OSTEOMYELITIS

METABOLIC BONE
DISORDERS

OSTEOMYELITIS
Infection of bone and marrow
Causative organisms
bacteria (pyogenic, mycobact)
viruses
fungi
parasites
Primary/secondary infection

Pyogenic osteomyelitis
Caused by bacteria
Organisms may reach the bone by
(1) hematogenous spread - healthy, long bones
(2) extension from a contiguous site
(3) direct implantation
Bacteremia - trivial injuries to mucosa
(defecation ,vigorous chewing of hard foods,
minor infections of the skin)
Open fractures, surgical procedures, and diabetic
infections of the feet

 Staphylococcus aureus - 80% to 90%

Escherichia coli, Pseudomonas, and
Klebsiella - genitourinary tract infections,
intravenous drug abusers
Mixed bacterial infections - surgery or open
fractures
Haemophilus influenzae and group B
streptococci - neonates
Salmonella - sickle cell disease
50% cases - no organisms isolated.

 Bacteria localise in bone - proliferate and

induce an acute inflammatory reaction
Entrapped bone undergoes necrosis within
first 48 hours
Bacteria and inflammation spread within
shaft, reaches the periosteum
(sizable subperiosteal abscesses in
children)
Lifting of periosteum further impairs blood
supply to the affected region
Suppurative and the ischemic injury
causes segmental bone necrosis
Dead piece of bone sequestrum

 Rupture of the periosteum - soft tissue abscess,

formation of a draining sinus
In infants, epiphyseal infection spreads into a joint septic or suppurative arthritis - destruction of the
articular cartilage and permanent disability
After the first week - chronic inflammatory cells,
release of cytokines - osteoclastic bone resorption,
ingrowth of fibrous tissue, and the deposition of
reactive bone in the periphery.
Newly deposited bone forms a sleeve of living tissue
around the segment of devitalized infected bone, it is
known as an involucrum

Morphologic variants
Brodie abscess - small intraosseous
abscess, frequently involves the
cortex and is walled off by reactive
bone
Sclerosing osteomyelitis of Garr
typically develops in the jaw
associated with extensive new bone
formation that obscures much of the
underlying osseous structure.

C/F:
hematogenous osteomyelitis :
acute systemic illness with malaise, fever,
chills, leukocytosis, intense throbbing pain
over the affected region
unexplained fever in infants
localized pain in the absence of fever in adult
X- RAY
lytic focus of bone destruction surrounded
by a zone of sclerosis
TREATMENT
antibiotics and surgical drainage is usually
curative.

COMPLICATIONS:
- chronic osteomyelitis
- pathologic fracture
- endocarditis, sepsis
- development of squamous cell
carcinoma
in the sinus tract
- secondary amyloidosis
- sarcoma in the infected bone

Tuberculous osteomyelitis
1% to 3% of individuals with pulmonary or
extrapulmonary tuberculosis have osseous
infection
More destructive and resistant to control than
pyogenic osteomyelitis.
MODE OF SPREAD :
blood borne (from a focus of active visceral
disease)
Direct extension (e.g., from a pulmonary focus
into a rib or from tracheobronchial nodes into
adjacent vertebrae)
Spread via draining lymphatics
MORPHOLOGY
usually solitary , AIDS - multifocal bone

 Potts spine - infection breaks through IV discs - involve

multiple vertebrae and extends into soft tissues forming
abscesses
C/F - pain on motion, localized tenderness, low-grade
fevers, chills, and weight loss
COMPLICATIONS
Severe destruction of vertebrae - permanent compression
fractures - severe scoliotic or kyphotic deformities and
neurologic deficits secondary to spinal cord and nerve
compression
tuberculous arthritis
sinus tract formation
amyloidosis

METABOLIC BONE
DISORDERS
1. Abnormalities of bone mass
- osteopenia/ osteoporosis
- osteosclerosis
2. Undermineralisation
- osteomalacia
3. Abnormal bone remodelling
- renal osteodystrophy
- hyperparathyroidism
- pagets disease

OSTEOPOROSIS
Disease characterized by porous bones and reduced
bone mass
Predispose the bone to fractures
Decreased amount of bone (trabecular bone) per
unit volume (of cancellous bone)
Increased osteoclastic bone resorption with reduced
rate of bone formation (decreased osteoblasts)
Generalized osteoporosis, in turn, may be primary or
secondary to a large variety of conditions

PRIMARY
Postmenopausal (dec E, inc
IL1,6;TNNF)
Senile (osteoblast, ECM GF)
low turnover
Idiopathic
SECONDARY
Endocrine disorders
Hyperparathyroidism
Hyperthyroidism

Hypothyroidism
Hypogonadism
Pituitary tumors
Diabetes, type 1
Addison disease
Neoplasia
Multiple myeloma
Carcinomatosis

Gastrointestinal
Malnutrition
Malabsorption
Hepatic insufficiency
Vitamin C, D deficiencies
Drugs
Anticoagulants
Chemotherapy
Corticosteroids
Anticovulsants
Alcohol
Miscellaneous
Osteogenesis imperfecta
Immobilization (mechl
forces- imp
stimuli)

Pulmonary disease
Homocystinuria
Anemia

 plain radiograms - 30% to 40% bone loss

specialized radiographic imaging techniques,
such as dual-energy X-ray absorptiometry
and quantitative computed tomography,
which measure bone density
Treatment
exercise, appropriate calcium and vitamin
D intake, bisphosphonates which bind to
bone and inhibit osteoclasts.

OSTEOMALACIA
Softening of bones
Failure of mineralisation of bone matrix,
abnormally wide osteoid seams around bone
trabeculae
Histologically, the unmineralized osteoid can be
visualized as a thickened layer of matrix (which
stains pink in hematoxylin and eosin
preparations) arranged about the more
basophilic, normally mineralized trabeculae

Vitamin D Metabolism

Osteomalacia
Skeletal pain, proximal muscle
weakness
X-ray Loosers zones
Laboratory low PO4-, (vitamin D
deficiency: low Ca2+, increased
alkaline phosphatase)
Treat underlying deficiency

Parathyroid Hormone
Increases tubular reabsorption of calcium
Increases renal phosphate excretion
Increases renal synthesis of 1,25dihydroxy-D3
Increases intestinal calcium absorption
Increases osteoclastic reabsorption of
bone
Stimulates osteoblast maturation
Parathyroid glands have calcium and
vitamin D sensing receptors

The skeletal changes characterized by

diffuse or focal resorptive loss
and fibrous replacement of bone due
to an excess of osteoclastic over
osteoblastic activity
caused by an over-production of
parathormone (PTH) in primary or
secondary hyperparathyroidism.

Hyperparathyroidism
Osteitis Fibrosa Cystica
Excess of Parathyroid Hormone
causing marrow fibrosis, expansion of
osteoid surfaces, and numerous
osteoclasts with resorptive surfaces

HYPERPARATHYROIDISM
Earliest change : excess osteoid seams around
bony trabeculae (resembles osteomalacia)
Later, osteclasts activated increased bone
resorption with
surface excavation (prominent howship lacunae)
tunneling into trabeculae by fibrous tissue &
osteoclasts)
Trabeculae transected as lacunae enlarge
Increased fibrosis, intertrabecular spaces
completely filled by fibrous tissue

 Moderate increase in vascularity of marrow, ?

macroscopic cysts visible
Microhemorrhages hemosiderin laden
macrophages within fibrous tissue, foreign body
type giant cells
Osteitis fibrosa cystica

Microscopy of "brown tumors

proliferated osteoclasts and
fibroblasts in a fibrous stroma
often located in a region of
hemorrhage, and characteristically
associated with hemosiderin
deposition (which imparts a brown
color).

 Primary hyperparathyroidism
most frequently occurs in adults ( third and fifth
decades)
rarely seen in children under 10 years of age.
female to male ratio of 2-3/1
Biochemistry
hypercalcemia, hypophosphatemia,
hypercalciuria, elevated serum alkaline
phosphatase activity (in the presence of bone
disease), and increased levels of PTH measured
by radioimmunoassays.

 The clinical presentations divisible into 3 categories:

Hypercalcemia - neuromuscular weakness, fatigue,
gastrointestinal symptoms, and, rarely, coma in severe
hypercalcemic crisis
renal stones (often bilateral); calcification of the kidneys
(nephrocalcinosis); and metastatic calcification of other tissues
bone resorption and fibrous replacement resulting in diffuse
osteopenia (which may be difficult to distinguish radiologically
from common osteoporosis);
in some cases, "cystic" or tumor-like lesions of bone ("brown
tumors");
pathological fractures
widespread alterations and deformities affecting the
demineralized and softened bones of the entire skeleton
(generalized osteitis fibrosa cystica).

RENAL OSTEODYSTROPHY
Complex manifestations
Combination of bone disease due to
1. secondary hyperparathyroidism (most common, may
advance to osteitis fibrosa cystica in severe cases)
2. osteomalacia (earliest change with thickened bony
trabeculae and increased osteoid seams)
3. Osteosclerosis (patchy, stromal fibrosis is common)

PAGETS DISEASE
Unknown etiology
Increased osteoclastic resorption of bone followed by
uncoordinated formation of disordered bone
Initial stages increased bone resorption
Trabecular bone with scalloped appearance
Deposition of disordered woven bone, increased
osteoblasts
Increased vascularity (arteries, arterioles, capillaries,
sinusoids) prolonged bleeding on bone marrow
biopsy
New bone (lamellar) formation in uncoordinated
haphazard fashion

The bone changes are divisible into three phases defined

radiologically:
osteolytic phase
mixed osteolytic and osteoblastic phase
final osteosclerotic phase
osteolytic focus characterized by the presence of numerous
large osteoclasts. Radiographically, circumscribed areas of
radiolucency, often first seen in the skull ("osteoporosis
circumscripta)
osteolytic phase followed by osteoblastic formation of
highly vascular new bone of woven type
numerous osteoclasts along with an abundance of
osteoblasts (which account for elevated levels of serum
alkaline phosphatase activity) and osteoid.

 Pain - microfractures, bony

impingement on nerves, or other
causes.
bone enlargement or deformity,
overt pathological fracture