Osteochondritis of different bones


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Osteochondritis of different bones

  2. 2. ANATOMY • A typical long bone, ossifies in three parts; the two ends and one shaft. • The ends ossify from secondary centers of ossification while the shaft ossifies from primary center of ossification
  3. 3. • In a young bone in which the process of ossification is not complete • Epiphysis • Diaphysis • Metaphyses • Epiphyseal plate of cartilage
  4. 4. • Epiphysis: • The ends and the tips of a long bone that ossify from secondary centers are known as epiphyses. Growth of the epiphysis arises from two areas: (1) the vascular reserve zone car- tilage, which is responsible for growth of the epiphysis toward the joint, and (2) the epiphyseal plate, which is responsible for growth in bone length
  5. 5. TYPES OF EPIPHYSIS • Pressure epiphyses: articular & take part in joint formation. These epiphyses are the weight transmitting epiphyses. Ex -head of the humerus, lower end of the radius etc. • Traction epiphyses: provide attachment to tendons of muscles. The traction epiphyses ossify later than the pressure epiphyses. Examples of these epiphyses are tubercles of humerus and trochanters of femur • Atavistic epiphyses: are phylogenetically independent but they become fused in man. Examples are coracoid process of scapula • Aberrant epiphyses: these epiphyses are not always present. Examples are epiphyses at the head of the first metacarpal bone and at the base of other metacarpal bones.
  6. 6. DEFINITION • The terms osteochondrosis or epiphysitis is a self limiting developmental dearrangement of normal bone growth primarily involving centres of ossification in the epiphysis • It is an aseptic ischemic necrosis • The disorder may be localized to a single epiphysis or occasionally may involve two or more epiphyses simultaneously or successively
  7. 7. CHARACTERISTICS • Predilection of immature skeleton • Involvement of epiphysis • Radiographic picture dominated by fragmentation ,collapse, sclerosis and reossification of osseous centres
  8. 8. CLASSIFICATION • BURROW’S CLASSIFICATION into pressure traction and atavistic types
  9. 9. SIFFER CLASSIFICATION • Articular osteochondroses: – Calvé-Legg-Perthes Disease (hip/femur) – Köhler's Bone Disease (ankle navicular bone) – Freiberg's Disease (2nd metatarsal head) – Panner's Disease (capitulum of humerus) • Non-articular osteochondroses: – Osgood-Schlatter Disease (tibial tuberosity) – Sever's Disease (calcaneus) – Sinding-Larsen and Johansson Syndrome (inferior tip of patella) • Epiphyseal osteochrondroses: – Scheuermann's Disease (vertebral bodies)
  10. 10. ARTICULAR OSTE0CHONDROSIS Legg Calve Perthes Disease Legg-Calvé-Perthes disease (LCPD) is the name given to idiopathic osteonecrosis of the capital femoral epiphysis in a child.
  11. 11. HISTORY
  12. 12. Blood supply to femoral head • Upto 4 years 1. Retinacular vessels mainly lateral epiphyseal vessels 2. Metaphyseal 3. Artery of ligamentum teres
  13. 13. Blood supply to femoral head • By 4 yrs Epiphyseal plate forms a barrier to metaphyseal vessels. • Pre-adolescent 1. After 7 yrs arteries of lig teres become more prominent and anastomose with the lateral epiphyseal vessels. Between 4&7 yrs blood supply is dependent on retinacular vessels only
  14. 14. Incidence • Male : Female = 4-5:1 • 2.5:1 in India • Age of onset earlier in females. • Age – Range – 2-13 years. Most common 4-8 years. Average – 6 years. • Bilateral in 10-12 % • Incidence more in Caucasians as compared to Negroid, mongoloid.
  15. 15. Etiology • Etiology not known. • Coagulation disorders. • Altered arterial status of femoral head. • Abnormal venous drainage. • Abnormal growth and development. • Trauma. • Hyperactivity or attention deficit disorder. • Genetic component. • Environmental influences. • As a sequelae to synovitis.
  16. 16. Pathogenesis • Waldenstrom staged the pathological process of the disease as 1. Initial or ischaemic stage 2. Resorption or fragmentation stage 3. Reparative stage 4. Remodelling stage
  17. 17. Stage of Avascular Necrosis Ischemia A part ( anterior) or whole of capital femoral epiphysis is necrosed. On X-ray – – The ossific nucleus looks smaller – Classically of Perthes’, looks dense – The articular cartilage remains viable & becomes thicker than normal – increased joint space. PATHOGENESIS
  18. 18. PATHOGENESIS Stage of REVASCULARIZATION / FRAGMENTATION • Ingrowths of highly vascular & cellular connective tissue. • Necrotic trabecular debris is resorbed & replaced by vascular fibrous tissue the alternating areas of sclerosis and fibrosis appear on X- ray as fragmentation of epiphysis. • New immature bone laid on intact necrosed trabeculae by creeping substitution further increases the density of ossific nucleus on X-ray.
  19. 19. PATHOGENESIS Stage of Ossification / Healing New bone starts forming and epiphyseal density increases in the lucent portions of the femoral head.
  20. 20. • Remodeling / Residual stage This is the stage of remodeling and there is no additional change in the density of the femoral head. Depending on the severity of the disease the residual shape of the head may be spherical or distorted. PATHOGENESIS
  21. 21. Remodelling stage (replacement by biologically plastic bone) If treated • Femoral head is congrous If untreated • Subluxation and deformity
  22. 22. CLINICAL FEATURES • Classic portrait of the child with Legg-Calvé- Perthes disease—small, often thin, extremely active, constantly running and jumping, and limping after strenuous physical activities
  23. 23. • Often insidious onset of a painless limp, excaberated by activity. • C/O pain in groin, thigh, knee • Few relate trauma hx • Can have an acute onset Presentation
  24. 24. • Tredelenburg with antalgic gait • Trendelenburg test often positive • Muscular atrophy of thigh/buttock/calf • Limb length discrepency • Decreased ROM, especially abduction and internal rotation: initially due to muscle spasm Physical Exam
  25. 25. Imaging – Radiographic Feature • Widening of the joint space and minor subluxation • Sclerosis • Fragmentation and focal resorption • Loss of height • Metaphyseal cyst formation • Widening of the femoral neck & head (Coxa Magna) • Lateral uncovering of the femoral head • Sagging rope sign • Acetabular remodelling
  26. 26. Sclerosis of epiphysis & widening of joint space in the early stages
  27. 27. Fragmentation of the femoral capital epiphysis
  28. 28. Caffey’s sign • As the disease progresses, a subchondral # may occur in the anterolateral aspect of the femoral capital epiphysis. • Is an early radiographic feature best seen on the frog-lateral projection. • This produces a crescentic radiolucency known as the crescent, Salter’s or Caffey’s sign
  29. 29. Metaphyseal cyst formation within the femoral neck
  30. 30. Stages of radiological changes in Perthe's disease: cont…  Late Stage–  Coxa magna  High-riding trochanter  Flattened femoral head  Irregular articular surface
  31. 31. ‘Sagging Rope Sign’ • This a curvilinear sclerotic line running horizontally across the femoral neck. • It is confirmed by 3D CT studies. • It is a finding in AP radiograph in a mature hip with Perthes’ disease.
  32. 32. Workup • Technetium 99 bone scan - Helpful in delineating the extent of avascular changes before they are evident on plain radiographs. – The sensitivity of radionuclide scanning in the diagnosis of LPD is 98%, and the specificity is 95%. • Avascular areas show cold spots
  33. 33. Ultrasound features • Effusion, especially if persistent • Synovial thickening • Cartilaginous thickening • Atrophy of the ipsilateral quadriceps muscle • Flattening, fragmentation, irregularity of the femoral head • New bone formation • Revascularisation with contrast enhanced power Doppler
  34. 34. CT Scan • Staging determined by using plain radiographic findings is upgraded in 30% of patients. • Not as sensitive as nuclear medicine or MRI. • CT may be used for follow- up imaging in patients with LPD.
  35. 35. Arthrography • Shows configuration of the femoral head and its relation with the acetabulum. • Containment • Congruity • Not routinely used .
  36. 36. MRI • It allows more precise localization of involvement than conventional radiography. • MRI is preferred for evaluating the position, form, and size of the femoral head and surrounding soft tissues. • MRI is as sensitive as isotopic bone scanning.
  37. 37. Morphological classifications of the extent of the lesion • Classification according to Catterall (Common) • Classification according to Salter & Thompson • Classification according to Herring
  38. 38. • Legg, who identified two types of femoral heads—a “cap” and a “mushroom.” • Goff also identified three types of femoral heads—spherical, cap, and irregular—that correlated with disease outcome.
  39. 39. Classification of extent of lesion - (Acc to Catterall) Grade Characteristics I Only anterolateral quadrant affected II Anterior third or half of the femoral head III Up to 3/4 of the femoral head affected, only the most dorsal section is intact IV Whole femoral head affected
  40. 40. Grade – I • Only anterolateral quadrant affected
  41. 41. Grade - II • Anterior third or half of the femoral head
  42. 42. Grade – III • Up to 3/4 of the femoral head affected, • only the most dorsal section is intact
  43. 43. Grade – IV • Whole femoral head affected
  44. 44. Classification according to Salter & Thompson Group Characteristics A Subchondral # involving <50% of the femoral dome B Subchondral # involving >50% of the femoral dome
  45. 45. Classification according to Herring Group Characteristics A Lateral pillar not affected B >50% of height of lateral pillar preserved C <50% of height of lateral pillar preserved
  46. 46. Classification according to Herring “A” Lateral pillar not affected
  47. 47. Classification according to Herring “B” >50% of height of lateral pillar preserved
  48. 48. Classification according to Herring “C” <50% of height of lateral pillar preserved
  49. 49. Prognostic Factors 1. Age at diagnosis <6 yrs – good 6 – 9 yrs – fair >9 yrs - poor 1. Extent of involvement 2. Sex 3. Catterall “head at risk” signs
  50. 50. Catterall “head at risk” signs • Clinical 1. Progressive loss of hip motion more so abduction. 2. Fixed flexion deformity and adduction deformities of hip 3. Obese child 4. Age on higher side
  51. 51. • Radiographic 1. Gage sign 2. Calcification lateral to epiphysis 3. Diffuse metaphyseal rarefaction 4. Lateral extrusion of femoral head 5. Growth disturbance of physis
  52. 52. Physeal disruption
  53. 53. Metaphyseal rarefaction
  54. 54. Femoral head extrusion
  55. 55. Gage’s sign • Rarefaction in the lateral part of the epiphysis and subjacent metaphysis.
  56. 56. Classification of End Results MOSE CLASSIFICATION • The Mose classification system is based on fitting the contour of the healed femoral head to a template of concentric circles. • In good outcomes, the shape of the femoral head deviates no more than 1 mm from a given circle on both AP and frog-leg lateral radiographs. • If the shape falls within 2 mm, it is considered a fair outcome. • If the deviation is greater than 2 mm, it is a poor outcome.
  57. 57. Stulberg classificaton • Class I – Shape of the femoral head was basically normal. • Class II – Loss of head height but within 2 mm to a concentric circle on AP and frog leg X-Ray • Class III – Deviates more than 2 mm and acetabulum contour matches the head contour • Class IV – Head Flattened, Flattened area <1cm. Acetabulum contour matches the head contour • Class V – Collapse of femoral head, Acetabular contour does not change
  58. 58. Stulberg classificaton • Class I & II – Spherically congruent. • Class III & IV – Congruous Incongruity OR Aspherical congruity. • Class V – Incongruous incongruity OR Aspherically incongruent.
  59. 59. Treatment • Goals of treatment – Achieve and maintain ROM – Relieve weight bearing – Containment of the femoral epiphysis within the confines of the acetabulum – Prevent secondary degenerative arthritis of the hip
  60. 60. Treatment • Caterall group 1 and group 2 ( < 7 years) No • Herring group 1 & Treatment group 2 (< 6 years)
  61. 61. Treatment Treatment is divided into 3 phases • Initial Phase – restore & maintain mobility • Active Phase – Containment and maintainance of full mobility. • Reconstructive phase – correct residual deformities.
  62. 62. Treatment ( Initial Phase ) • Physiotherapy – active and passive range of motion exercises to restore motion • Traction – B/L skin traction and gradually abducting over 1-2 weeks till full abduction isregained.
  63. 63. Treatment ( Active Phase ) • Consists of containment of the femoral head within the acetabulum. This can be achieved by orthosis or by surgery
  64. 64. Treatment (Orthosis) • Non Ambulatory weight releiving 1. Abduction broomstick plaster cast 2. Hip spica cast • Ambulatory Both limbs included 1. Petrie Abduction cast 2. Toronto orthosis 3. Newington orthosis 4. Birmingham brace 5. Atlanta Scotish Rite Brace
  65. 65. • Ambulatory unilateral 1. Tachdjian trilateral socket orthosis
  66. 66. Treatment (Orthosis) • Atlanta Scotish Rite Brace
  67. 67. Treatment (Orthosis) • Toronto Brace
  68. 68. Treatment (Orthosis) • Birmingham brace
  69. 69. Treatment (Orthosis) • Newington orthosis
  70. 70. Treatment (Orthosis) • Tachdjian trilateral socket orthosis
  71. 71. Treatment (Orthosis) • Orthotic treatment is discontinued when the disease enters the reparative phase and healing is established.
  72. 72. • The radiographic evidence of healing are 1. Appearance of irregular ossification in the femoral head. 2 . Increased density of femoral head should disappear. 3 . Medial segment of femoral head should increase in size and height. 4 . Metaphyseal rarefaction involving the lateral cortex of the metaphysis should ossify. 5 . There should be intact lateral column.
  73. 73. • If non-op tx cannot maintain containment • Surgically ideal pt: – 6-9years – Catterral II-III – Good ROM – In collapsing phase Operative Tx
  74. 74. Surgical Containment Femoral VDRO Pelvic osteotomies Varus 20 Salter’s Derotation 20-30 osteotomy
  75. 75. • varusderotation osteotomy :- – INDICATIONS- patients with a spherical femoral head, – little or no acetabular dysplasia (center-edge angle of at least 15 to 20 degrees), – lateral overloading, and – a valgus neck-shaft angle of more than 135 degrees.
  78. 78. DISADVANTAGES- varus angulation that may not correct with growth (especially in a older child), further shortening of an already shortened extremity, the possibility of a gluteus lurch produced by decreasing the leng of the lever arm of the gluteal musculature, the possibility of nonunion of the osteotomy, requirement of a second operation to remove the internal fixatio
  79. 79. • ADVANTAGE- • Anterolateral coverage of the femoral head, • lengthening of the extremity (possibly shortened by the avascular process), and • avoidance of a second operation for plate removal INNOMINATE OSTEOTOMY
  80. 80. • DISADVANTAGES-1)inability sometimes to obtain proper containment of the femoral head, especially in older children; • 2)an increase in acetabular and hip joint pressure that may cause further avascular changes in the femoral head; • 3)an increase in leg length on the operated side compared with the normal side that may cause a relative adduction of the hip and uncover the femoral head.
  81. 81. • Valgus extension osteotomy indication -hinge abduction of hip • Cheilectomy indication – malformed femoral head • Chiari osteotomy indication – malformed femoral head with lateral subluxation • Trochanteric advancement or Greater trochanteric epiphysiodesis indication – premature capital femoral physeal arrest • Shelf augmentation procedure indication – coxa magna & lack of acetabular coverage TREATMENT Reconstructive procedures
  82. 82. FREIBERG INFRACTION • Osteochondritis of the second metatarsal head. But may also involve 1st 3rd and 4th metatarsal heads • Usually occurs following trauma. • A misshapen metatarsal head frequently is an incidental radiographic finding, and careful questioning of the patient often reveals a period during adolescence when pain was noted in the forefoot.
  83. 83. PATHOPHYSIOLOGY • The second toe is the longest and the second ray the least mobile, excessive pressure on the metatarsal head on weight bearing cause repetitive microfractures, loss of blood supply to subchondral bone, collapse of this cancellous bone, and cartilage deformation.
  84. 84. • Synovitis accompanies the process, and if it is prolonged and severe, limitation of motion, especially in extension, results. • With this loss of extension of the metatarsophalangeal joint, weight bearing causes abnormal stress to be applied to the metatarsal shaft, which becomes widened from bicortical thickening.
  85. 85. PRESENTATION -Pain around the involved metatarsophalangeal joint primarily on weight bearing, local tenderness around the metatarsophalangeal joint, and limitation of motion. -If a synovitis is present, swelling becomes apparent
  86. 86. Irregular ossification of the primary ossification center of the metatarsal head,widening of the metatarsal shaft,and osteochondral fragmentation
  87. 87. TREATMENT • Modification of activities, semirigid orthoses, and metatarsal bars. • A short leg walking cast with a toe extension may be needed if other non operative treatment fails. • Occasionally, crutches are needed to rest the painful foot completely.
  88. 88. TREATMENT • If conservative management fails, surgical treatments include (1) Resection of the metatarsal head • (2) Elevation of the depressed fragment of the metatarsal head and bone grafting of the defect (Smillie procedure) • (3) Resection of the base of the proximal phalanx with syndactylization of the second and third toes • (4) Dorsal closing wedge osteotomy of the metatarsal head • (5) Joint débridement and metatarsal head remodeling
  89. 89. KOHLER’S DISEASE • Osteochondritis of tarsal navicular • The aetiology of Köhler's disease is unknown. Theories have included vascular trauma and retarded bone • It commonly affects children aged 3 to 5 years old, but is seen any time between age 2 and 10 years. • It is more common in boys; however, girls with this condition are often younger than boys with the disease
  90. 90. • Children present with a unilateral antalgic gait (a limp, avoiding putting weight on painful structures) • Local tenderness of the medial aspect of the foot, over the navicular bone • The child is able to walk by taking the majority of their weight on the lateral aspect of the foot. Frequently, there is swelling and redness of the soft tissues
  91. 91. • Plain X-ray -The navicular bone is initially flattened and sclerotic. Later it becomes fragmented and then re-ossifies.[4] • The lateral view shows a flat tarsal scaphoid. • The space between the talus and the cuneiforms is preserved.
  92. 92. Rest ,avoiding excessive weight bearing ,analgesia & immobilisation in a short leg cast moulded under the longitudinal arch for at least 6 weeks is recommended. If pain persists after a 6-week period of casting, a new cast must be applied for 6 supplementary weeks • The course is chronic, but rarely lasts longer than 2 year
  93. 93. • Arthrodesis is the only operation of value, and the midtarsal joints (talonavicular and calcaneocuboid) can be arthrodesed. • Here arthrodesis is difficult to secure; metallic internal fixation and inlay grafts of autogenous cancellous bone are helpful.
  94. 94. PANNER’S DISEASE • OSTEOCHONDRITIS OF CAPITELLUM • Panner's disease affects the dominant elbow of children, mainly boys, between the ages of five and 10.
  95. 95. PATHOPHYSIOLOGY • Interference in blood supply to growing epiphysis, which results in resorption & eventual repair & and replacement of the ossification center • In patients under 20 years of age, capitellum is only supplied by end arteries entering posteriorly;
  96. 96. • - inciting causes: - chronic repetitive trauma, congenital and hereditary factors, embolism (fat), and endocrine disturbances;
  97. 97. Clinical manifestations • Intermittent pain and stiffness in the affected elbow that lasts for several months • Symptoms are relieved by rest and aggravated by activity • local tenderness over capitellum, limited extension is typical, lacking 20 to 30 deg of full extension • There may be slight loss of pronation and supination w/ tenderness
  98. 98. RADIOLOGY • An irregular surface on the capitellum. The entire growth plate may appear fragmented and transparent. The capitellum may appear flattened out, which means that the bone has coapsed • The MRI can give a better view of bone irregularities. The MRI can also detect swelling.
  99. 99. TREATMENT • Children may need to stop sports activities for a short time. This reduces the pain and inflammation • NSAIDS to help reduce pain and swelling. Physical therapy such as heat, ice, and ultrasound may be used to ease pain and swelling. • In severe cases, when regular treatment is not effective, doctors may recommend that the child wear a long-arm splint or cast for three to four weeks.
  100. 100. OSGOOD–SGHLATTER DISEASE • Osgood–Schlatter disease or syndrome (OSD) is an irritation of the patellar ligament at the tibial tuberosity
  101. 101. Osgood Schlatters disease is a very common cause of knee pain in children and young athletes. It occurs during the period of rapid growth, due to a combined high level of sporting activity who play soccer, basketball, and volleyball, and who participate in gymnastics It occurs more frequently in boys than in girls, with reports of a male-to-female ratio ranging from 3:1 to as high as 7:1. [1]
  102. 102. PATHO-MECHANICS Following an adolescent growth spurt, repeated stress from contraction of the quadriceps is transmitted through the patellar tendon to the immature tibial tuberosity. This can cause multiple sub-acute avulsion fractures along with inflammation of the tendon, leading to excess bone growth in the tuberosity and producing a visible lump which can be very painful when hit. Activities such as kneeling may irritate the tendon further.
  103. 103. Sayantika D
  104. 104. What Makes OSD Worse? o squatting o running o walking up or down stairs o cycling o forceful contractions of the quadriceps muscle o jumping (basketball, volleyball) o kneeling o repetitive hard landings Anything that puts excessive stress on the insertion of the patellar tendon
  105. 105. Symptomso Main symptom - painful swelling over a bump on the tibia on one or both sides o Pain: mild and intermittent initially. o Later stages- the pain is severe and continuous in nature. o Pain usually resolve with treatment but may recur for 12–24 months before complete resolution at skeletal maturity, when the tibial epiphysis fuses. Palpation: The area is tender to pressure, and swelling ranges from mild to very severe.
  106. 106. Painful swelling
  107. 107. Radiographs Sayantika D
  108. 108. Conservative Management o Regular stretching, both before and after exercise and athletics, can help prevent injury o NSAIDS for pain relief &rest (3 days) and decreasing activity (1-2 weeks) o Ice - over the painful area, 2 to 3 times a day, 20 to 30 minutes at a time, o Bracing, Orthopedic casting o Infra patellar strap – 6 to 8 weeks
  109. 109. Surgical Management • Surgery may be considered if symptoms are persistent and severely disabling & include -Excision of intra- tendon ossicles -Tibial sequestrectomy
  110. 110. SEVERE’S DISEASE • Inflammation of the calcaneal apophysis which occurs in children and adolescents due to repeated 'microtrauma' at the site of the attachment of the Achilles tendon to the apophysis of the heel, often result of sporting activities
  111. 111. AETIOLOGY • The line of ossification in the calcaneal apophysis is thought to develop microfractures due to recurrent stresses on the heel, combined with the growth spurt of puberty. It is caused by decreased resistance to shear stress at the bone-growth plate interface.
  112. 112. CLINICAL FEATURES • Heel pain, usually in young physically active individuals, which is gradual in onset, and worse on exercise, especially running or jumping relieved by rest. Often bilateral. • Tenderness on palpation of the heel - particularly on deep palpation at the Achilles tendon insertion. • Pain on dorsiflexion of the ankle - particularly when doing active toe raises; forced dorsiflexion of the ankle is also uncomfortable. • Swelling of the heel - usually mild. • Calcaneal enlargement - in long-standing cases
  113. 113. • X-ray of the heel may show increased sclerosis and fragmentation of the calcaneal apophysis – but these features are nonspecific and it may be normal • CT or MRI scan may be useful to exclude osteomyelitis or fusion of the small bones of the hindfoot.
  114. 114. TREATMENT • Physiotherapy and exercises • Soft orthotics or heel cups. • Advice on suitable athletic footwear. In severe cases: temporarily limiting activity such as running and jumping. • Ice and non-steroidal anti-inflammatory drugs (NSAIDs), which can reduce pain • In very severe cases, a short period of immobilisation (eg 2-3 weeks in a case in mild equinus position)
  115. 115. Sinding-Larsen-Johansson Disease: • - osteochondrosis of the inferior pole of the patella - presents as anterior knee pain in the active adolescent - usually resolves with skeletal maturation ossification
  116. 116. • The mechanism in Sinding-Larsen Johansson disease is thought to be persistent traction at the cartilaginous junction of the patella and the patellar ligament/tendon It is essentially a chronic stress injury with overuse of the patella-patellar tendon junction
  117. 117. • Knee X-ray: can show calcification or ossification at the junction between the patella and the patella ligament • Physiotherapy is the mainstay of treatment, including quadriceps strengthening exercises
  118. 118. KIENBOCK DISEASE • Avascular Necrosis of Lunate • First Described by Robert Kienbock in 1910; as “traumatic softening” of Lunate bone
  119. 119. AETIOLOGY • Aetiology = unknown, but several cause have been proposed • Vascular compromise from repetitive trauma causes microfracture & excessive stress on microscopic architecture (sports injury) • Ulnar minus variant:- Individual having ulnar minus variance are at increased risk. Short Ulna  increases shear force across the lunate  Causes vascular insufficiency
  120. 120. EPIDEMIOLOGY • Age= 15-40 (young individuals) • Sex= Men • Location= Unilateral, Dominant wrist
  121. 121. CLINICAL FEATURE • There may be history of trauma with wrist in severe dorsiflexion The lesion presents with 1. Dorsal wrist pain:- Pain may be produced in lunate region by axial strike/injury at distal end of middle finger 2. Swelling 3. Decreased Grip strength 4. Decreased range of motion; particularly in extension. In later stage movement may be painful
  122. 122. IMAGING • X-ray at first show no abnormality but • Bone scan may reveals increased activity • Later x-ray may show either mottled or diffuse density of bone – to – osteoarthritic changes in wrist • MRI Most reliable way of detecting the early change
  123. 123. TREATMENT A Conservative Casting of wrist for several wks ; for early stages of disease ( St I or II, before sclerosis, fragmentation or collapse) But- Unacceptable & Ineffective B Operative • Surgery is only definitive treatment
  124. 124. Early Disease Stage I & II • Unloading the Lunate* • 1. Ulnar lengthening • Transverse osteotomy at distal ulna  Distraction  Cortical iliac graft  Tightening of plate screw
  125. 125. Early Disease Stage I & II 2. Radial Shortening Indication – Negative ulnar variance – Lunate compression fracture without fragmentation or flattening Procedure Transverse osteotomy 3” proximal to distal articulating surface shortening of radius by 2 cm fixing the bone with compression plate
  126. 126. • Vascularized grafts include the distal radius based on the pronator quadratus, the pisiform as a pedicle graft, and various other grafts from the distal radius, second metacarpal, and pisiform. • These procedures also are effective in relieving pain and improving function in approximately 90% of patients
  127. 127. In stage III 1. Ulnar lengthening 2. Silicon prosthesis - silicon synovitis - foreign body cyst 3. Interacarpal fusion 4. Lunate excision 5. Arthrodesis Tri scaphe Scaphocapitate
  128. 128. In stage IV • Proximal carpal row resection • Wrist arthrodesis
  129. 129. ISELIN DISEASE • Traction epiphysitis of the base of the fifth metatarsal occurring in young adolescents at the time of appearance of the proximal epiphysis of the fifth metatarsal • This bone is located within the cartilaginous flare onto which the peroneus brevis inserts
  130. 130. PRESENTATION • Tenderness over a prominent proximal fifth metatarsal. • Weight bearing produces pain over the lateral aspect of the foot. • The affected area over the tuberosity is larger on the involved side, with soft-tissue edema and local erythema. • The area is tender to palpation at the insertion of the peroneus brevis, and resisted eversion and extreme plantar flexion and dorsiflexion of the foot elicit pain.
  131. 131. • Oblique radiographs- enlargement and fragmentation of the epiphysis and widening of the cartilaginous-osseous junction. • Technetium-99m bone scanning-incresed uptake
  132. 132. DD
  133. 133. TREATMENT • For mild symptoms, limitation of sports activity, application of ice, and administration of NSAIDS • For severe symptoms, cast immobilization may be required. Internal fixation of the epiphysis is not indicated.
  134. 134. SCHEUREMANN’S DISEASE • It is essentially osteochondrosis of the vertebrae • It affects the thoracic or thoracolumbar spine causing increased kyphosis, poor posture and possible backache. It is the most common cause of structural kyphosis in adolescents.
  135. 135. PATHOPHYSIOLOGY • A defect in the secondary ossification centres of the vertebral bodies. A few vertebral bodies may be involved or the whole thoracolumbar spine. • Hereditary factors are thought to play a part • Taller height, as well as an association with increased levels of growth hormone, have also been suggested • Mechanical factors and trauma
  136. 136. Epidemiology • Usually presents in children aged 13-16 years old. • Occurs more commonly in boys.
  137. 137. Presentation • Poor posture with increased kyphosis (usually noticed by parents). • Pain is a more common presentation if the disease affects the lumbar spine. Pain is usually dull aching worse on activity and relieves on rest • Neurological symptoms may rarely be the presenting feature • Cardiorespiratory symptoms can also rarely occur.
  138. 138. Examination • It is normal to have a degree of kyphosis. Any degree of kyphosis of more than 40° is considered abnormal • Kyphotic deformity may be progressive. • Upper thoracic kyphosis is best seen in the forward flexed position; lower thoracic kyphosis may be seen at the thoracolumbar junction. • There is reduced flexibility of the spine. • There may be tenderness above and below the apex of the kyphosis. • Scoliosis may also be present • Neurological signs are rare.
  139. 139. RADIOGRAPHY • Wedge-shaped vertebral bodies • Rigid kyphosis • Narrow intervertebral disc spaces with calcifications • Prominent irregularities of the vertebral surfaces • Vertebral plates that are poorly formed and that develop multiple herniations of the nucleus pulposus known as Schmorl nodes
  140. 140. TREATMENT • Mild, nonprogressive disease can be treated by reducing weight-bearing ,stress and avoiding strenuous activity • For severe kyphosis , recommendations include casting, a spinal brace, or rest and recumbency on a rigid bed. Orthotic Mx usually requires 12-24 months of treatment. • Non-steroidal anti-inflammatory drugs may be used for pain relief
  141. 141. • Surgery ,if there is neurological deficit, uncontrolled pain, unacceptable cosmetic appearance or documented progression • Cord decompression for neurological deficit and • Spinal fusion techniques for kyphosis correction and pain control.
  142. 142. Complications • Chronic back pain. • Progressive and permanent deformity. • Neurological deficit. • Cardiorespiratory problems.
  143. 143. THANK YOU