psuedomonas
Mixed bacterial infection
H. influenza and group B streptococci
Salmonella
 2. Virus Cox sackei-B, CMV ,
3. Fungus Actinomycosis , Nocardia etc,
4. Parasites
Predisposing factors of pyogenic osteomyelitis:
Predisposing factors
1.Trauma fall , accidents , fractures ,
2. Pre existing infection boil, abscess,tonsil
3. Bacteremia, septicemia .
4. Decreased immunity AIDS / Others
5. Surgery of bones and joints ,compound #
6. Age of the patient
Pyogenic osteomyelitis:
Location of lesion:
Neonates metaphysis
Children metaphysis
Adults epiphysis and subchondral region
In chronic pyogenic osteomyelitis:
Chronic lesion
New bone formation
(Involucrum)
Chronic inflammatory cells
Fibrosis
Course of pyogenic osteomyelitis:
Entrapped bone undergoes early necrosis; the dead bone in infected sites is called a sequestrum
subperiosteal abscesses
draining sinus, cloaca
Reactive woven or lamellar bone can be deposited; when it forms a shell of living tissue around
a segment of devitalized bone it is called an involucrum
Morphologic variants of osteomyelitis:
Brodie abscess
- subacute pyogenic osteomyelitis
- small, solitary, intraosseous abscess localized to the metaphysis
Sclerosing osteomyelitis of Garre
Extensive new bone formation
Typically develops in jaw
Clinical features of pyogenic osteomyelitis:
Acute systemic illness with malaise, fever, leukocytosis, and throbbing pain over the affected
region.
Lab investigations leukocytosis, raised ESR, raised C- reactive protein
Radiologic findings: a destructive lytic focus surrounded by a sclerotic rim
biopsy and bone cultures are usually required to identify the pathogen
Complications with pyogenic osteomyelitis:
1. Pathologic fracture,
 2 Secondary amyloidosis,
3. Endocarditis,
4. Septicemia, suppurative arthritis
5. Development of squamous cell
carcinoma in the sinus tract,
6. And rarely osteosarcoma.
7. Bone deformity ,dwarfism
Tuberculous osteomyelitis:
Bone infection complicates an estimated 1% to 3% of cases of pulmonary tuberculosis
Organism- Mycobacterium tuberculosis
The organisms usually reach the bone through the bloodstream, although direct spread from a
contiguous focus of infection. It is always secondary to some foci of infection
Usually solitary
Multifocal Acquired immunodeficiency
Tends to be more destructive and resistant to control than pyogenic osteomyelitis
Age adolescents, young adults
Source of infection pulmonary or extrapulmonary
Route of infection of tuberculous osteomyelitis:
- blood borne: active pulmonary or extra pulmonary disease
- Direct extension: from lung into the rib, tracheobronchial nodes into adjacent vertebrae
Sites of tuberculous osteomyelitis:
Spine (thoracic or lumbar vertebrae) commonly known as POTT DISEASE.
The infection breaks through intervertebral discs to involve multiple vertebrae and extends
down into the soft tissues forming COLD ABSCESS- PSOAS ABSCESS
Knees and hips
Tuberculous osteomyelitis:
It affects the synovium first , with its higher oxygen pressures,
The infection then spreads to the adjacent epiphysis, where it causes a typical granulomatous
inflammation with caseous necrosis and extensive bone destruction
Pathogenesis of tuberculous osteomyelitis:
Primary at some site- Lungs, GIT, LN etc
Spread through Blood, Lymphatics, Direct extension from adjescent foci
Establish the foci in Synovium, or bone marrow
Granuloma formation and caseation necrosis, COLD ABSCESS ,sinus formation,Deformity etc
Pathology of tuberculous osteomyelitis:
The onset of tuberculous osteomyelitis is usually insidious.
The infection is unrelenting, necrotizing, and destructive of bone, cartilage, and soft tissue.
The tuberculous exudation and the inflammatory necrosis may extend through the medullary
and cortical bone, penetrate through the periosteum, and progress through the epiphysial and
articular cartilage (radiographic joint space).
Tunneling sinuses may extend into the adjoining soft tissue and drain to the skin surface
Laboratory diagnosis of tuberculous osteomyelitis:
Clinical features of Bone pain,Low grade fever,malaise, Wt loss, Cough+sputum,
 High ESR ( >100 mm ),Anemia,>CRP
X-ray findings-Osteolytic lesion
Bone scrapping
ZN stain- AFB demonstration
Bone Biopsy Granulomatous inflammation
Culture and sensitivity
Complications of tuberculous osteomyelitis:
1. Spine scoliosis, kyphosis and neurological deficits due to spinal cord and nerve compression.
2. Pathologic fracture,
3. secondary amyloidosis,
4. Spread of Tb - arthritis
5. Sinus, non healing ulcer,
6. development of squamous cell
carcinoma in the sinus tract (rare )