LEGG CALVE PERTHES DISEASE

(LCPD)
PRESENTER
DR. SIVARAM SIDDA
1ST YEAR PG

MODERATOR
DR.SHYAM KUMAR
 CONTENTS
• DEFINITION
• HISTORY, EARLY TREATMENT CONCEPTS AND
CONCEPT OF CONTAINMENT
• ETIOLOGY
• PATHOLOGY
• CLINICAL FEATURES
• INVESTIGATIONS
• CLASSIFICATIONS
• DIFFERENTIAL DIAGNOSIS
• TREATMENT
 DEFINITION
• Avascular event of head of femur → Cessation of
growth of ossific nucleus of head→ Bone becomes
dense→ Fragmented→ Gets resorbed→ New bone
formation.

• Due to all these mechanical properties of femoral head

are altered and head becomes flat and large.
• 10-12% are bilateral
• Male : Female→ 4/5 : 1
• Age 4 -12 yrs
• Imp etiology is silent coagulopathy.
 HISTORY
Arthur Legg
• American who described
salient features of LCPD.
• 5-8yrs age group
• H/Of trauma
• Painless limp
• Minimal/ no spasm or
shortening of limb.
Jacques Calve
• French surgeon who said
LCPD has minimal atrophy
and no palpable swelling
• His associate Paul Sourdet
gave radiological
illustrations
George Perthes • Schwarz→ Blood supply
• Thought LCPD as youthful of femoral head.
variant of degenerative
arthritis.
• Later described it as SELF • Waldenstrom→ Reported
LIMITING, NON radiographic changes and
INFLAMMATORY DISEASE mistook them for TB.
affecting femoral head
with stages of
degeneration and
regeneration leading to
restoration of bone
nucleus.
 EARLY TREATMENT CONCEPTS
• Bed rest
• Immobilization
• Weight relief → Patten-bottom brace is used.
Hip is suspended with opposite limb shoe
elevation. Contemporary biomechanics suggest
muscle compression, increased intraarticular
pressure than normal weight bearing. Protracted
recumbence and special carts to move about.
→ Snyder slings were used
 CONCEPT OF CONTAINMENT Rx
• Parker use Petrie casts 45º abduction and 5-10º internal
rotation.

• Harrison and Menon described head in acetabular cup as jelly

poured into cup molds same shape as a cup when it is allowed
to come out after reconstitution.

• Harrison designed ambulatory containment brace.

• Eyre and brook said 18 -24 months traction is needed and

treatment should be started while head is still soft.

• Goal→ maintain round head and preserve full range of

motion.
 Salter pig model experiments
• Experiment 1
Hips with AVN treated with

Non weight bearing and Weight bearing with hip

Neutral or adducted hip In flexion and abduction

Head deformed Head did not deform

• Experiment 2
Hips with AVN treated with

Normal Non weight bearing Weight bearing

weight bearing with hip in acute with hip in
flexion abduction

• 3rd group showed round femoral head

• Containment prevents deformation and maintains way for
biological plasticity of head
 During early phases of revacularisation.

Subchondral #res.

Non union of #res.

Femoral head collapses, flattens and extrudes out antero-

laterally from acetabulum.

Lateral subluxation of femoral head.

Increased pressure on edge of acetabulum.

Stress concentration on head leading to progressive deformity of head.

CONTAINMENT PREVENTS PRESSURE CONCENTRATION AND EVENTUAL

HEAD DEFORMITY
 ETIOLOGY
1. HEMATOLOGICAL CONDITIONS
• Leukaemias, lymphomas, ITP, thalassemias, sickle
cell anemia like condition leads to increased blood
viscosity and AVN.
• Venous thrombus formation is increased in Protein
C deficiency, Protein S deficiency, hypofibrinolysis,
increased Lipoprotein(a) etc.
venous thrombus→ venous HTN→ Hypoxic bone
death→ LCPD
• Other conditions like Factor V leiden mutation, IgG
ad IgM anticardiolipin antibodies.
• Coagulopathies are not absolute causes of LCPD conflicting results were noted in
various studies and further research is needed
• Arterial status of femoral head

Extracapsular ring formed by MCFA* and LCFA

Important supply by lateral segment of ring
Lateral retinacular vessels have narrow passage and is
particularly contracted in kids <8yrs
• Many pts with LCPD have incomplete subsynovial
ring.
 Angiographic studies show
• Obstruction of superior capsular arteries and lateral retinacular
vessels

• Stages of Revascularisation as disease progressed

• Decreased blood in MCFA, and decreased flow with hip

extension, abduction and Int rotation.

• African kids have blood to head by inf gluteal artery and they’re
less prone to LCPD

• Small for age underdeveloped kids have shallow neck and are
prone for lateral retinacular obstruction

• Minimum 2 infarcts are needed in femoral head for LCPD to

occur
Blood supply of femoral head

Anterior
Posterior
• 4 to 7yrs→ Physeal plate forms a firm barrier.
Only lateral epiphyseal artery supplies
femoral head in this age group.
• More prone to injury.
• Tc Scintigraphy:
Kids with transient synovitis
Scintigraphy
Decreased uptake of isotope
Scintigraphy after 6wks
Persistent decrease in uptake

LCPD
2. PREDISPOSED CHILD
• Child with growth & development abnormalities.
• Delay in bone age compared to chronological
age.(disease diagnosed before 5yrs more delay is seen,
less delay if disease is diagnosed after 8yrs)
• Delay is seen in carpal ossification.
• “Radiological Pause” seen in triquetrum and lunate.
• In bilateral LCPD trapezoid growth delay is seen.
• After phase of delay there is phase of accelerated
maturation to match chronological age.
• Most pts have LBW and short stature.
• Important cause is growth hormone (somatomedin A
and C reduction) and some studies show elevated
thyroxine.
3. TRAUMA in predisposed child→ disrupted vascularity of
head→ AVN→ LCPD

4. ADHD child is in perpetual state of motion like climbing and

falling leading to trauma and LCPD.

5. HERIDITARY: LCPD runs in families with assciation of X-linked

recessive factors, autosomal homozygous alleles, beta
fibrinogen gene polymorphism etc.

7. ENVIRONMENTAL: Passive smoking (decreased tissue plasminogen activator

activity→Hypofibrinolysis→venous stasis→ LCPD), urban areas, low socioeconomic
status, low nutrition (Mn).

8. SYNOVITIS & SEPTIC ARTHRITIS there is increased

intraarticular pressure leading to altered blood flow and LCPD.

9. HIV.
 PATHOLOGY
Staging by Perthes and Schwarz
1. STAGE OF INCREASED DENSITY:
• There is necrotic bone, dead marrow and
pulverized particles of dead bone in marrow
spaces called trummermehl.

• There is articular cartilage thickening and

subchondral fractures.
 NECROTIC
DENSE TRBECULAE
AND
FLAT
HEAD

ABSENCE OF NUCLEI IN TRABECULAE

2. FRAGMENTATION PHASE:
• There is repair, revascularization and creeping
substitution. New woven bone is laid admixed with
old dead tissue.
• Collapse and resorption if necrotic bone→ Loss of
femoral head height.
• Growth plate is disrupted, irregular and with
columns extending into metaphysis.

3.HEALING PHASE:
• New woven and lamellar bone is formed.
• Normal architecture is regained.
 VASCULAR
FRAGMENTED
CONNECTIVE
AND FLAT
TISSUE, GROWING
HEAD
INTO DEAD BONE

REMNANTS
OF NECROTIC
BONE
IMMATURE
NEW BONE
Findings suggestive of systemic cartilagenous process

• Epiphyseal cartilage below articular cartilage show

hypercellular fibrillated area with increased
proteoglycans, glycoproteins and abnormal collagen
fibrils. Border of lateral physis has large lipid inclusions.

• These are the localized manifestations of a generalizes

transitory epiphyseal cartilage disorder also seen in
vertebral end plates of juvenile kyphosis.

• This abnormal growth, disrupted ossification,

mechanical collapse and subsequent resorption lead to
flat femoral head.
DOUBLE INFARCTION:

• In dog model 2 infarcts with 4wks gap is comparable

to LCPD.

• 2 infarcts sustained at separate time is seen in pts

with LCPD.

• 2 infarcts→ Catterall group II and III

• >2 infarcts→ Catterall group IV
METAPHYSEAL CHANGES:

• Overabundant fatty bone marrow.

• Circumscribed osteolytic lesion with sclerotic

border.

• Wide growth plate with disarrayed ossification with

columns crossing into mataphysis seen as lucensies.

• Extension of growth plate down sid of neck of

femur.
DENSE FATTY PALE BONE MARROW OF METAPHYSIS
 CLINICAL FEATURES
• 2-12yrs (mean age 6yrs)
• Boys : Girls is 3.7 : 1
• Mild symptoms
• Meyer’s disease/dysplasia epiphysealis capitis
femoris is a delayed irregular ossification of
femoral head with out deformation of head.
• It’s a milder form of LCPD.
 Symptoms
• Pain in anterior groin, around GT and referred to
knee sometimes.
• Limp.
• Pain aggravated with activities and decreased with
rest and is more in the later part of day.
• Isolated incident of trauma.
• Waxing and waning of symptoms.
• H/Of ADHD activities (running, jumping and perpetual motion)
• Small stature and thin extremely active
PREDISPOSED CHILD.
• Family history is present in some cases.
 Signs

• Hyperactivity of child leads to other #res (M/C

wrist)
• Gait is a mixture of antalgic and Trendelenburg
type(occurs in late stages).
• Leans the body over involved side to decrease
abductor force and pressure in hip joint.
• Trendelenburg test is positive.
• In late stages there is gluteus, quadriceps and
hamstrings atrophy.
• RANGE OF MOVEMENTS are initially normal.
• As the disease progress Abduction and IR are
restricted.
• In severe cases with flexion hip goes into
obligatory external rotation.
• In late stages adduction contractures are seen.
• Flexion and extension are seldom affected
 Waldenstroms Clinical Stages Of LCPD

Initial stage Fragmentation stage

• 1 to 14 months (mean • 2 to 35 months (mean 8mo)
6months) • Head starts to collapse and
• Mild pain and limp with extrude from acetabulum.
remissions and relapses • Pronounced symptoms and
decreased ROM.
• X ray shows increased
femoral head density and • Rest doesn’t decrease symptoms
subsequent subchondral • Some patients have brief
fractures (salters sign) asymptomatic fragmentation
phase.
• Xray show
fragmentation→lateralization→Fla
ttening
Healing/Reossification stage Healed stage
• 2 to 122 months (mean Delay in reossification of
51months) central segments

• Symptoms start to alleviate. Pian

• ROM remain restricted until Loose fragment and

head is fully ossified. osteocondritis dessicans

• On Xray flattening improves Crepitus, Locking and Popping

and new bone is formed in of joint
subchondral regions.
• NATURAL HISTORY OF DISEASE

→Range from mild to severe forms.

→Symptoms for 12 to 18months→Resolution

→Early onset (<6yrs)– Mild disease, meyers dysplasia

6 to 9yrs– Moderate disease
>9yrs– Severe form

→Poorest results are seen in hips with greatest

radiological evidence of disease.

→More is duration of the disease poor is the outcome

 IMAGING
• Xrays (AP and Frog leg lateral views)
Initial stages
• Cessation of growth of epiphysis with small ossific
nucleus.
• Lateralization of femoral head.
• Increase joint space due to synovitis, thickening of
articular cartilage and ligamentum teres.
• Subchondral linear #res of femoral head on frog leg
lateral view.
• Subsequently head becomes dense.
• Cysts and lucencies in metaphysis.
• Lucencies in ossific nucleus.
• Mean duration 6 months, max 14 months.
Fragmentation phase
• Lucencies are seen in ossific nucleus.
• Central dense fragments are demarcated from medial
and lateral segments of head.
• Later stages new bone is seen in subchondral region.
• Mean duration is 8 months range (2 to 35 months)
• In mild disease fragmentation is seen only in frog leg
lateral views as only anterior segments of epiphysis is
involved
• In still milder forms there is no fragmentation phase
and dense bone phase is followed by new bone healing
phase.
Lt INCREASED BONE DENSITY
WIDENING OF JOINT SPACE. FRAGMENTATION STAGE
Healing Phase
• New subchondral bone.
• Reossification from center to medial and lateral and
last to ossify is anterior part.
• Lucencies are filled with woven bone and later with
trabecular bone.
• Lasts for 51 months
• Head gains round shape
• In late onset disease head is flattened.
Residual stage
• Shape of head evolves and permanent
contour fixed only after completion of skeletal
growth.
• Shape vary from completely normal to flat
head.
HEALING STAGE WITH WIDE EARLY RESIDUAL STAGE WITH
JOINT SPACE AND INCONGRUITY
BICOMPARTMENTAL
ACETABULUM
LATE RESIDUAL STAGE
WITH GOOD JOINT
CONGRUITY.
JOSEPH Radiographic classification of LCPD

→Ia - 4 months- Increased bone density without loss of

epiphyseal height
→Ib - 3 months- Increased bone density with loss of epiphyseal
height

→IIa – 4 months- Early fragmentation

→IIb – 4 months- Advanced fragmentation

→IIIa – 7 months- Early new bone formation

→IIIb – 11 months- Normal texture of >1/3rd of femoral head

→IV – Fully healed

In stage III maximum deformation of head is seen.

 Xray changes in metaphysis
• Initially thought as holes of decalcification or cysts
due to resorption and revascularization.
• Ponseti opined them as to be generated in physis
and fibrillated cartilage stretching into the neck
which is evident on MRI.
• SAGGING ROPE SIGN-Damaged growth plate seen
as radio dense line over proximal femoral
metaphysis.
• Edge of rope is overlarge femoral head projecting
over metaphysis.
METAPHYSEAL CYSTS ON XRAY ON MRI
• SAGGING ROPE SIGN.
 Physeal Abnormalities

• Premature closure or bridging of growth plate is

seen in 1/4th pts with LCPD.

• Central femoral neck physeal premature closure

leads to Short and round neck with GT overgrowth.

• Lateral femoral neck physeal premature closure

cause head tilt laterally, medial neck is longer and
GT overgrowth.
 PHYSEAL BRIDGING

LOSS OF GROWTH
OF UPPER TROCHANTERIC
FEMORAL NECK OVERGROWTH.
AND VALGUS TILT
OF HEAD
Acetabular changes
• Femoral head protrudes out causing
bicompartmentalization of acetabulum.
• Early closure of triradiate cartilage.
• Osteoporosis of actabular roof.

Limited changes on Xray

• Seen in Meyer’s dysplasia and routine classical
stages are not seen.
• Delayed appearance of ossific nucleus, less round
head, anterior part of head flattening and central
notch are some changes seen.
 Bilateral changes on Xray

• Type 1 → Xray findings are exactly same bilateral. This

is seen in multiple epiphyseal dysplasias. Other joints
also must be checked.
• Type 2 → B/L changes are same but fragmentation
occurs only in on hip.
• Type 3 → Classical xray features seen only in one hip
but healed changes are seen in both hips.
• Type 4 → B/L disease with a severe course in one hip

ONLY Type 3 and 4 are true B/L LCPD

 MRI

• Better than xray, Tc scintigraphy and arthrography.

• Gadolinium enhanced subtraction MRI is used to study
revascularization.
• Bipostional MRI is used to study femoral head
sphericity and containment.
• MRI is used to study congruity, containment, cartilage
hypertrophy, physeal involvement, extent of necrosis of
head and revascularization and reperfusion.
• 97 to 99% accuracy and early diagnosis.
• Sequential MRIs correlate with Catterall classification.
De sanctis MRI classification of LCPD based on extent
of head necrosis, lateral extrusion and physeal
disruption.

• Group A→ <50% of head necrosis.

• Group B→ (>50 %) of head is necrosed.

B0 to B3 based lateral extrusion and physeal
disruption. B3 being most severe form.
 Tc Scintigraphy
• Better than Xray
• Classify disease severity based on 1/4th—1/2—
3/4th—full epiphyseal involvement ( Gr1 to Gr4).
Revacularization of Head occurs by

Recanalisation Neovacularisation

“A” Pathway “B” Pathway

Good prognosis Poor prognosis

• Tc sacn can be use to study acetabular events.
Tc SCINTIGRAPHY SHOWING DECREASED UPTAKE FROM LATERAL PART OF EPIPHYSIS
 Arthrography
→Study the congruity of head and acetabulum.
→Study Containment, cartilage thickening, Joint space and
currently best used to study hinge abduction.

USG
→Study early stages of disease , joint effusion and cartilagenous
part of head.
→Doppler and microbubble contrast enhanced USG can be used
to study femoral head blood flow.

CT Scan
→Obtain 3D images of head and acetabulum.
→In later stages used to evaluate pain, locking and mechanical
symptoms.
→Delineate b/w incomplete ossification vs osteochondrotic
lesion
 “HEAD AT RISK”
• Correlated positively with poor results especially in patients in
groups II, III, and IV.

(1) Lateral subluxation of the femoral head from the

acetabulum.

(2) Speckled calcification lateral to the capital epiphysis.

(3) Diffuse metaphyseal reaction (metaphyseal cysts).

(4) A horizontal physis.

(5) Gage sign, a radiolucent V-shaped defect in the lateral

epiphysis and adjacent metaphysis
 CLASSIFICATIONS

EARLY CLASSIFICATIONS
• Legg classified LCPD based on shape of head
cap type and mushroom type(poor prognosis).

• Waldenstroms Type 1 and 2 good prognosis

and type 3 poor prognosis.

• Goff classification based on shape of head

Spherical / Cap / Irregular.
 Catterall Classification
• Milestone in treatment decision for LCPD
• Done during stage of fragmentation
• Low degree of interobserver agreement

Group 1→ Anterior portion of epiphysis only affected.

Group 2→Anterior and central sequestrum is seen.
Head may collapse but height is maintained.
Group 3→Most of epiphysis is sequestered except
medial and lateral ends
Group 4→Entire head sequestered
 Lateral Pillar Classification

• Femoral head has medial, central and lateral pillars which are
separated during stage of fragmentation.
• Lateral pillar remains intact and support weight bearing when
central pillar collapses

(A) → Minimal density change and no loss of height of lateral

pillar. Good prognosis.

(B) → Lucency and loss of height <50% in lateral pillar. Central pillar
collapse is present. Intermediate prognosis.

(B/C) → Very narrow lateral pillar of height >50% of normal or

normal thickness with Height of 50% of normal.

(C) → No separation between central and lateral pillars and lateral

pillar is lower height than central. Poor prognosis.
 LATERAL PILLAR
A B
B/C C
 CLASSIFICATION OF END RESULTS

• Mose classification: Done by fitting contour femoral head into a template of

concentric circles. Head deviates no more than 1mm from a given circle on
AP and lateral views

STULBERG CLASSIFICATION
( I ) → Normal Hips

( II ) → Deviation from circle is <2mm in AP and Lateral views

( III ) → Elliptical femoral head with >2mm deviation

( IV ) → Head flattening is seen with >1cm flattening over weight bearing

area. Normal flexion and extension. Abduction and rotations restricted.
Types (III) and (IV) Acetabulum and head are matching and “congruous
incongruity” is seen.
( V ) → “Incongruous incongruity”. Similar to AVN. Head is collapsed and
acetabular contour doesn’t match with head.
 Salter Thompson Classification
• Subchondral fracture in the superolateral portion of
the femoral head.

• Extent of the fracture (line) is less than 50% of the

superior dome of the femoral head is type A, and
good results can be expected.

• If the extent ofthe fracture is more than 50% of the

dome, the involvementis considered type B, and fair
or poor results can be expected
STULBERG 4
DIFFERENTATING STULBERG II AND III
(II) → Good prognosis.
(III) & (IV) → Mild to moderate degenerative
changes in adulthood.
(V) → Painful arthritis in early adulthood.
 Poor Prognostic Findings of LCPD

• Lateralization of head.

• Catterall 3 and 4 groups.

• Lateral calcification

• Saturn phenomenon- Lucent ring around epiphysis.

• Widening of femoral head and neck before

fragmentation.
 Differential Diagnosis
• AVN
• SCFE
• Multiple epiphyseal dysplasias
• Hypothyroidism (pseudofragmentation are seen which are
multiple ossification centres.
• Syndromes like Moquio, maroteaux-lamy, Schwartz-jampel,
trichorhinopharyngeal syndrome and osteochondromatosis
etc.
• Fracture
• Osgood Schattler disease
• Septic/reactive arthritis
• Rheumatic fever
• Lyme’s disease
• Toxic synovitis etc.
 TREATMENT
Based on lateral pillar classification and age of
onset of disease:
• Before 8yrs→ Symptomatic treatment in all
types.
• Group A >8yrs→ Symptomatic Rx
• Group B and B/C >8yrs→ Surgical RX
• Group C >8yrs→ Do not improve with or
without surgery. Outcome is Stulberg IV in
most of pts.
 SYMPTOMATIC TREATMENT
• Bed rest most effective in early stages before
subchondral #

• Traction for days to weeks until hip ROM improves.

Traction in extension there is increased
intraarticular pressure. 30 t 40 degree flexion and
slight ER is best suited for traction.

• Partial/non weight bearing and crutches.

• NSAIDS.
 CONTAINMENT
Hold the head in acetabulum during period of
biological plasticity while necrotic bone is resorbed
and living bone is restored through creeping
substitution.
• Femoral head is 125% of hemisphere and acetabulum is
75% of hemisphere. At a time only 63% femoral head is in
contact with
acetabulum.

• Containment treatments have no mechanical advantage.

Their main purpose is to hold the head in acetabulum
during healing.
 Orthotics for Containment
• Restore normal ROM of irritable hip by rest
and traction before applying orthotic.

• Orthotic must keep hip in abduction and allow

some amount of movement in hip.
Petries casts:
• 45 degree abduction &
5-10 degree IR.
• Bars b/w legs.
• Changed every 3-
4months to mobilize
knee and ankle.
• Continued till good
healing on xray (Avg 19
months).
Toronto brace:
• Heavy and complex.
• Allows hip and knee
flexion.
• Pt can sit and stand.
• Universal joint at the
base is often worn out.
Birmingham brace
• Provide perfect
immobilization.
• Leather corset keeps hip
in abduction and IR.
• Special crutch for
clearance to abduction
• Padlock and chains keep
knee in flexion and
provides non weight
bearing.
Newington brace
• Metal A frame.

• Complicated design.

• Reproduces Petrie’s
casts
Atlanta Scottish Rite Brace
• M/C used now.
• Has metal pelvic band,
hip hinges and thigh cuffs.
• Extensile bar b/w thighs
to allow abduction and
restrict adduction.
• Relative gives quicker
results and early ability to
walk.
• Generally required for 9
months to 1 yr.
 SURGERIES
→Timing- Early fragmentation phase.
• Varus derotation osteotomy
• Innominate osteotomy
• Chiari Osteotomy
• Shelf procedures
• Arthrodiastasis
• Valgus osteotomy
• Cheilectomy
• Trochanteric advancement or epiphysiodesis for GT
overgrowth.
 Femoral Osteotomy

• Restore ROM in irritable hip before surgery.

• Timing of Sx→ During early stages of

fragmentation.

• Post op varus should be 100 to 110 degrees ideally.

Complications
• Excessive varus.
• Persistence of ext rotation.
• Shortening
• Abductor lurch and limp
• GT overgrowth
• Fixation complications like non union
• Loss of external rotation and abduction.
• Decreased articular and trochanteric distance
leading to Trendelenburg gait.
 SALTER INNOMINATE OSTEOTOMY
Indications→ Moderate to severely affected head, age
>8yrs and loss of containment.

Prerequisites→ Minimum deformity of head, non

irritable hip, No/minimal restriction of hip
movements.

Complications→ Loss of fixation, displacement of

distal fragment, limb lengthening, decreased flexion,
joint stiffness and hinge abduction.
 Arthrodiastasis
• Distraction of the joint widens,
unloads the joint space,
reduces the pressure on the
femoral head, allows fibrous
repair.
• Hip Orthofix external fixation
device.
• Immediately distract the joint
space 4 to 5 mm & Continue
distraction at 1 mm per day
until the Shenton line is
overcorrected.
Combined Femoral and Innominate Osteotomy:
Done is severe cases with lateral subluxation,
calcification and metaphyseal changes. Provides
greater femoral coverage.

Valgus osteotomy:
Main indication is Hinge abduction i.e head and and
acetabulum are congruent in adduction but
incongruent in neutral and abduction positions.
This sugery improves gait, roundness of head, healing
of central fragment, decrease subluxation, increased
joint space, good limb length and motion.
 Chiari Osteotomy
Provide coverage of a large flattened femoral head in
an older child when the femoral head is subluxating
and painful.
 Shelf Arthroplasty
• Used for older children who
are not candidates for
femoral osteotomy because
of insufficient remodeling
capacity.
• It is used to give coverage for
COXA MAGNA
Beneficial effects:
(1) lateral acetabular growth
stimulation.
(2) prevention of subluxation.
(3) shelf resolution after
femoral epiphyseal
reossification.
 Cheilectomy
LCPD child is sometimes left with a malformed
femoral head, usually a large mushroom shape
(coxa plana) or a lateral protuberance of the
femoral head outside the acetabulum.

This excess is excised and this is called cheilectomy.

Though short term results are good, long term

results are not satisfactory. Myositis ossificans
occurs at the site
 TROCHANTERIC OVERGROWTH
• In Perthe’s GT over growth is due to premature closure of femoral
capital epiphysis.
Consequences
• Elevation (overgrowth) of the trochanter decreases tension and
mechanical efficiency of the pelvic and trochanteric muscles.
• Trochanter coming closer to the center of rotation of the hip,
decreases the lever arm and mechanical advantage of the muscles.
• Line of pull of the muscles becomes more vertical, increasing the
pressure forces concentrated over a diminished areaof hip joint
surface.
• Impingement of the trochanter on the rim of the acetabular roof
during abduction.

• Transfer of the greater trochanter distally restores normlacy and

avoids above complications.
 Osteochondrotic lesion of femoral head

Loose body Softened fibrocartilage

Delineated by arthrography

Removed by arthroscopy Drilling the affected

Or arthrotomy and area triggers ingrowth
Debridement of lesion of blood vessels and
Bed healing