DISEASES OF

BONE

Brig Shahid Jamal

MBBS, FCPS (Pak), FRCPath (UK)
Professor of Histopathology
AM College Rawalpindi
 Osteomyelitis
It is infective disease of bone, can be caused
by many types of organisms including
 Viruses, Parasites, Fungi, and Bacteria
 but most common are pyogenic and
tuberculous osteomyelitis
 Osteomyelitis

Pyogenic osteomyelitis:
Bacteria reach the bone by:
a. Haematogenous spread
b. Extension from the surrounding
foci
c. Direct implantation
 Osteomyelitis
Organisms:
Staphylococcus is responsible in 80-90% cases
Other bacteria include, E.coli, pseudomonas,
Klebsiella, H.Influanzae, Group B
streptococci, and salmonella
Location: In children metaphysis,
In adults, epiphyseal ends
 Osteomyelitis
(Morphology)
Will depend on stage (acute, subacute or
chronic)
Sequence of events:
Focus of inflammation – localized abscess formation
(Brodie abscess)
– spreads to the surrounding cortex
– uplifting of periosteum – necrotic cortical fragment
(sequestrum) – ultimate fibrosis,
osteoclastic/osteoblastic activity, new bone formation
(invalcrum) –
healing with or without permanent deformity
Osteomyelitis
(Morphology)
 Osteomyelitis
(Morphology)

Microscopy:
Acute stage: Necrotic bone surrounded
by neutrophils, pus cells and
congested blood vessels
Chronic stage: necrotic bone replaced
by fibrosis, new bone formation.
Lymphocytes and some macrophages
are seen
 Osteomyelitis
(Morphology)
X-Rays: shows lytic lesion
surrounded by zone of
sclerosis
Complication:
a. Septicemia

b. Suppurative arthritis
c. Pathological fracture
d. Secondary amyloidosis
e. Malignancy (SCC in
the sinus)
 Tuberculous
osteomyelitis
 More common in underdeveloped and
developing countries
 M. Tuberculosis reach the site of lesion by
haematogenous spread (common mode) or by
direct extension of lungs or GI tract lesion (rare
mode)
 Adolescents and young adults are mostly
affected
 Spines and bones of extremities are most
commonly involved
Tuberculous osteomyelitis
(Morphology)
Gross:
 Tuberculous
osteomyelitis
 Chronic caseating granulomatous
inflammation
 AFB may be found on special stains
Tuberculous osteomyelitis
Complications:
 Psoas abscess, lumber cold abscess

 Systemic amyloidosis

 Pathological fractures
 Collapse vertebrae (kyphosis) with
neurosurgical symptoms
 TB arthritis
 Metabolic and endocrine
diseases of bone
 Osteoporosis
 Osteomalacia & Rickets, Scurvy
 Hyperparathyroidism
 Pituitary dysfunction, Thyroid disorders
 Renal osteodystrophy, Skeletal fluorosis

Osteoporosis is a disease characterized

by increased porosity of skeleton due
to reduced bone mass
 Osteoporosis
Causes:
Primary:
 Postmenopausal
 senile
 idiopathic
Secondary:
Endocrine- hyperparathyroidism, hypo-
hyperthyroidism, hypogonadism, diabetes,
Addison’s disease
Neoplasia – multiple myeloma, carcinomatosis
GI diseases- malnutrition (Ca, Vit D), malabsorption
Drugs- corticosteroids, chemotherapy, anticoagulants
Others- immobilization, anaemia, pulmonary diseases

DENGO = Pnemonic
Osteoporosis (senile &
postmenopausal)
 Osteoporosis
(morphology)
Any bone can be affected
but certain bone are more
severely involved
depending upon the cause
Gross:
Bones more porous and are
thinned out
Microscopy:
Thin bone trabeculae with
intervening fibrous tissue
 Osteoporosis (clinical
features)
 Depending upon the bone involved
 Pathological fractures
 Osteoporosis weakens the
vertebrae, resulting in;
 Compression fractures of
vertebra.
 Back pain
 Over time, shortening of
stature, dorsal kyphosis, and
cervical lordosis
 Rickets & Osteomalacia

It is due to deficiency of Vit-D or

deranged functions of Vit-D
Causes:
Vit-D deficiency – decreased exposure to
sunlight, dietary deficiency, poor maternal
nutrition
Decreased absorption – cholestatic liver
disease, pancreatic, billiary diseases, celiac
disease
Deranged Vit-D metabolism – impaired
synthesis of 25(OH)D & 1,25(OH)2D and
some other enzymes
End organ resistance to 1,25(OH)2D –
inherited absence of receptors
 Rickets & Osteomalacia
(morphology)
 There is excess of un-mineralized matrix
(Osteoid matrix)
 In rickets epiphyseal cartilage overgrows as it
is not calcified (costochondral junction)
 Abnormal overgrowth of capillaries and
fibroblasts secondary to wear and tear and
microfractures
 Rickets & Osteomalacia
(morphology)

 Craneotabes –occipital
bone is flattened, parietal
bone pushed inward
 Rickety rosary- chest
deformity at casto-chondral
junction
 Pigeon breast deformity
due to upward pull of
sternum
 Bowing of legs in older
children
Renal osteodystrophy
Charing Cross Hospital, London