A description of the development, anatomy, physiology, factors influencing its growth, pathology and disorders affecting physis in brief

1. Physeal Cartilage
Dr.Anandu Mathews Anto,MBBS
Orthopedics Resident
Government Medical College Kottayam

2. Content
• Structure and Composition
• Growth influencing factors
• Pathology
• Injury
In detail
briefly

3. 1. The physis
Primary function of growth cartilage
Primary function of growth cartilage is the continuous and controlled
elaboration of a solid scaffold (calcified cartilage) in preparation for
bone deposition.
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Embryological development
The cartilaginous precursors (anlagen) of the long
bones appear early in embryonic life.

4. The cartilaginous anlage is invaded in its central
segment by blood vessels.
This process results in ossification of the
cartilage, producing the early diaphyseal bone.
The histological specimen here is of a young rat’s
tibia.

5. By 13 weeks, in the human fetus, the
primary ossification in the diaphyses can
be seen clearly.

6. Postnatal development
Postnatally, the next skeletal event is the
invasion of the cartilaginous end caps
(epiphyses) by blood vessels, resulting in
the formation of the epiphyseal ossific
nuclei (secondary ossification centers).

7. 2. Physeal structure
The cartilaginous zones between the bony
diaphysis and the ossifying epiphyses
differentiate into complex chondral organs –
the physes.
Each physis is highly organized into
transverse zones

8. Physeal zones
These zones are respectively, from epiphysis to
metaphysis:
The reserve zone
The zone of proliferation
The zone of hypertrophy
The zone of provisional ossification
Each zone contributes different aspects of
longitudinal growth.

9. Vascular anatomy of physis
Trueta, of Oxford, England, first described the
vascularity of the physis. He noted that no
significant vessel pierced the physeal disc and
that there exist no significant anastomoses
between the epihyseal and metaphyseal vascular
trees within the bone.

10. The portion of the physis adjacent to the
epiphysis is nourished by diffusion from the
epiphyseal circulation and the zone of
provisional ossification is supplied by the
metaphyseal circulation.

11. The effect of this is that any shearing
disruption of the physis, which usually occurs
through the zone of hypertrophy, leaves each
of the separated portions of the physis with a
functional vascular supply.
1.The reserve zone and the proliferation zone are rich
in surrounding ground matrix and hence the cells are
attached strongly to each other.
2. The zone of calcification is strong due to the calcium
deposits
Hence the relatively weaker area is the zone of
hypertrophy where the cells are hypertrophying with
minimal matrix tissue
why through the zone of hypertrophy?

12. There are some epiphyses that are totally covered by articular
cartilage, notably at the proximal femur and the proximal
radius, where the vessels feeding the epiphysis are bound
down tightly to the perichondrium of the periphery of the
physis.
In such sites, a shear injury of the physis is highly likely to
devascularize the epiphysis and thereby deprive the reserve and
proliferating zones of the physis of nutrition. This commonly results in
physeal growth arrest and avascular necrosis of the affected
epiphysis.
Dale and Harris Type of blood suppy-TYPE A

13. Dale and Harris Type of blood suppy-TYPE B

14. 3. Functional anatomy of
growth cartilages
The reserve zone of the physis lies adjacent to the bone of
the secondary ossific center: it comprises small, scattered
round cells, densely nucleated, and with an abundant
endoplasmic reticulum, a clear indication that they are
actively synthesizing protein.
Their function remains obscure – they do not proliferate at
any rate that could contribute to the cell populations of the
other zones of the physis.
Longitudinal growth

15. The proliferating zone of the physis is the zone in
which the cells reproduce more rapidly and the
more mature ones align themselves in columns, in
preparation for hypertrophy.

16. The proliferating zone cells are the
fundamental “power-house” of the
physis. If they cease to reproduce, for
example if deprived of nutrients as a
result of lost blood supply to the
epiphysis, then longitudinal growth will
cease.

17. In the hypertrophic zone, the
cells are aligned in columns.

18. The hypertrophic cells each
lie in a lacuna, separated
longitudinally by septa and
laterally by interterritorial
matrix.

19. As the cells mature, they enlarge: this
enlargement is greater in length than in
width and it is this increase in their
longitudinal dimensions that is the
principle factor resulting in longitudinal
bone growth.

20. The most mature hypertrophic cells lie
adjacent to the zone of provisional
ossification.
At this junction the hypertrophic cells
undergo programmed cell death –
apoptosis.

21. The programmed cell death begins with the ingrowth
of capillary buds into the cell lacuna.
Also at this level, the septa and the interterritorial
matrix start to calcify.

22. Cells within the walls of the invading capillaries
send pseudopodia through the adjacent
septum into the lacuna of the most mature
hypertrophic cell, which then dies.
This is an active process, triggered by a
stimulus that is ill-understood.

23. The interterritorial matrix of some of
the cylinders occupied by the
capillary loops, is broken down by
chondroclasts, thereby enlarging the
channels.

24. Diametric growth
There is a specialized fibrous area surrounding the periphery of the
growth plate, comprising the groove of Ranvier and the perichondrial
ring of LaCroix. There are cells in this area that are specialized
chondrocytes, which increase laterally by appositional growth, thereby
resulting in an increase in the diameter of the physis as maturity
progresses.

25. Polarity of physeal plate

26. Growth influencing factors
Factors
Local
chemical/hormones
Systemic
chemicals/hormones
Mechanical

27. 1.Growth Factors and Local Regulators Associated with Growth Plate Maturation and/or Epiphyseal Fu
Ihh-indian headge hog
Runx- a transcription factor

28. Local Factors influencing bone
growth

29. • 2. Hormones Involved in Growth Plate Maturation and
Epiphyseal Fusion-
• Estrogen-promote accelerated physeal senescence
• androgen-stimulate growth in early age and accelerate physeal
closure in late phase of puberty
• growth hormone
• IGF-1

30. Mechanical factors
• Heuter-Volkmann law-history
In the skeletally immature, bone growth is relatively inhibited in areas of
increased pressure and relatively stimulated in areas of decreased pressure or
tension.
Also, the rate of inhibition during compression across physis is more than the
rate of bone growth when distraction is applied across physis

31. Pathology
• Disorders affecting growth plate can be classified as
• Developmental dysplasias
• Metabolic
• Hormonal
• Infections
• traumatic

32. Developmental Dysplasias
• Osteochondrodysplasias refer to abnormalities of cartilage or bone
growth and development
How to evaluate disproportionate short stature
1.Full set of xrays of skull,spine,pelvis,extremities,hands,feet
2.Identify location of lesion within each bone-
epiphysis,metaphysis,diaphysis
3.Recogonition o unique pattern of abnormal skeletal ossification
4.Review of serial radiographs taken at different age

33. Histopathology
-SOX9 gene mutation causes dysplasia-short and curved bones
-FGFR3 gene mutation causes
chondroplasia,hypochondroplasia,thanatophoric dysplasia
-PTHR1 mutation causes metaphyseal dysplasia
-RUNX2 gene mutation causes cleidocranial dysplasia

34. ⚫The chondro-osteodystropathies can be broadly classified
according to the recognizable clinical and x- ray
findings.,as follows:-
⚫1.Dysplasias with predominantly physeal and
metaphyseal changes
⚫2.Dysplasias with predominant epiphyseal changes.

35. 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:-

36. ⚫Hereditary multiple exostosis(Disphyseal Aclasis)
⚫Achondroplasia
⚫Hypochondroplasia
⚫Dyschondrosteosis
⚫Metaphyseal chondroplasia(Dysostosis)
⚫Dyschondroplasia(Enchondromatosis;Olliers disease)
⚫Maffucci’s syndrome

37. Hereditary Multiple
Exostosis(Disphyseal Aclasias)
⚫This is the most common&least disfiguring of all the
skeletal dysplasias.
⚫The underlying fault is unrestrained transverse growth of
the physeal plate.
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

39. Achondroplasia (Autosomal dominant)
⚫In this condition.,the adult height is usually around 122
cm(48 inches)
⚫This is the commonest form of abnormal short stature.
⚫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
tubular bones.

40. ⚫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
epiphysis.
⚫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.

41. Hypochondroplasia
⚫This is a very mild form of achondroplasia.
⚫There will be shortness of stature and noticeable
lumbar lordosis.
⚫Head&face are not affected.

42. Dyschondrosteosis
⚫autosomal dominant defect.
⚫disproportionate shortening of limbs.,but it is mainly the
middle segments(forearms and legs)which are
affected(mesomelia).
⚫Stature is reduced but not as markedly as in
achondroplasia.
⚫The most characteristic X-ray findings are shortening of
forearms and leg bones,bowing of radius and which may
reqiure operative treatment.

43. Metaphyseal chondroplasia (Dysostosis)
⚫This describes a type of short limbed dwarfism in
which bony abnormality is virtually confined to
metaphysis.
⚫The epiphysis are unaffected but the metaphyseal
segments adjacent to the growth plates are broadened and
mildly scalloped.,somewhat resembling rickets.

44. Dyschondroplasia
(Enchondromatosis;Ollier’s disease)
⚫defective transformation of physeal cartilage columns
into bone.
⚫ 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.

45. ⚫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.

46. Maffucci’s
Syndrome
⚫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.

47. Dysplasias with predominantly epiphyseal
changes
⚫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
⚫2.Spondyloepiphyseal Dysplasia
⚫3.Dysplasia epiphysealis Hemimelica
⚫4.Chondrodysplasia Punctata(Stippled Epiphysis)
⚫5.Mucopolysaccharidoses

48. Multiple Epiphyseal Dysplasia
⚫There is widespread involvement of the epiphyses but the
vertebrae are not at all, or only mildly affected.
⚫C/F:- first sign-delay in walking
⚫Children are below average height and the parents
may have noticed that the lower limbs are
disproportionately short compared to the trunk

50. ⚫X-Ray:-delay in appearance of ossification centres
⚫When they do appear-small, fragmented,mottled and flattened
⚫Proximal femur is most affected.
⚫Acetabular changes are seen in Med (vs perthes)

51. Spondyloepiphyseal
Dysplasia(SED)
⚫Short trunk+rhizomelic+melomelic with sparing of hands and feet
⚫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).

52. SED
CONGENITA
SED TARDA-milder form

53. DYSPLASIA EPIPHYSEALIS
HEMIMELICA(TREVOR’S DISEASE)
⚫non-hereditary disease that is characterized by
osteochondromas arising from the epiphyses
⚫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.

54. CHONDRODYSPLASIA
PUNCTATA(STIPPLED EPIPHYSIS)
⚫Stippled calcifications within epiphysis in infancy+ short
stature+dry scaly skin+ heart defects+cataracts
⚫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.

55. METABOLIC
DISORDERS
⚫1.Rickets
⚫ 2. Renal Bone diseases-
i)The Renal Osteodystrophy
ii)The Lignac-fanconi Syndrome
iii)Hypophosphatasia

56. RICKETS
⚫Rickets refer to the condition where it occurs before
closure of growth plate so that abnormalities of skeletal
growth are super-imposed.

57. Renal Oseodystrophy
⚫The bone changes are due to combination of
hyperparathyroidism,osteitis
fibrosa,osteomalacia,osteosclerosis,osteoporosis and
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.

58. Hormonal
⚫The various hormonal disorders which affect the
growth plate are:-
⚫1.Hypopituitarism
⚫2.Hyperpitutarism
⚫3.Hypothyroidism
⚫The clinical effects of these hormonal imbalances
mainly depend upon the stage of skeletal maturity at
which the abnormality occurs.

59. Hypopituitarism
⚫Anterior pituitary hyposecretion results in development of two
distinct clinical disorders.
⚫1.Lorain Syndrome:- The predominant effect is on
growth.
⚫Proportionate dwarfism is seen.,sexual development may be
unaffected.
⚫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 or
knee.

60. Infections
⚫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
cases.
⚫Metaphyseal tenderness and resistance to joint movement
can be seen.
⚫Compensatory increase in activity of physis of affected site is
seen due to hyperemia after acute osteomyelitis

61. Physeal injuries classification systems

62. Salter and Harris described 5 patterns of injury to
the physis:
Type I – a physeal shear without bony injury
Type II – a partial physeal shear associated
with a largely vertical metaphyseal bony
fracture
Type III – a partial physeal shear plus an epiphyseal
fracture.
Type IV – a vertical fracture plane passing through the
epiphysis, the physis and the metaphysis.
Type V – a physeal and metaphyseal crush injury,
destroying the related portion of the physis: sometimes
evident by a small metaphyseal bulge. Such injuries are
frequently diagnosed in retrospect

63. 1)There exist also complex multiplanar injuries of the physis,
epiphysis and metaphysis, not categorized by Salter and Harris.
Such complex injuries are exemplified by the
triplane group of injuries seen at the distal tibial
physis.
Disadvantages of salter and harris
2)No significant prognostic value

64. Peterson classification(1994)
• Sound anatomical basis
• Type 1-minor involvement
• Type 2- to progressive more involvement
• Type 3 –to complete transphyseal disruption
• Type 4 –to transphyseal disruption with epiphyseal fracture that
ensures damage to the germinal layer of cells
• Type 5 –to longitudinal disruption of the epiphysis, physis and
metaphysis
• Type 6 – to removal or loss of some of the physeal cartilage

66. Treatment
●
●
Stabilize first
General principles
●
●
● Children # heal rapidly
Cast immobilization
Accurate reduction
●
Complication – growth disturbance, neurovascular compromise

67. Summery
• Anatomy and development of physis
• Physeal growth
• Physeal vascularity
• Hormonal and mechanical factors influencing physis
• Heuter Volkmann law
• Physeal pathology including developmental disorders infections
trauma

68. References
1. Ao reference
2. Epiphyseal growth plate fractures by Hamilton A Peterson
3. Tachdjian’s Pediatric Orthopedics-5th edition
4. Hyphenated history: the Hueter-Volkmann law.
Article in American journal of orthopedics (Belle Mead, N.J.) ·
December 1997

69. Thank you