Metabolic Bone Disease

1. Osteopenia and Osteoporosis

Definition
Age realated decrease in bone mass secondary to uncoupling of
osteoclast-osteoblast activity
Epidemiology
Male : female ratio 1:4
Age bracket : postmenopausal osteoporosis is highest in women aged 50-
70 years
Location of fractures vertebral body (60-70 y.o) > hip ( 70-80 y.o) > wrist
fractures (50-60 y.o)
WHO FRAX Score Risk Factors

Labs
25 hydroxyvitamin D level -> low
Imaging:
Radiographs : AP and Lateral View
Indications :
 Suspicion of fracture
 Loss of height
 Pain in thoracic or lumbar spine
Dexa Scan

Differential
Osteoporosis Osteomalacia
Definition Reduce bone mass, Bone mass variable,
normal mineralization reduce mineralization
Age Postmenopausal Any age
Etiology Age, endocrine Vit D deficiency or
abnormally, abnormality of vit D
idiopathic, activity,pathway,
alcohol, calcium hypophosphatemia,
deficiency hypophosphatasia,
renal tubular acidosis
Symtoms and sign Pain and tenderness in Generalized bone pain
fracture site and tenderness
Radiographic Axial fracture Appendicular fracture
Fractures predominance predominance,
symmetric, includes
pseudofractures
Labs
Serum Ca Normal Low/Normal
Serum PO4 Normal Low/Normal
ALP Normal Elevated; ex in
hypophosphatasia
Urinary Ca High/Normal Normal or low
Bone Biopsy Tetracycline labeling Tetracycline labeling
normal abnormal

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Treatment
Non-Operative
 Lifestyle Modification and vitamins ( Calcium and Vit D)
 Pharmacologic treatment
o 1st line : Biphosphonates
o Indication :
 Hip or vertebral fractures
 T-score <2.5 at femoral neck or spine fractures
 Low Bone mass ( T-score between -1.0 and -2.5)
o Hormon replacement Therapy
o Estrogen-Only replacement
o Salmon calcitonin
o Raloxifene
o Teriparatide
o Denosumab

Operative
 Osteoporotic vertebral compression fracture
 Femoral neck fracture
 Distal radius fracture

2. Osteomalacia
Definition
A metabolic diseases where defective mineralization results in a large
amount osteoid

Risk Factors
 Vit D deficient diets
 Malabsorbtion eg celiac disease
 Renal osteodystrophy
 Hypophosphatemia
 Chronic alcoholism
 Tumor

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  Drugs ( phenytoin, phyenobarbital, rifampisin, cholestyramine,
cadmium, glucocorticoids)

Presentation
Symptoms
 Generalized bone and muscle pain
 Fractures of long bones, ribs and vertebrae
 Proximal muscle weakness
 Fatigue

PE: inspection waddling gait > from hip pain and thigh weakness
Diffculty rising from chair and climbing stairs

Imaging:
Radiographs
Findings
Looser’s zone ( insufficiency fractures)
 Medial femoral
 Pubic ramus
 Scapula
 Fractures
 Biconcave vertebral bodies
 Trefoil pelvis
 Protrusion acetabuli
Bone scan: increase activity

Labs

Histology
Widely separated osteoid seams
Greater amount of unmineralized osteoid than normal

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Treatment
Large doses of oral vit D ( 1000 iu/day), treat underlying cause

3. Rickets
Definition
A defect mineralization of osteoid matrix caused by inadequate calcium
and phosphate
Prior to closure of physis known as rickets
After physeal closure called osteomalacia

Pathophysiology
 Disruption of calcium/phosphate homeostasis
 Poor calcification of cartilage matrix of growing long bones
 Occurs at zone of provisional calcification
 Leads to increased physeal width and cortical thinning and bowing

Classification
 Familial hypophosphonatemic ( Vit D-resistant)
 Vit D deficient ( Nutritional)
 Vit D dependent ( type 1 and type II)
 Renal osteodystrohy
 Hypophosphatasia

Presentation
 Orthopedic manisfestation include
 Brittle bones with physeal
cupping/widening
 Bowing of long bones
 Ligamentous laxity

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  Flattening of skull
 Enlargement of costal cartilage ( rachitic rosary)
 Kyphosis (cat back)

Imaging
Radiographs : recommended views are AP and Lateral
view of affected bone.
Findings:
 Physeal widening
 Metaphyseal cupping
 Looser’s zones
 Decrease bone density
 Prominance of rib heads at osteochondral joint
( rachitic rosary)
 Bowing ( often genu varum)

Laboratory studies

Familial hypophosphatemic Rickets ( Vit D resistant)

X-linked Hypophosphatemic causes inability of renal tubules to absorb
phosphate.
Treatment
 Non-Operative : medical treatment
Calcitrol
Phosphate replacement

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  Operative :
Corrective surgery to correct tibial bowing in severe deformity

Vit D dificiency Rickets

Nutritional rickets is associated with decrease dietary intake of vit D.
Low vit D > decreased intestinal absorbtion of calcium > low calsium level
> increase PTH and bone resorption > increased alkaline phosphatase
level
Clinical findings
 Enlargement of costal cartilage ( rachitic rosary)
 Bowing of knees
 Codfish vertebrae
 Retared bone growth
 Muscle hypotonia
 Dental disease
 Pathologic fracture
 Waddling gate

Treatment : Vit D ( 5000 IU) daily

Hereditary Vit D Dependent Rickets ( Type I dan Type II)

Rare disorder. Autosomal decessive
Clinical Features similar to Vit D deficient Rickets but more severe
Clinical characteristics
Type I : caused by defect in renal 25-OH vit D alpha-hydroxylase >
prevents convertion inactive form of vit D to active form
Clinicals : joint pain/deformity, hypotonia, muscle weakness, growth
failure and hypocalcemic seizure or fracture in early infancy.
Labs: decrase level of 1,25 OH2 Vit D
Type II : caused by defect in intracellular receptor for 1,25 OH2 Vit D

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Clinicals : bone pain, muscle weakness, hypotonia, hypocalcemic sizure,
growth retardation, several dental caries or teeth hypoplasia
Labs: increase levels of 1,25-OH2_vit D

Treatment:
Type I : Physiologic doses of 1,25-OH2-Vit D
Type II : daily high dose Vit D + elemental calcium

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Joint disease

1. Gout
Definition
A monosodium urate cystal deposition disorder
 Primary gout : an idiopatic disorder of nucleic acid metabolisme
that lead hyperuricemia and deposition of monosodium urate
cyrstals in joints ( a purine breakdown product)
 Secondary gout : associated with a disease with high metabolic
turnover.

Epidemiology
 Man > women
 Location:
Lower limb as podagra and cyrstal deposition as tophi

Pathophysiologi
 Dyfunctional nucleic acid metabolisme causing hyperuricemia
 Deposition of monosodium urate cystals in synovium of joint
 Cystal lead to an inflammatory respons activating

Presentation
Symptoms
 Pain in joint
 Can resemble septic arthritis
 Symptoms of renal stones

PE:
 Decreased ROM due to pain

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  White toothpaste like apperance of tophus most common site is
MTP 1

Imaging
Radiographs : AP and lateral of affected joint
Findings : may see punch out periarticular erosion and soft tissue cyrstal
deposition

Labs
Elevated serum uric acid
Crystal analysis made by joint aspiration and cystal
analysis
May see monosodium urate crystal : thin, tappered,
needle-shaped, strongly negatively birefringent

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Treatment
 Acute gout
o Colchicine
o Oral, intraarticular or IV glucocorticoid if patient unable to
take NSAID or colchicine
 Chronic gout
o Allupurinol ( an xanthine oxidase inhibitor)
o Colchicine

2. Pseudogout ( CPPD)
Definition
A metabolic disease resulting in deposition of calcium pyrophosphate
dihydrate ( CPPD) cystal within the joint space

Epidemiology
Commonly affects the elderly

Presentation
Symptoms
 Acute, onset joint tenderness
 Warm, erythematous joint
 Commonly on knee and wrist joint
PE
 Erythematous, monoarticular arthritis
 Joints tender to palpation
 May observe superficial mineral deposits under the skin at affected
joints

Imaging
May see calcification of fibrocartilage structures. Commonly TFCC in wrist
joint and meniscus in the knee

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Evaluation
Joint aspiration cyrstal analysis : positively birefrigent rhomboid-shaped
crystals

Treatment
Acute pseudogout
 NSAID
 Splint
 Intraarticular steroids

Chronic pseudogout
 Colchicine
 Intraarticular Yttrium-90 injections

3. Reiter’s
Definition
A seronegative spondyloarthropathy characterized by
 Urethritis
 Conjungtivitis or uveitis
 Arthritis
Epidemiology
 Rare
 Man > women in young man < 40 y.o
 Location:
o Arthritis
o May be unilateral or bilateral
o One or multiple joint

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Pathophysiology
 Associated infections
 Genetics ( HLA-B27)

Presentation
Symptoms
 Urinary discomfort or pain
 Inflammation or dryness of the eye
 Joint pain
 Other non-spesific pain symptoms including
o Heel pain ( achiless tendon pain)
o Low back pain
PE:
 Non-GO Urethritis
 Conjungtivitis or uveitis
 Arthritis
 Skin lessions on palms/soles
 May resemble psoriasis and genital skin lesions
 Low-grade fever

Imaging
Radiographs : may identify arthritis of the joints

Labs
 HLA-B27 positive
 CRP elevated
 ESR elevated
 Urinalysis : identify signs of active infection

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Treatment
Non-operative
 Antibiotics, symptomatic treatment, observation
 Systemic steroids

Systemic Disease

1. Rheumatoid Arthritis
Definition
A chronic systemic autoimmune disease with genetic predisposition

Epidemiology
Most common form of inflamatorry arthritis
Affects 3% of women and 1% of men

Pathophysiology
Immunology
Cell-mediated ( T-cell MHC type II) immune response against soft tissues
(early), cartilage (later), and bone (later)
 Rheumatoid factor ( immune complex is then deposited in end
tissues, IgM antobody against negative IgG antibodies)
 Mononuclear cells ( primary cellular mediator of tissue destruction)
 IL-1, TNF-alpha ( part of cascade that leads to joint damage)
 Immune response thought be related to infectious etiology or HLA
locus ( HLA-DR4 & HLA DW4)

Pathoanatomy
Cascade of events includes

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Antigen-antibody and antibody-antibody reactions > microvascular
proliferation and obstruction > synovial pannus formation (histology
shows prominent intimal hyperplasia) > joint subluxation, chondrocyte
death/joint destruction and deformity > tendon tenosynovitis and
rupture

Presentation
Symptoms
 Insidious onset of morning stiffness and polyarthropathy
 Usually affects hands and feet
 DIP joint of hand is usually spared
 May also affect knees, cevical spine, elbows, ankle and shoulder
PE:
 Subcutaneous nodules in 20% (strong association with positive
serum RF)
 Ulnar deviation with MCP subluxation, swan neck deformity,
boutonniere deformity
 Hallux vagus, claw toes, MTP subluxation
 Joint become affected at later stage in disease process

Imaging
Radiographs findings:
 Periarticular erosions and osteopenia
 Protrusio acetabuli (median migration of femoral head past the
radiographic teardrop)
 Joint space narrowing
 Central glenoid erosion

Labs
 Anti-CCP ( cyclic citrullinated peptide)
 Anti-MCV ( mutated citrullinated vimetin)

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  Elevated ESR
 Elevated CRP
 Positive RF titer
 Joint fluid testing
o Decreased complement
o May have elevated RF levels

Diagnostic Criteria
 Morning Stiffness > 1h
 Swelling in > 3 joints
 Rheumatoid nodules
 Radiographic changes of the hand including bony erosion and
calcification
 Symmetric arthritis
 Serum RF
 Arthritis of hand (MCP,PIP) and wrist
Have > 4 of 7 criteria for a 6 week period

Treatment
Non-operative
Pharmacologic treatment
 1st line : Low dose steroids
 2nd line : Disease modifiying anti-rheumatic drugs ( DMARDs)
 3rd line : DMARDS/ Biologic agents/ TNF antagonist
 4th line : DMARDS/ Biologic agents/ IL-1 antagonists
Operative
Operative treatment dictated by specific condition
Cervical Spondylisis
Includes
 Atlantoaxial subluxation
 Basillar invagination

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  Subaxial subluxation
 Finger conditions
Rheumatoid nodules
 Arthritis mutilans > pencil in cup deformity ( digits develop gross
instability with bone loss)
 Ulnar drift at MCP joint
 Boutonniere deformity
o synovitis in PIP leads to central slip (EDC) and dorsal capsul
attenuation > increasing PIP flexion
o lateral band subluxate volar to axis of rotation of PIP
o oblique retinacular ligament contracture causes extension
contracture of DIP
o Elson’s test
 Swan neck deformity
o Terminal tendon rupture from DIP synovitis leads to DIP
flexion /PIP hyperxtension
o FDS, volar plate and collateral ligament attenuation from
synovitis leads to decreased volar support of PIP, and
hyperextension deformity
o Lateral band subluxate dorsal to PIP axis rotation
o Contracture of triangular ligament, attenuation of transverse
retinacular ligament
Treatment : Early : Splint, Late: Reconstruction, arthrodesis for rigid
deformities

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Thumb conditions

Flexor Tendon Conditions

 Triggering
 Mannerfelt syndrome
 FDP rupture
 FDS rupture
Extensor Tendon Conditions
 Extensor Tendon Rupture
 Frequency EDM > EDC (ring) > EDC ( small) > EPL
 Radial sagittal band failure
 Vaughan-Jackson Syndrome > rupture of digital extensor tendons
from ulnar to radial ( EDM is first extensor rupture)
Differentials for loss of digital extension
 PIN neurophaty
 Extensor tendon rupture
 Extensor tendon subluxation
 MCP volar subluxation
Wrist Conditions

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  Caput-ulna syndrome
Synovitis in the DRUJ>ECU subluxation>volar carpal
subluxation>increased pressure over the extensor compartments >
tendon ruptures > PIN compression neurophaty ( seen in RA due
elbow synovitis)
 Radiocarpal destruction
Elbow Conditions
 Rheumatoid elbow
Shoulder Conditions
 associated with rotator cuff tears.
 Radigraphs finding : central glenoid, periarticular osteopenia, cysts
Hip conditions > protusio acetabuli
Knee conditions
 Joint space narrowing
 Periarticular osteoporosis/osteopenia
 Joint erosions
 Ankylosis
Foot and Toe conditions
 Toe hyperextension deformity
 Talonavicular arthritis

Complications
SSI ( surgical site infection)

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2. Systemic Lupus Eryhematous ( SLE)
Definition
Chronic autoimmune disorder of unknown origin leads accumulation of
autoimmune complexes in joints, skin, kidney, lungs, heart, blood, vessels
and nervous system

Etiology
Multiple HLA involved
HLA class II, HLA class III, HLA-DR, HLA-DQ

Presentations

Imaging
Osteonecrosis of hips is common

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Treatment
Similar to RA

3. Acute Rheumatic Fever

Definition
Acute systemic disease that may follow untreated group A-beta hemolytic
strep infections ( 2-6 wk latent period)
Characterized by migratory arthritis that involve multiple large joints

Jones Criteria

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Synovial Fluid Analysis

Treatment
Non-Operative
Penicillin ( 250.000 U orally BID) and salicylates.

Metabolic diseases

1. Hypercalcemia
Causes:
 Malignancy
Caused by parathyroid-related hormone protein (PTHrP)
Chractarized by:
Hypercalcemia, hypophosphatemia, low PTH
Examples :
o Paget’s disease
o Multiple Myeloma
o Squamous cell cancer of the lung
o Multiple endocrine neoplasia
o Pturitary adenoma
 Medical conditions
o Primary hyperparathyroidism

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 o Sarcoidosis
o Familial hypocalciuric hyoercalcemia
o Hyperthyroidism
o Addison’s disease
o Zollinger-Ellison syndrome
 Drugs
Thiazide diuretics
 Dietary
Calcium ingestion ( milk-alkali syndrome)
Hypervitaminosis D
Hypervitaminosis A

Presentation
Symptoms:
CNS
o Confusion
o Stupor
o Weakness
Gastrointestinal
o Constipation
o Anorexia
o Nausea
o Vomiting
Kidney
o Polyuria
o Kidney stone
o Polydipsia

Treatment
Hydration

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 o Saline diuresis
Drug Therapies
o Loop diuretics
o Bisphosphonates
o Mithramycin
o Calcitonin
o Gallium nitrate
Dialysis ( severe)

2. Hypocalcemia
Causes of hypocalcemia include
Decreade PTH that can caused by
o Hypoparathyroidism
o Psudohypoparathyroidism
o Renal osteodystrophy
spectrum of disease seen in patients with chronic renal disease.
Hypocalcemia > damaged kidney cant convert Vit D3 to calcitrol,
Hyperparathyroidism and secondary hyperphosphatemia >
hypocalcemia caused lack of phosphate excretion, uremia
related phosphate retention.
Imaging : radiographs finding : Looser’s zones, brown tumor,
osteosclerosis (osteomalacic bone and rugger jersey spine),
widened growth plate and zone of provisiona; calcification, varus
deformity, fracture, soft-tissue calcification, osteopenia. CT :
osseous resorption

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 o Decreased vit D3

Presentation
Symptoms
o parasthesia ( fingertip, toes, perioral)
o Abdominal pain, biliary colic
o Muscle cramps, tetany
o Dyspnea
o Convulsions
o Mental status changes
PE:
Trousseau’s sign
o Carpopedal spasm after blood pressure readings > inflate BP cuff
20mmHg above systolic BP 3-5 min
o Hand adopts a MCP flexed, DIP and PIP extended position
Chovstek’s Sign
Facial muscle contractions after tapping on the facial nerve
Dermatologic
o Fungal nail infection
o Hair loss
o Blotchy skin

Imaging
CT: basal ganglia calcification

Evaluation:
Serum Ca, phosphate, vit D and PTH
Serum albumin > hypoalbuminemia
pH > alkalosis
EKG : prolonged QT interval

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Treatment
Non-operative
o Ca gluconate infusion
o Activated Vit D ( calcitrol)

3. Hypoparathyroidism
Decreased production of PTH of the parathyroid gland resulting in
o Decrease plasma calsium levels
o Increade plasma phosphate levels
o Decreased 1,25 OH2 vit D levels

Etiology > thyroidectomy

Pathophysiology
o PTH decreased > urinary exretion of phosphate at kidneys decreased
> phosphate level increased
o PTH decreased > convertion inactive vit D to active form decreased

Presentation
Symptoms
( same as hypocalcemia)

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Labs
o Decreased PTH, Calcium, 1,25 Vit D, urinary calcium
o Increased serum phosphate
o Normal : alkali Phospatase

Treatment
Calcium and Vit D supplementation

4. Hyperparathyroidism
Increased PTH production that maybe primary, secondary or tertiary
causes

Pathophysiology
Excessive PTH leads to over-stimulation of bone resorption

Associated condition
Brown tumor > giant cell tumor relating to focal demineralization of bone
in the setting of hyperparathyroidism

Presentation
Symptoms
o Often asymptomatic
o Weakness
o Kidney stones
o Bone pain
o Constipation
o Secondary hypertension

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Labs

Urinalysis
Hypercalciuria ( renal stones)

Imaging
Radiographs findings > cystic bone spaces ( salt and pepper)

EKG shortened QT

Treatment
Acute hypercalcemia
o IV fluids and loop diuretics

5. Hypophosphatasia
Metabolic diseases characterized by generalized impairment of bone
mineralization
Pathophisiology
o Low levels of alkaline phosphate result decreased synthesis
inorganic phosphate
o Osteoid that forms in hyperthropic zone of growth plate flail to
mineralize
o The zone of proviosional calcification never forms and growth is
inhibited
o Genetics > autosomal recessive caused by mutation tissue non-
specific isoenzyme of alkaline phosphate

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Presentation
Similar to rickets
Abnormal tooth formation

Imaging
Radiographs findings
o Deossification of bone
o Physeal widening

Labs
Decreased serum alkaline phosphatase
Urin > phosphatenolamine in the urine

Treatment
No approved therapies

6. Psudohypoparatiroidism
PTH resistance
Defect in GNAS1

Classification

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Skeletal defect:
Short 4th and 5th metacarpals and metatarsals or short 4th metacarpal
only.

Presentation
Same as hypocalcemia

Treatment
Oral calcium and 1 alpha-hyroxylated vit D
IV calcium replacement

7. Scurvy
Definition
Vit C deficiency

Epidemiology
o 8% of men and 6% of women
o 4:3
o Infants 5-10months
o Location : wrist, knees, sternal ends of ribs
o Risk factors
o Elderly ( chronic malnutrition)
o Alcoholic
o Smokers
o Malabsortive conditions

Pathophysiology
o Humans are unable to synthesize L-ascorbic because enzyme L-
gluconolactone oxidase is nonfunctional
o Vit C deficiency > decrease in chondrotin sulfate and collagen synthesis

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o Impaired intercellular hydroxylation of collagen peptide
o Greatest effect occuring in the metaphysis and defect in spongiosa of
the metephysis at growth plate because the demand of type 1 collagen
is greatest during new bone formation.

Presentation
History
o Infant diet consisting of evaporated or condensed milk
o Tea and toast diet
Symptoms
o Malaise and fatigue
o Pain
o Bone pain
o Myalgia > reduced carnitine production
o Bleeding
PE
o Petechiae and ecchymosis
o Joint effusion
o Swelling over long bones because of subperiosteal hemorrhage
o Scorbutic rosary ( costochondral separation) angular step-off
deformity
o Defferentiated from rachitic rosary, which is rounded and nodular

Imaging
Radiographs
Recommended views
o Wrist
o Knee
o Sternal end of ribs

Findings

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 o The white line of Frankel
Widened zone of provisional calcification
Between epiphysis and metaphysis
o Trummerfeld zone
Transverse radiolucent band in the metaphysis adject to the frankle
line also known as the scurvy line
o Wimberger ring
Ring of increased density surrounding epiphysis
o Pelkin spur and fracture > metaphyseal spurs and fractures
o Corner sign of park > metaphyseal clefts
o Thin cortices ( pencil-point cortex)
o Decreased trabeculae with ground-glass ostepopenia
o Subperiosteal elevation
o Epiphyseal separation
o Fractures and dislocation

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Treatment
Vit C replacement with oral vitamin C

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Joint Conditions : Osteoarthritis

Definition
Degenative disease of synovial joints that causes progressive loss of
articular cartilage

Epidemiology
Incidence
 Hip OA
88 per 100,000 per year
 Knee OA
240 per 100,000 per year

Risk factors
Modifiable
 Articular trauma
 Muscle weakness
 Heavy physical stress at work
 High impacted spoting activities
 Large body mass
 Occupation, repetitive knee bending
 Metabolic syndrome
Non-modifiable
 Gender: female>male
 Increased age
 Genetics
Development or acquired deformities
 Hip dysplasia
 SCFE

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  Legg-Calve-Perthes

Pathophysiology
Pathoanatomy
 Articular cartilage
 Increase water content
 decreased in amount of proteoglycans
 collagen abnormalities
 organization and orientation are lost
 binding of proteoglycans to HA

Synovium and capsule

 Early phase of OA
Mild inflammatory chnges in synovium
 Middle phase of OA
Moderate inflammatory changes of synovium
Synovium becomes hypervascular
 Late phases of OA
Synovium becomes increasingly thick and vascular
Bone
 Subchondral bone attempts to remodel
 Forming lytic lesion with sclerotic edges
 Bone cysts form in late stages

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Cell biology
Proteolytic enzymes
Genetics
 Inheritance non mendilian potentialy link to OA
 Vit D receptors
 Estrogen reseptor 1
 Infflamatory cytokines
o IL-1
o IL-4
o Matrilin-3
o BMP-2, BMP-5

Presentation
History
Identify age, functional activity, pattern of arthtitic involement, overall
healt and duration of symptoms

Symptoms
 Fuction-limiting hip/knee pain
 Pain at night or rest
 Hip/knee stifness
 Mechanical
 Instability, locking catching sensation
PE
 Inspection
 Body habitus
 Gait
 LLD
 effusion
 Skin ( scars)
 Primary ostheoarthritis in hand

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 o Heberden’s nodes : Swelling in DIP joints
o Bouchard’s nodes : swelling in PIP joints

ROM
 Lack of full extension
 Lack of full flexion
 Ligament integrity
 Limited internal rotation
Neurovascular : normal
Deformity : varus genu
Kellgren-Lawrence Classification

Imaging
Radiographs : Standing AP + Lateral views
Findings
 Joint space narrowing
 Osteophytes
 Subchondral sclerosis
 Subchondral cysts

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Treatment
Non-operative
 NSAIDs and or/tramadol
 Walking stick
 Weight loss, activity modification and exercise program/physical
therapy
 Corticosteroid joint injection

Operative

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2. Hip Osteonecrosis
Also known as avascular necrosis that occurs in hip

Epidemiology
 20.000 new cases per year in US
 Male > female
 35-50 y.o
 Location
 Bilateral hips involved 80% of the time
 Multifocal osteonecrosis
Risk factors
Direct causes
 Irradiation
 Trauma
 Hematologic disease
 Dysbaric disorder
 Marrow-replacing disease
 Sickle cell disease
Indirect causes
 Alcoholism
 Hypercoagulable statse
 Steroid
 SLE
 Transplant patient
 Virus
 Idopathic

Pathophysiology
 Idopathic AVN > intavascular coagulation
 AVN associated with trauma

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 Due injury of femoral head blood supply ( medial femoral
circumflex)
 Femoral head fractures 75-100%
 Basicervical fracture 50%
 Cervicotrochanteric 25%
 Hip dislocation 2-40% (2-10% if reduced within 6 hours of injury)
 Intratrochanteric fracture : rare

Classification

Presentation
Symptoms

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  Insidious onset of pain
 Pain with stairs, inclines and impact
 Pain common in anterior hip
PE:
 Mostly normal
 Advanges stage similar to hip OA

Imaging :
Radiographs :
Recommended views
 AP hip
 AP and lateral of contralateral hip
MRI : highest sensitvity and specificity
Bone Scan

Treatment
Non-operative
 Biphosphonates ( for Ficat stage 0-II)
Operative

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