Physis-Development,Anatomy,Physiology,Pathology,Diseases

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 . T he p h y sis P rimary func tion o f g r o w t h car tilage Primary function of growth cartilage is the continuous and controlled elaboration of a solid scaffold (calcified cartilage) in preparation for bone deposition. L o gin Cookies help us improve your website experience. By using our website, you agree to our use of cookies. C onfirm X Embr y ol ogical d e v elopment 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. P ostnatal d e v elopment 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 . P h y s eal s tructure 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. P h y s e al zone s 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. V ascular ana t o m y o f p h y sis T ruet a , o f O x f o r d, England, fi r st de scri b e d t he v ascularity o f t he p h y si s . He n o t e d t hat no significant v e ssel pie r c e d t he p h y s e al disc and t hat t he r e e xist no significant anas t omose s b et w e en t he epi h y s e al and metap h y s e al v ascular t r e e s wi t hin t he b on e .

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 . F unctional anato m y o f gr o wth c artilage s 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. L ongitudinal g r o w t h

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 g r o w t h 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

27. 1.Growth Factors and Local Regulators Associated with Growth Plate Maturation and/or Epiphyseal Fusion 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 M etabolic 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.D y splas i as with p r edom i na n t ep i p h y seal chan g e s .

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. Th e c o n diti o n s a r e : -

36. Hereditary multiple exostosis(Disphyseal Aclasis) Achondroplasia Hypochondroplasia Dyschondrosteosis Metaphyseal chondroplasia(Dysostosis) D y schond r o p lasi a (Ench o nd r oma t os i s; O l liers disease) M af f u c ci ’ s synd r ome

37. Hereditary Multiple Exostosis(Disphyseal Aclasias) Thi s i s th e mos t c ommo n &least dis f iguri n g of all the skeletal dysplasias. The underlying fault is unrestrained transverse growth of the physeal plate . poorly modelled,broadened metaphysis,with sessile or peduncula t ed e x os t oses aris i n g f r om th e c orti c e s . ii)A bony mottled appearance around a bony excrescence indicates calcification in the cartilage cap

38. 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.

39. 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 metap h y sis and p h y seal lines a r e i r r eg ula r ., w i t h n o rmal 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.

40. Hypochondroplasia This is a very mild form of achondroplasia. The r e will b e shortness of sta t u r e and not i c eable lumbar lordosis. H ead&fa c e a r e n ot af f ec t ed .

41. Dyschondrosteosis autosomal dom i na n t de f ect. 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.

42. Metaphyseal chondroplasia (Dysostosis) Thi s describe s a typ e of short limbed dw ar f is m i n 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 .

43. Dyschondroplasia (Enchondromatosis;Ollier’s disease ) defective transformation of physeal cartilage columns into bone. i)Typically this disorder is unilateral.,indeed only o n e limb or e v en o n e b o n e i s i n v o l v ed . ii)An affected limb is short,and if the growth plate is asymmetrically involved,the bones grows bent . The condition is not inherited .

44. 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 .

45. Maffucci’s Syndrome This rare disorder is characterized by development of mul t i p le encho n d r omas and soft tiss u e hemang i omas of skin & viscera. Lesions appear during childhood; boys and girls are affected with equal frequency .

46. Dysplasias with predominantly epiphyseal changes This group of disorders is characterized by abnormal development and ossification of epiphysis,resulting in distortion of bone ends. V ar i ous d y splas i as a r e enlis t ed as f oll o ws 1.Multiple Epiphyseal Dysplasia 2.Spondyloepiphyseal Dysplasia 3.Dysplasia epiphysealis Hemimelica 4.Chondrodysplasia Punctata(Stippled Epiphysis) 5.Mucopolysaccharidoses

47. Multiple Epiphyseal Dysplasia The r e i s widesp r ead i n v o l v ement of th e ep i p h y ses b ut 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

48. 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 )

49. Spondyloepiphyseal Dysplasia(SED) Short trunk+rhizomelic+melomelic with sparing of hands and feet wellmarked vertebral changes – delayed ossification, flattening of the vertebral bodies (platyspondyly), ir r egular ossi f icati o n of th e ri n g ep i p h y ses and indentations of the end-plates (Schmorl’s nodes ).

50. SED CONGENITA SED TARDA-milder form

51. 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.

52. 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 i r r eg ular i t i es and dy splasi a .

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

54. RICKE T S Rickets refer to the condition where it occurs before cl o su r e of g r o wth p l a t e so tha t abn o rmal i tie s of skeletal growth are super-imposed .

55. 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.

56. 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.

57. Hypopituitarism Anterior pituitary hyposecretion results in development of t w o distinc t cli n ica l diso r der s . 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 s k eletal matu r i t y associa t ed with adiposity and immat u r i ty 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.

58. 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

59. Physeal injuries classification systems

60. 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

61. 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

62. 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

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

64. 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

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

66. Thank you