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Northern Italy and Japan  Rare in Chinese and blacks First born, breech del,   Unilateral > bilateral    Left > right       

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SURGERY NEWLIFE

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CONGENITAL DEFORMITIES Pathology    



Abnormalities present at birth  birth   Etiology   Etiology

     

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1.  Genetic influences  influences  chromosome anomalies multiple, severe, incompatible with life downs syndrome/ trisomy 21  Single gene disorder 



 



 



 



Genetic mutation  



2.  Intrauterine  Intrauterine  Drugs, infection, irradiation  Depends on stage of fetal development

3.  Combined genetic and environmental  Congenital Dislocation of the Hip/ Developmental Dysplasia of the Hip  Hip   



Dislocatable/congenital hip Dislocatable/congenital dysplasia  -1/100  -10% - progress to true dislocation

 



   Dislocated   rare Irreducible    Later in childhood  Congenital subluxation  Acetabular dysplasia  Teratologic hip dislocation    Rare,severe, pathologic changes of advanced disloc.   – 

 



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Incidence /etiology  /etiology 

1  – 2/ 1000    Girls 5x more affected     Ligamentous laxity, twins,  

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parents with dislocated hip

 



 



 



Pathologic changes vary with age   Elongated ligamentum teres  Slightly increased femoral anteversion  Acetabulum becomes shallow/ roof sloping  Femoral head  – upward and backward, underdevelopment, flattening  Capsule  – elongated, thick and fibrous, hourglass shape  Muscles  – (adductors)shortened (adductors)shortened and contracted  Secondary acet- developed on the ilium  Pelvis  – underdeveloped on the affected side; forward tilting  Postural deviation of the lumbar spine toward the affected side; Increase of lordosis 

Clinical Features  Features    Neonatal period   IDENTIFY DISLOCATABLE HIP    BARLOWS TEST    ORTOLANIS TEST 



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Infancy Asymptomatic  Asymmetry of thigh folds  Greater trochanter is prominent    Bilateral dislocation    Each step patient lurch toward the

     

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weight bearing side  Wide perineum, broad buttocks, transverse gluteal fold is altered    Increased lumbar lordosis, protrusion of the abdomen  (+) Barlows and Ortolani sign ( early stage)  Limited abduction(< 45 degrees)  Galleazi sign  Telescoping/ piston mobility  Slight delay in walking   





 

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Abductor lurch  – may not be obvious    Trendelenburg test 

 

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Roentgenographic picture  picture   



3 classic signs    Delayed growth of the ossification center of the capital epiphysis    Upward and outward displacement of the femoral head    Obliquity of the acetabular  – 

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roof   Increased acetabular index (>30 deg)  Decreased CE angle  Disrupted Shentons line  Head located located at the superior lateral quadrant

Dynamic ultrasonography ultrasonography    before ossification of femoral head    Acetabular dysplasia    Capsular laxity    Assessing reduction    Arthrography    Assess reduction  Treatment   



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Fist 6 mos    Conservative/ non surgical    Frejka pillow, pavlik harness    Plaster cast    3 to 6 mos in cast or splint    Over 6 mos    Traction, close reduction and casting   



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Surgical of adductor muscles,section close reduction and casting    Open reduction and casting    . 18 mos to 2 years    Open reduction and casting    Open reduction,osteotomy( femoral shortening or innominate osteotomy) and casting    2 to 6 years old  old     Clinical picture   

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Absent Limp   stability tests 

 

Shortening  Asymmetric thigh crease  Telescoping (absent in subluxation)    (+) trendelenburg test    Treatment   Traction, adductor tenotomy and open reduction       

Talus- shortened and deviated medially, wedge shape,externally rotated    Navicular bone displaced medially    Forefoot  – medially    Subtalar surfaces- medially,

 

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Varus osteotomy Innonimate osteotomy 

  varus and equinus Calcaneuspoints downward and medially,   Tibia  –externally rotated    Proliferative bony changes    bursa 

 

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Congenital Talipes  Talipes 

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Talipes 

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talus –   – ankle ; pes- foot 

Four Cardinal Position of the Foot 1.  Varus/ inversion  inversion 

Roentgenographic pictures  pictures 

Little value in newborn  Evaluate treatment    Kite`s angle  – line drawn on

   

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2. Valgus /eversion 

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3. Equinus/ plantar flexion 

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4. Calcaneus/ dorsiflexion 

long axes of the talus and calcaneus on AP view  – 20  – 30 deg    Lateral view in maximum dorsiflexion >35 deg    Angle of Meary 0  – 20 deg 

Talipes Equinovarus/TEV ( congenital clubfoot)  clubfoot)    



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Etiology    Asso with other disorders     Isolated(idiopathic)    20%-hereditary    Pathogenesis    Arrest or anomalous development    Failure of inward rotation of the foot    Muscle imbalance   – 

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  Incidence   1/1000 birth    2x in boys    > 50% bilateral    R = L    Pathology    Achilles tendon shortened,,anterior and posterior tendons contracted, anomalous tendon insertion    Ligaments and capsule on the medial side shortened,   – 

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Clinical picture    Heel  – drawn up    Foot  – inverted, adducted,    concave medial border    Diagnosis    Paralysis, myelodysplasia, cerebral palsy,    old injury to distal tibial physis,  



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osteomyelitis,fracture, muscular dystrophy   

 

Evans  – resection of calcaneo-cuboid  joint;surgiacl release of talonavicular joint    Triple arthrodesis  –  subtalar,calcaneocuboid,talonavicular joint    More than ten years

Prognosis    Flexibility    Early treatment    Treatment    Ponsetti technique    cavus deformity must be corrected prior to correcting the other deformities;  

 



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- forefoot is supinated and the first metatarsal is dorsiflexed;    to correct the varus and adduction, the foot in supination is abducted while counterpressure is applied with the thumb against the head of the talus;   casting involves a toe-togroin plaster cast w/ knee flexed 90 degrees and the foot in maximum external rotation; 



old  Talipes Calcaneovalgus

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  correction of equinus: of tendon   Tenotomy of achilles -    Maintenance of reduction    Dennis brown splint  method    Kites method    Serial gentle manipulation and casting until a position of overcorrection is obtained.held in correction for 3-4 mos.,fitted with clubfoot shoes attached to a Dennis brown splint    Reduction of talonavicular joint  –   

Mild; self limited  Dorsiflexed ankle; eversion of the foot  Lenghtening of TA  Excessive pronation  treatment    No treatment    Gentle manipulation    Light corrective cast    Dennis brown splint   – 



Metatarsus Varus  Varus 

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key to success Rocker bottom  deformity  – hindfoot in equinus, forefoot dorsiflexion    Postero-medial soft tissue release    6 mos to two years old    Lengthening of TA, posterior tibial tendon, FHL, FDL    Release of posterior capsule, medial structures

     

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Dwyer Osteotomy- calcaneus 

in the transmetatarsal joint  1/3 of clubfoot?  Metatarsus primus adductus  Sometimes asso with clubfoot, calcaneo valgus of the opposite extremity  Residual of clubfoot deformity  Acquired (asso with valgus of hindfoot)  Cause of pigeon toe  Treatment   Manipulation; casting; surgical   – 

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Adduction of forefoot

Congenital Vertical Talus  Talus 

Excessive plantar flexion of the talus    Calcaneus- equinus position    Talonavicular and calcaneocuboid calcaneocuboid  

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 dislocated dorsally    Longitudinal arch is reversed    Forefoot is dorsiflexed 

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Simulates rocker bottom deformity  Treatment   Serial casting  Surgical     Surgical   Subtalar arthrodesis -. 10 years old   – 

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Congenital Clubhand  Clubhand   



Absence of radius    Complete / partial    Boys; bilateral(50%); right(2x)    Radial dev. of the hand; shortening of the f/a    Thumb ray, radial carpal bone(navicular),muscle controlling the thumb, radial artery and nerve  – absent    Elbow often abnormal; hand is useful   – 

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Ulna- bowed  Treatment   Passive stretching,serial casting,prosthesis, surgical   Absence of ulna    Elbow instability     

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Congenital Abnormalities of Fingers and Toes   Toes  



Camptodactyly - Digital flexion

deformity   PIP  of little finger- most common    Kirner’s deformity- dorsalulnar curvature of the distal phalanx   Clinodactyly  –curvature in the radioulnar plane    Syndactyly  – most common   – 

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middle ring most common    Simple  – soft tissue; complex  – bony fusion    Polydactyly  – 



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Preaxial- thumb; postaxial   small finger; central 

   

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Macrodactyly  – digital enlargement  Thumb hypoplasia  – undergrowth 

 

Arthrogryposis Multiplex Congenita  Congenita 

Cervical muscles is shortened  Abduction of shoulder is greatly affected,    glenohumeral motion not affected affected    Diagnosis    P.E, Xray    Vs paralysis of serratus anterior,obstetrical paralysis    

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Incomplete congenital fibrous ankylosis of joints    Trunk is spared    Symmetric,mild to severe    Unknown etiology; not hereditary    









Pathologic changes, mostly extraarticular    Joint capsules  –  thickened,contracted    Muscles decreased in bulk, absent, replaced by fat    Defective formation of the anterior horn cells    Clinical picture   Treatment   



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Treatment   Postural training, exercise    Surgical intervention-before 5 yrs old 

Congenital Synostosis of the Cervical Spine (Klippel-Feil Syndrome)  Syndrome) 

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Recurrence, unsatisfactory  unsatisfactory  Improve functional status  status  -Obtain stable well-aligned joints

Arrest of development  Fusion of all or of only the lower cervical spine into one homogenous mass or bone    Lamina not developed  – spina bifida   Classic triad   Short web neck   line    Low posterior hair   Limited cervical movement    Treatment    symptomatic    Plastic surgery     

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-Cast, extensive soft tissue release,arthrodesis



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Cleidocranial Dysostosis  Dysostosis  Partial/complete absence of clavicle    Exaggerated development of the transverse diameter of the cranium with delayed ossification of the fontanels    Clinical presentation    Treatment   

CONGENITAL ANOMALIES  ANOMALIES  GENERAL AFFECTION OF BONES









Congenital High Scapula (Sprengel s Deformity)  Deformity)  ’

Scapula elevated 1-4 inches  Inferior angle rotated medially Fails to descend to its normal position    Asso with other cong. Anomalies    Scapula  – small;; vertical length  –  decreased ;,width- increased    May unite with lower cervical vertebra  –omovertebral bone       

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Hereditary/genetic    Hormonal/endocrine    Enzymatic    Nutritional/ metabolic   

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Unknown WOLLF`S LAW    Every change in the form and function of bones or in their function alone is followed by certain definite changes in their internal architecture and equally definite changes in their external formation in accordance with mathematical laws.   Bone hypertrophy  – bone formation > resorption     



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Bone atrophy (osteoporosis)   resorption > formation  

 

Achondroplasia   Achondroplasia

2.  Osteopathia striata  striata    Coarse longitudinal striation in cancellous bone    Bony contour is normal  •

 



 



 



 



 



 



 



Most common form of short-limb dwarfism  Congenital, inherited, autosomal dominant  Enchondral osteogenesis is retarded  Membranous osteogenesis is unaffected  Pathologic process begins early in intra uterine life  – slowed, disorderly development of epiphyseal cartilage  Retardation of longitudinal growth of long bones Changes can can be recognized as early as 3 mos of intra uterine life by xray. 



3.  Osteopoikilosis  Osteopoikilosis    Small and scattered area of condensation-spotted •

appearance metaphysis  in the   Asso with small whitish skin lesion    AD 





Progressive myositis ossificans/fibrodysplasia ossificans progressiva Transformation of muscles and fascia into immobile structures of bony consistency    AD, male > female,    Begins early childhood   





Multiple Exostosis/ diaphyseal aclasis  aclasis       

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Multiple, osteocartilaginous masses  Metaphyseal, long bones  Broadening of metaphyses, shortening and bowing of of the shaft  Histologically a normal bone with a cartilaginous cap  Continues to enlarge by enchondral oss  Arise from epiphyseal plate Excision if symptomatic  Malignant degeneration



 



 



 



 



 



Under development and malalignment of great toes   Heralded by the appearance of painful, tender, subcutaneous masses  – regress, fixed  – undergo ossification  Neck and back are first involved  Bedridden, intercurrent infection  –  death  Steroids, diphosphonate compounds 

Osteogenesis Imperfecta (Fragilitas ostium/brittle bones)  bones)  Osteosclerosis   Regions of increased bone density density    Unknown cause,familial/hereditary    Excessive fluoride intake  •

 



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1.  Osteopetrosis(Albers-Schonberg dse,marble bones)  bones)    Failure of osteoclastic resorption  – narrowed medullary canal,splayed metaphysis    Early death in AR    Bone within bone appearance    Treatment of complications ,bone marrow transplant  •



 



   

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Hereditary,generalized connective tissue disorder  osteoporosis, with generalized thinning of the cortex, decreased diameter of the shaft, coarse trabeculation  Unknown etiology, AD,AR  Impaired maturation of the collagen fibers( type I)  Affects - ligaments, scleras, inner ear, skin  Woven, increased bone turnover, excessive bone formation and resorption taking place at all ages 

 

 



Osteocytes abnormally plentiful, lacunae are enlarged 

Types of OI  OI  Type AD/AR sclerae

Features  Features 

I

preschool age (tarda) 

AD

blue

A teeth involved, B not affected  II

AR

blue

lethal 

III AR N fractures at birth, progressive short stature  IV AD N mild form, normal hearing, IV-A teeth involved, IV-B not invloved  Treatment symptomatic; corrective osteotomies, medullary nailing Marfans Syndrome(Arachnodactily)  Syndrome(Arachnodactily) 

AFFECTIONS ASSOCIATED WITH DIETARY OR METABOLIC ABNORMALITIES  AVITAMINOSIS AND HYPERVITAMINOSIS   



VIT A 

Effect on osteoblast, osteoclast, chondroblast of growing bone    Pattern of bone growththick/short bones    Hypervitaminosis  – elevated periosteum-subperiosteal calcification, pain, irritability    Ulna and metatersals  – most commonly involved    VIT C    Regulating formation of intercellular substance    Conversion of prolene to hydroxyprolene  – collagen formation    Lack of -Interfers with osteoblastic activity    Decreased formation of osteoid or bone matrix    Defective capillary wall formation   Hemorrhage    Scurvy    Vitamin D   

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AD  Bones- assymetry of the skull,long fingers,scoliosis, coxa vara Joints- hypermobile,lax Eyes-Lens dislocation  cardiovascular (dissecting aneurysm)  Treatment directed at individual deformity hormonal to prevent excessive growth

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Mucopolysaccharidoses  Lysosomal storage dse  Enzymatic deficiency in the lysozymes    Intracellular accumulation of excessive amounts of mucopolysaccharides    Excretion of abnormal amounts of mucopolysaccharides mucopolysaccha rides in urine    Defective bone growth, joint contractures, hepatosplenomegaly, mental retardation, corneal clouding, cardiovascular cardiovascular abnormalities     

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Rickets (infantile/nutritional rickets)  rickets)  Dietary deficiency/malabsorption deficiency/malabsorption defects    Subnormal calcification with relative increase of osteoid tissue     Increase plasticity of bone that could not withstand normal stresses    

Increased bone resorption- sec hyperparathyroidism   Widened osteoid seams, thinned cortices, soft bones    Heart shape pelvis, shortened/telescoped spine, bowing of tibia and femur    Dxes  – iliac bone biopsy  –   

















  Disordered or delayed ossification Epiphyseal cartilage cells proliferate and hypertrophy but there is failure of mineralization    Widening and overgrowth of growth plate    Normal/ low calcium content,decrease phosphorus, increase alkaline phosphatase   







 



 



 



histomorphometric studiesquantification of amount of osteoid/ unmeniralized matrix on trabecular bone  Pain(shooting)/tenderness  – pelvis, back or hips  Muscular weakness, deformities,pathologic fractures  Xray   Loosers zone/pseudofractures  –  pathologic/fatigue  Treatment    Directed toward the  – 

Radiographic/clinical findings  findings   



Metaphysis - Widened,curved with irregular margin 

 



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Epiphysis - Widened ,obscurely outlined, contains one or more areas of indistinct oss., mottled appearance  Shaft  – thickened, fracture line, abnormal curvature  Recognized near the end of first year   Lethargy, weakness, tetany  Rachitic rosary  Harrissons groove  Craniotabes  Bowleg, knock knee,coxa vara,scoliosis  Treatment   Prevention- vit D(calciferol),  – 

phosphorus, calcium, exposure to sun     Proper posture, bracing    surgical (osteotomy) 

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Osteomalacia (adult rickets)  rickets)  Excess of unmeniralized bone matrix   Gastrointestinal malabsorption, anticonvulsant therapy, excessive intake of chelating agent, decreased sunlight exposure, dietary deficiency    Low/normal Ca, decreased P, alk phos and parathyroid hormone  –     

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elevated 

underlying source  Vit D- 5000 units daily  Calcitriol - .25 -1microgram daily   Calcuim -3grams daily 

   

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Osteomalacia associated with renal disorders   disorders Hypophosphatemia, refractory to Hypophosphatemia, treatment with ordinary dosage of vit.D, dysfunction of renal tubules     Hypophospha Hypophosphatemic temic rickets   





Sex linked dominant  Defect in renal absorption of P    Serum Ca and alk phos is normal, serum P is low    Tx  – oral P 2-4 g, high dose vit D    Vit D dependent rickets    AR,defect in conversion of 25OH,vit D  – 1,25 dihydroxy form   Hypercalcemia, phosphaturia, aminoaciduria, Increase PTH    Hypophosphatasia    

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Gradual resorption of bone trabeculae and a replacement of bone and marrow by fibrous tissue    Thin lamellae,scalloped surfaces,numerous osteoclast    Hemorrhagic cyst with

- AR,extremely low alkaline phosphatase,fatal phosphatase,fa tal in infantile form    Renal osteodystrophy    Chronic failure in adults/children, 5 yrs after the onset of renal failure    Low/N- calcium, high P and alk phos 

 

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Deposition soft tissues of calcium salts in

Scurvy   Scurvy  



 



 



 



 





       

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numerous tumors)  giant cells(brown   Areas new bone formation, weakened bone, bowing/deformity, pathologic fractures    Clinical picture    Women, middle ages,    General lassitude, muscular hypotonia    Treatment   Parathyroidectomy    Prevention of deformity    Phosphates/alendronates  – 

Deficient in takeof Vit C/ascorbic acid- 4- 6 mos  Changes in mesenchymal tissues of the body  Osteoporosis and depressed oteoblastic activity  Defective bone formation on the metaphyseal side of the growth plate Scorbutic line  – calcified zone of provisional calcification  Separation of epiphysis junction at the   epiphyseal-metaphyeal Subperiosteal hemorrhage  Clinical appearance 6-18 mos  Irritability, poor feeding, pain/ poor wound healing, hemorrhage, petechiae  Treatment    prevention   Vit C    symptomatic   – 

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Infantile Cortical Hyperostosis (Caffeys Dse)  Dse)  Self limited  Painful swelling and subperiosteal new bone formation    Shaft of long bones and mandible    Less than 6 mos old     Boys>girls    Irritability and swelling; tender wooden induration    Ruleout  – battered child,osteomyelitis, hyprvitaminosis A    No treatment,surgery contraindicated,steroids contraindicated,s teroids in severe form  Histiocytosis (Reticuloendotheliosis)  (Reticuloendotheliosis)     

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Hyperparathyroidism (generalized osteitis fibrosa cystica)  



 



 



 



 



   

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Excessive amounts of parathyroid hormone  Generalized osteoporosis and localized areas of bone destruction  Increase serum calcium and alk phos; phosphorus decrease/increase  Increase urinary calcium, hydroxyproline  Nephrolithiasis and renal insufficiency  Intestinal/psychiatric disturbances  Pathology 





 



Eosinophilic granuloma    Benign, solitary, children, young adult, males    Circumscribed area of bone destruction, 1  – 4 cm, sharply punched out appearance    Vertebral plana   – 

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Hemorrhagic granulation tissue, (mic)- large

 

mononuclears, collection of eosinophils, multinuclear giants cells    Disappear, excision, curettage, bone grafting    Hand-Schullers-C Hand-Schullers-Christian hristian dse    Multiple bone defects    Skull, skin, tendons, viscera    – 



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Bone is replaced by abnormal proliferation of fibro-osseous tissues   polyostotic   Girls, later years of growth period, predominantly unilateral, long bones    Albrights syndrome with caf é  au lait spots, endocrine  





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Diabetis insipidus, exophthalmos, gingivitis    Pituitary gland involvement;  jaundiced    Fatal; prednisone, chemotherapy, radiotherapy    Letterer-Siwe dse    Rapid, progressive,fatal    Liver, spleen, lymph nodes    Anemia, leukopenia ,anemia 

  bone  disorder Cancellous Gray lesions, soft and gritty; (mic) fibroblastic matrix embedded in scattered spicules of immature bone, (+)osteoid    Xray- radioluscent areas of ground glass appearance,thinned appearance,thinne d cortices, deformed contours ( Shepherd crook), pathologic fractures   Curettag,bone grafting and fixation

 

   

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Enchondromatosis (Olliers dse, Dyschondroplasia)  Dyschondroplasia)   



     

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Disorderly and excessive proliferation of the cartilage cells in different epiphyseal plates; young to mature chondrocytes  Within the metaphysis  Vs. exostosis  Maybe present at birth but not apparent  Failure of resorption during the process of enchondral oss.  Myxomatous degeneration;calcification  Predominantly on one side of the body- unequal leg length,bowing, angular deformities  Enlargement of digits and loss of function  Xray  – elongated radiolucent areas from epiphyseal line to the metaphysis; directed along the long axis of the bone  No specific treatment; osteotomy, limb lengthening  Malignant degeneration  – Mafucci syndrome( enchondromatosis plus hemangiomas) 

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Chronic, one or  many skeletal lesion; unknown cause

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Osteitis Deformans (Pagets dse)  dse) 



Fibrous Dysplasia  Dysplasia 

  Monostotic   Osteofibrous dysplasia/ossifying fibromatibial diaphysis

Chronic skeletal skeletal dse of of middle and late life  Begins insidiously, progressive structural changes and typical deformities  Mostly asymptomatic  Accelerated resorption and excesssive abnormal regeneration  During active phase- blood flow to the bone- high output cardiac failure Gradual thickening and bowing of the shaft of the long bones   Severe intractable pain, fatigue, stiffness and clumsiness  Deformity and enlargement of the bone  Kyphosis, barrel chest,  Deafness ,tinnitus, impairment of vision  Xray  – increase in curvature, cortex thickened to 5x, blurred, fluffy appearance, medulla narrowed,greatly increased cranial bones 

 

Increase alkaline phos,urine hydoxyproline,hypercalcemia    Diffvs hyperparathyroidism hyperparathyroidism ,metastatic Ca, osteomalacia, syphilis    Treatment   Serial obsrvation    Calcitonin,  







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piphosphonates,mothramyci n    Surgical    Good prognosis    Development of malignancy osteogeniccarcinoma   – osteogeniccarcinoma

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Senile Osteoporosis  Osteoporosis   

Acquisition of bone mass up to 40 yrs old    Accentuation of physiologic loss of bone mass    Senile/postmenopausal







   

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  stature, white   osteoporosis Women, small Smokers ,heavy drinkers  Sedentary  Commonest metabolic affectation of bone  Cancellous bone is greatly affected  Quantitative not a qualitative defect  Develops when bone that is being lost by normal catabolism is not replaced in equal measure by new bone formation  Decrease osteoblastic activity  Mild prolonged negative calcium balance    Decrease absorption, inadequate intake  Changes in gonads and adrenal gland  Inactivity in old age   Deficiency in estrogen  – defective protein metabolism  Mechanism of Bone Mass Regulation  Types    Type I  – (postmenopausal) (postmenopausal) affects trabecular bone,  – 

 



   

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vertebral fracture  and distal radius

Type II  – (age related) more than 75 yrs old, both trabecular and cortical bone, hipand pelvic fracture    Clinical picture    Fractures    Pain, kyphosis, deformity   

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Diagnosis   Normal serum Ca, P, alkaline phosphatase    Xray- more than 30% bone loss    Single photon (appendicular) absorptiometry    Dual photon (axial) absorptiometry    Quantitative CT scan    Dual energy xray absorptiometry (DEXA)    Histologic- thinning of trabecuale, decrease size of osteons, enlargement of haversian canal and  

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marrow spaces  Treatment

Posttraumatic painful osteoporosis (sudecks atrophy,reflex sympthetic dystrophy)   dystrophy)  



 



   

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Prolonged local pain, swelling,vasomotor instability, trophic changes, diffuse patchy rarefaction and atrophy of the bone after an injury of an extremity or peripheral nerve  Trauma is minor;disturbance is greater than the expected from the injury  Hands and foot  Atrophy develops very rapidly  Disturbed function of the sympathetic nerve supply 

 

Vs atrophy of disuse and causalgia  Heals spontaneously,  Brief splinting; prolonged physical therapy; active exercise    Sympatholytic drugs, sympathetic block, ganglionectomy, sympathectomy      

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PROVERBS 3:5-6 Trust in the Lord with all your heart and lean not on your own understanding in all your ways acknowledge Him in He will direct your path. 

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