Transcript Bone Pathology

Bone Pathology
Normal anatomy
• Parts of a long bones: diaphysis (shaft),
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physis (growth plate), epiphysis (ends of bone,
partially covered by articular cartilage),
metaphysis (junction of diaphysis and epiphysis,
most common site of primary bone tumors)
Cross section: periosteum, cortex (composed
of cortical bone or compact bone), medullary
space (composed of cancellous or spongy bone)
HISTOLOGY
• INFECTIONS
• BONE TUMORS
OSTEOMYELITIS:
Denotes inflammation of bones and
marrow.
• May be a complication of any systemic
infection but frequently manifests as a
primary solitary focus of disease.
• Pyogenic Osteomyelitis.
• Tuberculous osteomyelitis
• PYOGENIC OSTEOMYELITIS:
is almost always caused by bacteria.
1. Hematogenous spread.
2. Extension from a contiguous site.
3. Direct implantation.
• E.coli, Klebsiella and Pseudomonas.
• Mixed bacterial infections.
• Salmonella infections.
Sites of involvement:
• Influenced by the vascular circulation,
which varies with age.
• Neonates: the metaphyseal vessels
penetrate the growth plate, resulting in
frequent infection of the metaphysis,
epiphysis or both.
• In children: metaphyseal.
• Adults: epiphyses and subchondral
regions.
• Clinical Course:
• Fever ,chills, malaise, marked to intense
throbbing pain over the affected region.
Diagnosis;
• Sign/symptoms.
• X-ray
• Blood cultures
• biopsy
Complications:
• Pathologic fracture.
• Secondary amyloidosis
• Endocarditis
• Sepsis
• Squamous cell carcinoma.
• Rarely sarcoma in the affected bone
Tuberculous osteomyelitis:
Routes of entry;
• Usually blood borne and originate 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) or spread
via draining lymphatics.
Bone tumors
Although the cause of most bone tumors is unknown.
Genetic alterations e.g. bone sarcomas in the Li-Fraumeni and
hereditary retinoblastoma which are linked to mutations in p53 and
Rb genes.
Bone infarcts
chronic osteomyelitis
pagets disease
radiation and
metal prostheses are also associated with increased incidence of
bone neoplasia.
Classification of primary tumors involving
bones:
• Bone Forming tumors.
• Cartilage forming tumors.
• Fibrous and fibro-osseous tumors.
• Miscellaneous tumors.
JOINTS/TYPES
•
Synovial or nonsynovial
Synovial joints: also called diarthroses;
contain joint space between ends of bones,
joints covered by hyaline cartilage, strengthened
by dense fibrous capsule continuous with
periosteum of bones and an inner synovial
membrane; joint is reinforced by ligaments and
muscles; presence of joint space allows wide
range of motion.
JOINTS/TYPES
• Nonsynovial joints: also called solid
joint or synarthrosis; no joint space
present; provides structural integrity and
minimal movement
Arthritis
• SUPPURATIVE ARTHRITIS
• TUBERCULOUS ARTHRITIS
• OSTEOARTHRITIS
• RHEUMATOID ARTHRITIS
ARTHRITIS
• Suppurative arthritis:
• Due to seeding of joint during bacteremia, most
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commonly due to Staphylococcus, Streptococcus, gram
negative rods; rarely syphilis
Also due to postsurgical infection
Neonates: often due to osteomyelitis
Young women: most commonly due to gonorrhea
(gram negative intracellular diplococci, which is
associated with multiple joint involvement, including the
knee)
Sickle cell disease: Salmonella
ARTHRITIS
• Tuberculous arthritis:
• Insidious onset of chronic progressive arthritis, usually
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monoarticular in knee and hip; usually after
osteomyelitis
Leads to fibrous ankylosis of joint with obliteration of
joint space
Can detect from culture and examination of synovial
fluid.
PCR is sensitive; apparent false positives in clinically
negative patients may represent early disease.
ARTHRITIS
Degenerative joint disease:
• Also called osteoarthritis.
• Nonneoplastic disorder of progressive erosion of articular
cartilage associated with aging, trauma, occupational
injury.
• Usually age 50+ years (present in 80% at age 65 years)
• Cartilage degradation may be mediated by IL-1.
• Sites: men-hips, women-knees and hands; also first
metatarsophalangeal joint, lumbar spine; usually one
joint or same joint bilaterally, at least initially
Osteoarthritis
• Symptoms: pain worse with use of joint,
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crepitus, limited range of motion, nerve root
compression; Heberden nodes in fingers of
women only (osteophytes at DIP joints)
Secondary degenerative joint disease:
younger patients with predisposing condition
(trauma, congenital, diabetes, obesity,
ochronosis, hemochromatosis), such as knees of
basketball players
Osteoarthritis
• Gross: early changes are even degeneration of hyaline
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cartilage of articular surface, with fragmentation
later thinning of cartilage and articular surface is
often soft and granular with altered shape, sloughing of
cartilage .
cysts: (synovial fluid forced into fractures via ball valvelike mechanism),
osteophytes: (bony outgrowths at margins of articular
surface)
Osteoarthritis
• Loose bodies: may form if portion of
articular cartilage breaks off; normally
loose body is nourished by synovium and
continues to grow.
GOUT
• Gout and gouty arthritis
• Transient attacks of acute arthritis initiated by
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crystallization of urates and neutrophils, followed
by chronic gouty arthritis with tophi in joints and
urate nephropathy
Causes 2-5% of chronic joint disease
Sites: 50% have initial attack in first
metatarsophalangeal joint; also ankles, heels,
knees, wrists, fingers, elbows
GOUT
• Primary gout (90%): idiopathic (85%) with
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overproduction of uric acid or known enzyme
defects.
Secondary gout (10%): increased nucleic
acid turnover due to leukemia/lymphoma,
chronic renal disease.
GOUT
• Gout is due to hyperuricemia and deposition of
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monosodium urate crystals in joints and viscera
and uric acid kidney stone formation.
Need serum urate > 7 mg/dl for deposition
(saturation threshold for urate at 98.6 F)
Risk factors for gout with hyperuricemia are age
> 30 years, familial history of gout, alcohol use,
obesity, thiazide administration, lead etc.
Rheumatoid arthritis
• Chronic systemic inflammatory disorder affecting
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synovial lining of joints, bursae and tendon sheaths; also
skin, blood vessels, heart, lungs, muscles
Produces nonsuppurative proliferative synovitis, may
progress to destruction of articular cartilage and joint
ankylosis
75% are women, peaks at ages 10-29 years; also
menopausal women
Sites: small bones of hand affected first (MCP, PIP
joints of hands and feet), then wrist, elbow, knee
Rheumatoid arthritis
• Xray: joint effusions, erosions
• narrowing of joint space; destruction of
tendons, ligaments and joint capsules
produce radial deviation of wrist, ulnar
deviation of digits, swan neck finger
abnormalities
Rheumatoid arthritis
• Diagnosis: morning stiffness, arthritis in
3+ joint areas
• arthritis in hand joints,
• symmetric arthritis,
• rheumatoid nodules, rheumatoid factor,
typical radiographic changes
OSTEOPOROSIS
Is a term that denotes increased porosity of
the skeleton resulting from reduction in
the bone mass.
It may be localized →disuse osteoporosis
of a limb.
or
may involve the entire skeleton, as a
metabolic bone disease.
OSTEOPOROSIS
• Primary
• Secondary
PRIMARY: post menopausal
Senile
OSTEOPOROSIS
• Secondary:
• Endocrine Disorders
OSTEOPOROSIS
Pathophysiology:
• AGING
• ↓ replicative activity of the
osteoprogenitorcells
• ↓ synthetic activity of the osteoblasts.
• ↓ activity of the matrix bound growth
factors.
OSTEOPOROSIS
• Menopause:
• ↓ serum estrogen
• ↑ IL-1,IL-6 levels
• ↑ osteoclast activity
Genetic factors
Nutritional effects
OSTEOPOROSIS
Prevention Strategies
• The best long-term approach to osteoporosis is
prevention.
• children and young adults, particularly women,
with a good diet (with enough calcium and
vitamin D) and get plenty of exercise, will build
up and maintain bone mass.
• This will provide a good reserve against bone
loss later in life. Exercise places stress on bones
that builds up bone mass