Bone develops by transformation of pre-existing
When bone formation occurs in primitive connective
tissue it is called intramembranous ossification.
Ex:-The bones with vault of skull,maxilla,majority of
mandible and the clavicle.
When it takes place in pre-existing cartilage it is called
Ex:-Long bones,vertebrae,pelvis and bones of the base
Endochondral ossification is responsible for the
initial bone development from cartilage in utero and
infants and the longitudinal growth of long bones in
the epiphyseal plate.
The plate's chondrocytes are under constant division
These daughter cells stack facing the epiphysis while
the older cells are pushed towards the diaphysis.
As the older chondrocytes degenerate, osteoblasts
ossify the remains to form new bone.
In puberty increasing levels of estrogen&cotisol, in
females and males respectively, leads to increased
apoptosis of chondrocytes in the epiphyseal plate.
Depletion of chondrocytes due to apoptosis leads to
less ossification and growth slows down and later
stops when the entire cartilage have become replaced
by bone, leaving only a thin epiphyseal scar which later
Once the adult stage is reached, the only way to
manipulate height is modifying bone length via
The epiphyseal plate (or physeal plate, physis, or
growth plate) is a hyaline cartilage plate.,its an area of
developing tissue near the ends of long bones in
between the widened part of the shaft of bone (the
metaphysis) and the end of the bone(the epiphysis).
The growth plate regulates,helps and determines the
length and shape of mature bone.
The long bones of the body do not grow from the
Instead growth occurs at each end of the bone around
the growth plate.
The growth plate is the last portion of the bone to
ossify.,which leaves it vulnerable to fractures.
The growth plate is composed of cartilage cells which
are arranged in well ordered long columns seperated
from each other by an intracellular matrix of loosely
packed collagen fibres containing proteoglycans.
The columns are parallel to each other and to the axis
of growth of each particular bone end.
2.Zone of proliferating cartilage
3.Hypertrophic cell zone(maturation zone)
4.Zone of provisional calcification.
immediately adjacent to epiphysis.Its a germinal
layer.Ratio of extracellular matrix to cell volume is
high.Injury to this layer leads to cessation of growth.
Zone of Proliferating cartilage:-Location in which
bone length is created by active growth.mitotic activity
takes place here and cells are aligned to welldifferentiated columns called as Zone of cellular
Hypertrophic Zone:-No active growth in this
layer.chondrocytes begin to get differentiated.Cells
nearer the metaphysis begin to undergo changes that
ultimately lead to their calcification process.
Zone of provisional calcification:-It is in this area
the extracellular chondroid matrix becomes
impregnated with calcium salts&development of bony
vasculature occurs in this stage of bone formation.
Disorders affecting growth plate
They can be classified as
Osteochondrodysplasias refer to abnormalities of
cartilage or bone growth and development.
They are divided into
i)Defects of the growth of tubular bones and/or spine
which are frequently referred to as chondrodysplasias.
ii)Dysostoses refers to malformations of individual
bones,single or in combination and does not refer to a
generalized disorder of skeleton.
The chondro-osteodystropathies can be broadly
classified according to the recognizable clinical and xray findings.,as follows: 1.Dysplasias with predominantly physeal and
2.Dysplasias with predominant epiphyseal changes.
Dysplasias with predominant
physeal and metaphyseal changes
In these disorders there is abnormal physeal
growth,defective metaphyseal modelling and
shortness of tubular bones.
The axial skeleton is also affected but the limbs are
disproportionately short compared to spine.
The conditions are:-
This is the most common&least disfiguring of all the
The underlying fault is unrestrained transverse growth
of the physeal plate.
The condition is transmitted as autosomal dominant
Mutations are seen on the chromosomes 8,11 and 19.
i)poorly modelled,broadened metaphysis,with sessile
or pedunculated exostoses arising from the cortices.
ii)A bony mottled appearance around a bony
excrescence indicates calcification in the cartilage cap
iii)The distal end of ulna is sometimes tapered or
carrot shaped and reduced in length and the radius is
usually bowed and this discrepancy may lead to sublaxation of radiohumeral joint.
TREATMENT: If the deformities of forearms or legs is so severe which
demands osteotomy.,it should be postponed till late
In this condition.,the adult height is usually around 122
This is the commonest form of abnormal short stature.
Severe,disproportionate shortening of limb bones may
be diagnosed by x.ray before birth.
The main pathology lies in the abnormal
endochondral longitudinal growth.
The physis show diminished,and less regular cell
proliferation which accounts for diminished length of
Achondroplasia occurs in about 1 in 25,000 births.
There is autosomal dominant inheritance
The main fault is the point mutation in the gene coding for
fibroblast growth factor receptor 3.,which plays key role in
endochondral cartilage growth.
X-ray findings:-i)The tubular bones are short,with wide
metaphysis and physeal lines are irregular.,with normal
ii)The proximal limb bones are disproportionately
affected(rhizomelia),changes are also seen in wrist and
hands,where the metaphyses are broad and cupshaped.
These features are best defined on CT/MRI.
This is a very mild form of achondroplasia.
There will be shortness of stature and noticeable
Head&face are not affected.
X-ray may show slight pelvic flattening and thickening
of long bones
This condition is transmitted as autosomal dominant
Lower-limb lengthening surgery can be done in few
cases with considerable chance of success.
This condition also is transmitted as an autosomal
In this disorder there is disproportionate shortening of
limbs.,but it is mainly the middle segments(forearms
and legs)which are affected.
Stature is reduced but not as markedly as in
The most characteristic X-ray findings are shortening
of forearms and leg bones,bowing of radius and which
may reqiure operative treatment.
This describes a type of short limbed dwarfism in
which bony abnormality is virtually confined to
The epiphysis are unaffected but the metaphyseal
segments adjacent to the growth plates are broadened
and mildly scalloped.,somewhat resembling rickets.
Operative correction by osteotomy may be required for
coxavara or tibiavara.
This is a rare but easily recognized disorder in which
there is defective transformation of physeal cartilage
columns into bone.
C/F:- i)Typically this disorder is unilateral.,indeed only
one limb or even one bone is involved.
ii)An affected limb is short,and if the growth plate is
asymmetrically involved,the bones grows bent.
The condition is not inherited,indeed it is probably an
embryonal rather than a genetic disorder.
The characteristic X-ray change is radiolucent
streaking extending from the physis into the
metaphysis.,the apperance of persistent,incompletely
ossified cartilage columns trapped in bone.
If only half the physis is affected,growth is
asymmetrically retarded and bone becomes curved.
Rx:-Bone deformity may need correction but it should
be deferred until growth is complete otherwise it is
likely to recur.
This rare disorder is characterized by development of
multiple enchondromas and soft tissue hemangiomas
of skin & viscera.
Lesions appear during childhood; boys and girls are
affected with equal frequency.
Patients with maffucci’s syndrome should be
monitored regularly throughout life for any change in
bone or visceral lesions because.,
There is a strong tendency for malignant change to
occur in both soft-tissue and bone lesions; the
incidence of sarcomatous transformation in one of the
enchondromas is probably greater than 50 per cent,but
fortunately these tumours are not highly malignant
Dysplasias with predominantly
This group of disorders is characterized by abnormal
development and ossification of epiphysis,resulting in
distortion of bone ends.
Various dysplasias are enlisted as follows
1.Multiple Epiphyseal Dysplasia
3.Dysplasia epiphysealis Hemimelica
4.Chondrodysplasia Punctata(Stippled Epiphysis)
Multiple Epiphyseal Dysplasia
Multiple epiphyseal dysplasia (MED) varies in severity
from a trouble-free disorder with mild anatomical
abnormalities to a severe crippling condition.
There is widespread involvement of the epiphyses but
the vertebrae are not at all, or only mildly affected.
C/F:-Children are below average height and the
parents may have noticed that the lower limbs are
disproportionately short compared to the trunk
X-Ray:-Changes are apparent from early childhood.
Epiphyseal ossification is delayed, and when it appears it is
irregular or abnormal in outline.
In the growing child the epiphyses are misshapen; in the
hips this may be mistaken for bilateral perthe’s disease.
The vertebral ring epiphysis may be affected,but only
Genetics:-This appears to be a heterogenous disorder but
most cases have an autosomal dominant pattern
Management:-At maturity,deformity around the hips,knees
or ankles sometimes require corrective osteotomy.
The term ‘spondyloepiphyseal dysplasia’ (SED)
encompasses a heterogeneous group of disorders in
which multiple epiphyseal dysplasia is associated with
wellmarked vertebral changes – delayed ossification,
flattening of the vertebral bodies (platyspondyly),
irregular ossification of the ring epiphyses and
indentations of the end-plates (Schmorl’s nodes).
The mildest of these disorders is indistinguishable
from MED; the more severe forms have characteristic
This autosomal dominant disorder can be diagnosed
in infancy.,the limbs are short,but the trunk is even
shorter and the neck hardly there.
X-Ray shows widespread epiphyseal dysplasia and
characteristic vertebral changes.
Odontoid hypoplasia is common and may lead to
atlanto-axial sublaxation and cord compression.
Management may involve corrective osteotomies.
An X-linked recessive disorder, SED tarda is much less
severe and may become apparent only after the age of
5 years when the child fails to grow normally and
develops a kyphoscoliosis.
X-rays show the characteristic platyspondyly and
abnormal ossification of the ring epiphyses, together
with more widespread dysplasia.
Treatment may be needed for backache or (in older
adults) for secondary osteoarthritis of the hips.
This is a curious “hemidysplasia” affecting only one
limb and only one half(the medial or lateral half) of
It’s a sporadic disorder which usually appears at the
ankle or knee.
The child (most often a boy) presents with a bony
swelling on one side of the joint; several sites may be
affected – all on the same side in the same limb, but
rarely in the upper limb.
X-rays show an asymmetrical enlargement of the bony
epiphysis and distortion of the adjacent joint. At the
ankle, this may give the appearance of an abnormally
large medial malleolus.
Treatment is called for if the deformity interferes with
joint function. The excess bone is removed, taking care
not to damage the articular cartilage or ligaments.
Chondrodysplasia punctata (or Conradi’s disease) is a
generalized, multisystem disorder producing facial
abnormalities, vertebral anomalies, asymmetrical
epiphyseal changes and bone shortening.
These children die during infaancy due to the associated
The characteristic x-ray feature is a punctate stippling of
the cartilaginous epiphyses and apophyses.This disappears
by the age of 4 years but is often followed by epiphyseal
irregularities and dysplasia.
Orthopaedic management is directed at the deformities
that develop in older children: joint contractures,limb
length inequality or scoliosis.
The polysaccharide GAG’S form sidechains of
macromolecular Proteoglycan’s,a major component in
bone matrix,cartilage,inter-vertebral discs &
Defective PG’S are degraded by lysosomal enzymes.
Any deficiency of these enzymes causes a defective
degradative pathway and leads to accumulation of
PG’S & irregular bone matrix.
C/F:-Excessively short stature with vertebral
deformity,coarse facies,hepatosplenomegaly and
mental retardation in some cases.
All except Hunter’s syndrome (an X-linked recessive
disorder) are transmitted as autosomal recessive.
X-Ray show bone dysplasia affecting the vertebral
bodies,epiphyses and metaphysis;typically bones have
a spatulate pattern.
Rickets is a condition characterized by defective
mineralization of bone matrix which is seen
histologically as excessive unmineralized osteoid.
Rickets refer to the condition where it occurs before
closure of growth plate so that abnormalities of
skeletal growth are super-imposed.
Aetiology-1.Deficiency of vit.D
The bones are soft and porotic,bend easily due to body
weight or external forces.
Normally epiphyseal line of long bone is a well-defined
strip of narrow cartilage 2mm deep.,but in rickets it
forms a wide irregular band and the metaphysis is
broad & irregular from excessive proliferation of cells
of epiphyseal line.
The cartilage in the proliferating zone is
hyperplastic,but instead of normal palisade
arrangement of cells,they are aranged more hapazardly
and the extent of zone is increased.
In the zone of calcified cartilage,the deposition of
calcium in intercellular matrix is greatly deficient or
In the zone of ossification.,the bone deposited by the
osteogenic cells from the diaphysis is poor in quality.
In the metaphysis,the bony trabeculae are weakened
by lack of calcium,the continued strain stimulates the
connective tissue hyperplasia so that the extremity of
bone appears mis-shapen and unmodelled.
1.Large head,open fontanelles & craniotabes
3.Seperation of recti muscles over the protuberant
6.Beaded ribs-the rickety rosary
7.Bowing of long bones with genu valgum
8.Delayed dentition with irregular,soft decaying teeth
9.pale skin,flabby subcutaneous tissue,typical wizened
1.Acute Stage-Normal rounded appearance of epiphysis is
replaced by a cloudy area containing one or more indistinct
centres of ossification.
2.Second Stage-Epiphysis appears as a mottled irregular,illdefined shadow.The metaphysis is ragged but is now
broader than normal.
3.Third Stage-The shadow becomes denser and at the end
of metaphysis a dense line appears.
4.Fourth stage-The characteristic increase in breadth of
metaphysis is still present,but the bone is now clearly
defined & shows normal content of calcium salts.
Treatment by 3 modalities: 1.Medical
2.Prevention of deformity-when the bones are so soft
that they are easily bent by pressure/muscle
strain,child’s movements should be controlled that
little or no pressure is exerted on limbs.In difficult
children it is often advisable to fit ‘rickets’ splints.
3.Treatment of existing deformity-Deformity is usually
corrected by splints or by osteotomy.
Renal Bone Diseases
Patients with chronic renal failure develop
abnormalities of skeletal homeostasis,termed renal
osteodystrophy which are not cured and may even get
severe by dialysis which can cause dialysis arthropathy
and systemic amyloidosis.
The bone changes are due to combination of
peripheral new bone formation.The bone changes are
associated with extraskeletal calcification.
C/F:-stunted growth,very low body weight,dwarfism at
puberty,toxic inhibition of growth plates,slip of the
capital femoral epiphysis.
Radiological changes:-Changes may be absent in early
condition.,but becomes evident as disease progresses.
The characteristic feature of hyperparathyroidism is
bony erosion which commonly affects the tufts of
femoral phalanges where collapse of overlying soft
tissue may cause clubbing.
Periarticular phalangeal erosions are also common &
erosions may also involve proximal tibia,neck of femur
or humerus and outer end of clavicle.
The Lignac-Fanconi Syndrome
In this,there is proximal tubular deficiency with
polyuria,polydypsia,anorexia & vomiting.
The children exhibit rickets as well as dwarfism and
usually die before puberty.
The primary lesion appears to be an impaired
reabsorption of glucose and phosphate because of
some failure of phosphorylation in tubules.
Massive doses of Vit.D may improve the skeletal
This is an inherited rachitic disease of bone as a
marked mineralization disturbance with the bony
changes in the long bones and skull.
Radiographically and patholgically the lesion suggests
severe rickets with dwarfism.
There is a large urinary excretion of
phosphoethanolamine without the other aminoacids
commonly seen in other forms of renal rickets.
Large doses of Vit.D will improve radiographic
appearances,with a fall in alkaline phosphatase levels.
The various hormonal disorders which affect the
growth plate are: 1.Hypopituitarism
The clinical effects of these hormonal imbalances
mainly depend upon the stage of skeletal maturity at
which the abnormality occurs.
Anterior pituitary hyposecretion results in development of
two distinct clinical disorders.
1.Lorain Syndrome:- The predominant effect is on
Proportionate dwarfism is seen.,sexual development may
2.Frohlich’s adiposogenital syndrome:-There is delayed
skeletal maturity associated with adiposity and immaturity
of the secondary sexual characters.
weakness at the physis combined with disproportionate
adiposity may result in epiphyseal
displacement(epiphysiolysis/slipped epiphysis) at the hip
Investigations should include direct assays & tests for
X-Rays of skull may show pituitary fossa expansion &
erosion of adjacent bones.CT/MRI may reveal the
Treatment:-If the cause is a tumour and its
identified.,it can be removed or ablated.
The deficiency of GH can be overcommed by
administration of somatotropin and response is
checked by serial growth plots.
Cause-Oversecretion of GH due to acidophil adenoma.
GH over secretion causes excessive growth of entire
skeleton in children & adolescents.
Its quite easy to diagnose the patients early and its
important to track child’s development by regular
clinical & x-ray examination as the patient may
develop deformity of hip due to epiphyseal
There may be mental retardation & sexual immaturity
Treatment-early removal of pituitary tumour.
The effects depend on the age of onset.
1.Congenital hypothyroidism(cretinism)-child becomes severely
dwarfed and mentally retarded
X-rays may show irregular epiphyseal ossificaion.
Child should be treated immediately wih thyroid hormone
2.Juvenile hypothyroidism-its usually less severe than congenital
Growth & sexual development are retarded.
X-rays show typical epiphyseal fragmentaion apperance.
The growth plate is disorganized in the reserve zone
chondrocytes & proliferating chondrocytes.
Acute osteomyelitis-almost invariably a disease of
children.,organisms usually settle in metaphysis,most often
in proximal tibia or at proximal/distal femur.
C/F:-severe pain,fever,malaise & toxaemia in neglected
Metaphyseal tenderness and resistance to joint movement
can be seen.
Multiple infection sites are uncommon.
Diagnostic Imaging-X ray may show a faint extra-cortical
outline due to periosteal new bone formation.,classical
x.ray sign of pyogenic osteomyelitis.
USG-may detect a sub-periosteal collection of fluid in
the early stages of osteomyelitis.
Radioscintigraphy with 99Tc-HDP.
MRI can distinguish soft tissue infection from
Typical feature is a reducd intensiy signal in T2weighted images.
Aspiration of pus from the metaphyseal sub-periosteal
abscess or adjacent joint.
Treatment & Complications
Rx:-supportive treatment for pain and hydration
Splintage of affected part
Complications:-Altered bone growth in
infants,physeal damage may lead to arrest of growth
and shortening of bone.
In older children.,the bone occasionally grows too long
because metaphyseal hyperaemia has stimuated the
In children.,over 10% of fractures may involve injury to
the growth plate.,as the physis is relatively weaker part
If the fracture traverses the celluar reproductive layers
of plate,it may result in pre-mature ossification of the
injured part & serious disturbances of bone growth.
Physeal fractures usually results from falls/traction
X-rays:-comparision with the other normal side gives the
valuable details about the fracture as the epiphysis itself is a
Tell-tale features are widening of epiphyseal incongruity of joint
or tilting of epiphyseal axis.
Rx:-Displaced fractures should be reduced as soon as possible.
With types 1 & 2.,this can usually be done closed;the part is held
splinted securely for 3-6 weeks.
Type 3 & 4 require perfect anatomical reduction as they may
result in premature fusion/asymmetrical growth of bone end.
Type 5 fractures causes premature fusion and retardation of
1.Samurl L.Turek-Text book of Orthopaedics
2.Apley’s sysem of orthopaedics & fractures
3.Mercer’s orthopaedic surgery