Growth plate & Various disorders affecting growth plate by Dr.Vinay


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A short PPT on Growth plate/Physeal plate and various disorders affecting growth plate.

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  • dear dr. viancy ; i had found you presentatiom about physeal injury valuable for me. could you please allow me to get a copy .this is my e.mail to send a copy ( thanks a lot. gamal aladl. egypt
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  • dear dr. vinacy ;i found your presentation valuable to me. can you please allow me to get a copy for teaching purpose. thanks a lot. gamal aladl egypt..
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Growth plate & Various disorders affecting growth plate by Dr.Vinay

  1. 1. Chair Person:-Prof.Dr.Mahesh K.U. Presenter:-Dr.Vinay 1st Year PG. Dated 08/10/2013 SSMC,TUMKUR.
  2. 2. Structure of a long bone
  3. 3. Ossification-Types  Bone develops by transformation of pre-existing     connective tissue. 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 endochondral ossification. Ex:-Long bones,vertebrae,pelvis and bones of the base of skull.
  4. 4.  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 by mitosis.  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.
  5. 5.  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 disappears.  Once the adult stage is reached, the only way to manipulate height is modifying bone length via distraction osteogenesis.
  6. 6. Physeal plate  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 centre outward.,  Instead growth occurs at each end of the bone around the growth plate.
  7. 7.  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.
  8. 8. Microscopic Structure
  9. 9.  1.Undifferentiated/Resting cartilage  2.Zone of proliferating cartilage  3.Hypertrophic cell zone(maturation zone)  4.Zone of provisional calcification.
  10. 10.  Undifferentiated/Resting cartilage:-Lies 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 proliferation
  11. 11.  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.
  12. 12. Disorders affecting growth plate  They can be classified as 1.Developmental dysplasias 2.metabolic 3.hormonal 4.infections 5.Traumatic
  13. 13. Developmental Dysplasias  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.
  14. 14.  The chondro-osteodystropathies can be broadly classified according to the recognizable clinical and xray findings.,as follows: 1.Dysplasias with predominantly physeal and metaphyseal changes  2.Dysplasias with predominant epiphyseal changes.
  15. 15. 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:-
  16. 16.  Hereditary multiple exostosis(Disphyseal Aclasis)  Achondroplasia  Hypochondroplasia  Dyschondrosteosis  Metaphyseal chondroplasia(Dysostosis)  Dyschondroplasia(Enchondromatosis;Olliers disease)  Maffucci’s syndrome
  17. 17. 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.  The condition is transmitted as autosomal dominant disorder.  Mutations are seen on the chromosomes 8,11 and 19.  X-ray shows i)poorly modelled,broadened metaphysis,with sessile or pedunculated exostoses arising from the cortices.
  18. 18.  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 adolescence.
  19. 19. Achondroplasia  In this condition.,the adult height is usually around 122     cm(48 inches) 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 tubular bones.
  20. 20.  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 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.
  21. 21. Hypochondroplasia  This is a very mild form of achondroplasia.  There will be shortness of stature and noticeable     lumbar lordosis. 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.
  22. 22. Dyschondrosteosis  This condition also is transmitted as an autosomal dominant defect.  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 achondroplasia.  The most characteristic X-ray findings are shortening of forearms and leg bones,bowing of radius and which may reqiure operative treatment.
  23. 23. 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.  Operative correction by osteotomy may be required for coxavara or tibiavara.
  24. 24. Dyschondroplasia (Enchondromatosis;Ollier’s disease)  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.
  25. 25.  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.
  26. 26. 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.  Patients with maffucci’s syndrome should be monitored regularly throughout life for any change in bone or visceral lesions because.,
  27. 27.  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
  28. 28. 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
  29. 29. 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
  30. 30.  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 mildly Genetics:-This appears to be a heterogenous disorder but most cases have an autosomal dominant pattern inheritance. Management:-At maturity,deformity around the hips,knees or ankles sometimes require corrective osteotomy.
  31. 31. Spondyloepiphyseal Dysplasia(SED)  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 appearances.
  32. 32. SED CONGENITA  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.
  33. 33. SED TARDA  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.
  34. 34. DYSPLASIA EPIPHYSEALIS HEMIMELICA(TREVOR’S DISEASE)  This is a curious “hemidysplasia” affecting only one limb and only one half(the medial or lateral half) of each epiphysis.  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.
  35. 35.  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.
  36. 36. CHONDRODYSPLASIA PUNCTATA(STIPPLED EPIPHYSIS)  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 cardiac anamolies.  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.
  37. 37. MUCOPOLYSACCHARIDOSES  The polysaccharide GAG’S form sidechains of macromolecular Proteoglycan’s,a major component in bone matrix,cartilage,inter-vertebral discs & synovium.  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.
  38. 38.  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.
  39. 39. METABOLIC DISORDERS  1.Rickets  2. Renal Bone diseases- i)The Renal Osteodystrophy ii)The Lignac-fanconi Syndrome iii)Hypophosphatasia
  40. 40. RICKETS  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 2.Malabsorption 3.Renal diseases.
  41. 41. Skeletal changes  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.
  42. 42.  In the zone of calcified cartilage,the deposition of calcium in intercellular matrix is greatly deficient or even absent.  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.
  43. 43. Clinical Features  1.Large head,open fontanelles & craniotabes  2.Prominent abdomen  3.Seperation of recti muscles over the protuberant       abdomen. 4.Narrow chest 5.Enlarged epiphysis 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 look.
  44. 44. Radiological Appearances  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.
  45. 45.  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.
  46. 46. 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.
  47. 47. 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.
  48. 48.  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.
  49. 49. 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 disorder.
  50. 50. Hypophosphatasia  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.
  51. 51. 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.
  52. 52. 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.
  53. 53.  Investigations should include direct assays & tests for hormone functions  X-Rays of skull may show pituitary fossa expansion & erosion of adjacent bones.CT/MRI may reveal the tumour.  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.
  54. 54. Hyperpituitarism  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 displacement(epiphysiolysis)  There may be mental retardation & sexual immaturity too.  Treatment-early removal of pituitary tumour.
  55. 55. Hypothyroidism  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 supplementaion. 2.Juvenile hypothyroidism-its usually less severe than congenital type. Growth & sexual development are retarded. X-rays show typical epiphyseal fragmentaion apperance. The growth plate is disorganized in the reserve zone chondrocytes & proliferating chondrocytes. Treatment-Hormonal supplementation.
  56. 56. 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. 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.
  57. 57.  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 osteomyelitis Typical feature is a reducd intensiy signal in T2weighted images. Aspiration of pus from the metaphyseal sub-periosteal abscess or adjacent joint.
  58. 58. Treatment & Complications      Rx:-supportive treatment for pain and hydration Splintage of affected part Antibiotic therapy Surgical drainage. 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 growth disc.
  59. 59. Traumatic  In children.,over 10% of fractures may involve injury to the growth plate.,as the physis is relatively weaker part of bone.  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 injuries.
  60. 60. Salter-Harris Classification
  61. 61.  X-rays:-comparision with the other normal side gives the      valuable details about the fracture as the epiphysis itself is a radioluscent area. 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 growth.
  62. 62. REFERENCES  1.Samurl L.Turek-Text book of Orthopaedics Fourth edition-Vol.I  2.Apley’s sysem of orthopaedics & fractures Ninth edition  3.Mercer’s orthopaedic surgery Ninth edition-Vol.I
  63. 63. THANK YOU…