SKELETAL DISORDERS OF METABOLIC AND ENDOCRINE ORIGIN DR. NAVNI GARGDNB RESIDENT, MEDANTA –THE MEDICITY

MATURE BONE

Lies within the medullary canal

Meshwork of primary longitudinal and secondary transverse trebaculae

Normally in ends of long bones and axial skeleton

Consists of haversian system : haversian canal surrounded by bony lamellae with volkman’s canal connecting them

TREBACULAR/ CANCELLOUS/ SPONGY CORTICAL

PARTS OF LONG BONE

GROWTH PLATE / PHYSIS Located at end of long bones between epiphysis

and metaphysis Site at which proliferation and orderly maturation of

cartilage cells occur Functionally part of shaft of long boneFour zones Resting/ germinal zone Proliferating zone Hypertrophic zone : zone of maturation,

degeneration and provisional calcification Zone of primary and secondary spongiosa

GROWTH PLATE Proliferating : cartilage

cells multiply Hypertrophic : marks

the end of lucent growth plate and beginning of calcified metaphysis

Spongiosa : calcified cartilage column, produce bone via enchondral calcification

BONE FORMATION

CLASSIFICATION Defect in osteoid formation : scurvy Defect in mineralization : rickets/

osteomalacia Disorder with increased bone resorption :

hyperparathyroidism Disorder with decreased bone mass :

osteoporosis Miscellaneous : fluorosis, heavy metal

poisoning, hypervitaminosis

CAUSES OF RICKETS AND OSTEOMALACIA

NUTRITIONAL RICKETS

PATHOLOGY Characteristic changes of rickets are identified

in the growth plate prior to closure Disorganisation of growth plate and adjacent

metaphysis Zone of maturation affected with disorganised

increase in number of cartilageneous cells : increase in length and width of growth plate

Zone of provisional calcification shows deficient mineralisation : Increased uncalcified osteoid and decrease in calcified osteoid

CLINICAL FEATURES First 6 months : tetanic convulsions Irritability, weakness Delayed development Small stature Bony deformities and pain Rachtic rosary Swelling of wrist and costocartilage

RADIOLOGICAL FEATURES MC and non specific finding : osteopenia Changes seen at open growth plate Especially visible at fast growing growth

plates like costochondral junction of the middle ribs, distal femur, proximal humerus, both ends of tibia, distal ulna and radius

Earliest sign : distal ends of radius and ulna. Ulnar growth plate grows more rapidly so manifestations are seen earlier in ulnar growth plate

WIDENING OF GROWTH PLATE Earliest and specific radiological change Due to increase in cartilageneous cell

mass

METAPHYSEAL FRAYING Irregular

metaphyseal margins occuring due to fraying and disorganisation of spongy bone in the metaphyseal region

METAPHYSEAL CUPPING AND WIDENING

Protrusion of bulky mass of cartilageneous cells in the zone of hypertrophy into the poorly mineralized metaphysis

Cupping is common in both ends of fibula and distal end of ulna and tibia

Not seen in bones of elbow

EPIPHYSEAL ABNORMALITIES Osteopenia Irregural and indistinct borders Delayed appearance of ossification

centres

SHAFT ABNORMALITIES Rarefaction of shaft due to loss of

mineral content Cortex becomes thin with a coarse

texture

SKELETAL DEFORMITIES Skull : Craniotabes Long bones : bowing deformities Ribs : rachitic rosary Spine : scoliosis and vertebral end plate

deformities (when weight bearing becomes prominent)

Pelvis : triradiate configuration

CRANIOTABES Excess osteoid

deposition in frontal and parietal regions with posterior flattening of skull due to supine posture of infant

Squared configuration of skull

Demineralisation of skull

BOWING OF LONG BONES Result of

displacement of growth centres owing to asymmetrical musculotendinous pull on the weakened growth plate

RACHITIC ROSARY Bulbous

enlargement of costochondral junction especially middle ribs

May indent pleural surface or thymic shadow

TRIRADIATE PELVIS Protrusion of hip

and spine into the soft pelvis with protrussio acetabuli

SIGNS OF HEALING RICKETS Seen within 2-3 weeks of adequate therapy Total calcification is usually complete in 2

monthsSigns : Reappearance of dense zone of provisional

calcification : first evidence Increase in cupping of healing metaphysis Recalcifiaction of subperiosteal osteoid

resulting in thick cortex surrounding the shaft Sharply defined ossification centres

REAPPEARANCE OF DENSE ZONE OF PROVISIONAL CALCIFICATION

Seen as a transverse line of increased density which appears beyond the visible end of shaft with a metaphysis interposed between two radiolucent areas

Complete healing and restoration of normal structure is the rule in rickets even if severe changes are present during the active stage !!!!

HEREDITARY VITAMIN D DEPENDANT RICKETS

1 alpha hydroxylase deficiency

Dec levels of 1,25 dihydroxy D 3

Presents within 3 months Convulsions and muscle

weakness, severe rachitic bone changes, pathologic fractures

Rx : 1,25- dihydroxy D3

End organ resistance to 1,25-dihydroxy D3

Elevated levels of 1,25 dihydroxy D3

Severe rickets,growth retardation, dental changes, alopecia

Rx : Calcium supplements

TYPE 1 (Psuedo vitamin D deficiency )

TYPE 2 (Calcitriol resistant rickets )

X LINKED HYPOPHOSPHATEMIA

Familial Vitamin D resistant/ refractory rickets MC form of renal tubular rickets and osteomalacia X linked dominant Rickets develops between 12-18 months of age Lifelong hypophosphatemia due to impaired

reabsorption of phosphate from proximal tubules Also impaired conversion of 25 hydroxy D3 into

1,25 dihydroxy D3 Low serum phosphate, normal serum calcium,

normal PTH

RADIOLOGIC FEATURES Bowing of legs Coarsening of trebacular

pattern with increasing age Generalized

increase/normal bone density especially axial skeleton

Calcification and ossification in paravertebral ligaments, ligamentum flavum, iliolumbar and sacroiliac ligaments

Osteoarthritis in ankle, knee, wrist, sacroiliac joints

ONCOGENIC OSTEOMALACIA Seen in adults with some vascular

neoplasms like hemangiopericytoma Tumors produce phosphatonin which

inhibits absorption of phosphate in proximal tubule resulting in hypophosphatemia

Advanced rachitic changes may be present

Refractory to vitamin D therapy Respond to tumor removal

DRUG INDUCED RICKETS Due to high doses of ifosfamide Nephrotoxic Metabolites cause tubular

damage Results in fanconi syndrome and

hypophosphatemic rickets

METAPHYSEAL CHONDRODYSPLASIA

Generalised symmetric disturbance of enchondral bone formation primarily at metaphysis

Seen in childhood : short stature, bowing of long bones

Normal serum calcium, phosphorus, ALP levels Widening of growth plate with multiple bony

projections growing from metaphysis into growth plate Metaphysis is well mineralised and shows increased

density with absence of loosers zone Spontaneous improvement, no response to vitamin D

therapy

HYPOPHOSPHATASIA

Defective skeletal mineralisation with normal serum calcium and phosphorus, low levels of alkaline phosphatase

Increased amount of phosphoethanolamine amino acid in blood and urine

Usually presents in infancy and childhood

Neonatal death may occur in severe disease

RADIOLOGICAL FEATURES Growth plate changes

similar to rickets with multiple radiolucent extensions into the metaphysis (uncalcified bone matrix)

Coarse trebacular pattern

Bowing deformity, fractures

Wormian bones, craniosynostosis

ATYPICAL AXIAL OSTEOMALACIA

Axial skeletal involvement with sparing of appendicular skeleton

Dense coarse trebacular pattern : most marked in cervical region , may be seen in Lumbar spine, pelvis or ribs

Normal serum calcium, phorphorus, ALP No response to vitamin D therapy

OSTEOMALACIA

PATHOLOGY Abnormalities are seen in mature areas

of trebacular and cortical bone Defective mineralisation of cortical and

spongy bone with Increase in unmineralised osteoid

C/F : fatigue, malaise , bone pain , proximal muscle weakness

RADIOLOGICAL FEATURES Osteopenia : Uniform involving all the bones Coarse indistinct trebacular pattern Thin cortex of long bones Pseudofractures Bone deformities : medial acetabular

migration (protrussio acetabuli ), triradiate pelvis, bowing of legs

Spine : kyphoscoliosis , increased endplate concavity

Pseudofractures / umbauzonen/loosers zone/milkman’s fracture

More specific but less common manifestation

Loosers zone : linear areas of undermineralised osteoid that occur in bilateral, symmetric distribution

Oriented at right angles to the cortex Occur due to vascular pulsation acting on

the softened bones May show mild-moderate sclerosis with

absence of callus formation

Site of increased stress resulting in fracture

Accelerated bone turnover

Inadequately mineralised osteoid

Radiolucent area

LOOSER’S ZONESites : Axillary margins of

scapula Superior and

inferior pubic rami Inner margin of

proximal femur Posterior margin of

proximal ulna Ribs

SPINE

Defective mineralisation

Overall decrease in number of bony trebaculae within all the bones enhancing the contrast of remaining trebaculae giving coarse mottled appearance

Decreased bone mass without any defect in mineralisation

Trebaculae are thin and sharp

OSTEOMALACIA OSTEOPOROSIS

HYPERPARATHYROIDISM

Occurs due to excessive production of PTH

Primary : due to excess production by abnormal gland like adenoma, hyperplasia , carcinoma

Secondary : abnormality in gland induced by sustained hypocalcemic stimulus like CRF, malabsorption states

Tertiary : due to long standing secondary HPT who develop autonomous parathyroid function

ACTIONS OF PTH

CALCIUM METABOLISM

RADIOLOGICAL FEATURES Bone resorption Brown tumors Joint disorders Osteosclerosis Renal osteodystrophy

BONE RESORPTION Hallmark of hyperPTH Due to increased osteoclastic activity Can be subperiosteal, intracortical,

endosteal , subchondral and trabecular Cortical bone is affected more than

cancellous bone Seen as poor definition of cortical

surfaces , increased cortical striations (tunneling ), cortical thinning , distortion and blurring of trabecular bone

SUBPERIOSTEAL RESORPTION

Pathognomic of HPT Earliest site : radial

aspect of middle phalanges of middle and index fingers and terminal tufts of fingers

Others : medial aspect of proximal end of tibia, humerus and femur, superior and inferior margins of ribs, lamina dura

LOSS OF LAMINA DURA Seen in dental sepsis, pagets disease,

fibrous dysplasia, osteomalacia also

INTRACORTICAL BONE RESORPTION

Osteoclasts tunnel through volkman’s and haversian canals causing tiny linear striations within the cortex parallel to long axis of bones

Tubular bones of hands and feet esp cortex of second metacarpal

Almost always associated with subperiosteal resorption

ENDOSTEAL BONE RESORPTION Leads to cortical thinning, scalloping and

irregularity of the endosteal surface esp bones of hand

Mostly occurs in conjuction with subperiosteal and intracortical resorption

SUBCHONDRAL BONE RESORPTION

Common manifestation of hyperPTH Seen in joints of axial skeleton,

sacroiliac, sternoclavicular , acromioclavicular , pubic symphysis, discovertebral junctions

Surface irregularity with increased joint space

Most severe in distal ends of clavicle

SUBPHYSEAL BONE RESORPTION Seen in children with primary or

secondary hyperHPT Irregular radiolucent areas in metaphysis

adjacent to growth plate

SUBLIGAMENTOUS AND SUBTENDINOUS BONE RESORPTION

Occurs at sites of tendon and ligament attachment to bone

Involves femoral trochanter, ischial and humeral tuberosities, elbow , inferior surface of calcaneum, inferior aspect of distal end of clavicle

TREBACULAR BONE RESORPTION Occurs throughout skeleton in advanced

stage of disease Osteoclasts dissect through the centre of

trabecula giving a stippled, mottled, granular appearance of skull ( SALT AND PEPPER SKULL)

Definition of inner and outer table is lost

SALT AND PEPPER SKULL

BROWN TUMORS Osteitis fibrosa cystica Cystic lesions within the bone due to

extensive bone resorption May cause swelling, pathological fracture

or pain Represent hemorrage and deposition of

breakdown products of hemoglobin Risk of pathological fracture is more

when brown tumor involves more than two thirds of the cortex of long bone especially in weight bearing areas

Multiple Iytic, expansile ,cystic lesion

Eccentric or cortical location

Sites : mandible, clavicle, ribs, pelvis and tubular bones

JOINT DISORDERS Erosive arthropathy of hands, wrists and

shoulders Almost always associated with typical

subperiosteal resorption of phalanges and occur on ulnar aspect of metacarpal heads

Chondrocalcinosis or calcification of hyaline/fibrocartilage of knee, pubic symphysis or wrist due to calcium pyrophosphate dihydrate deposition

OSTEOSCLEROSIS Increased bone density due to

stimulation of osteoblastic activity by PTH in addition of osteoclastic activity

Sec HPT : diffuse increase in bone density

Pri HPT : localized / patchy sclerosis Focal bone sclerosis seen in metaphyseal

regions of long bones, skull , vertebral end plates

Skeletal features Less florid skeletal

features Sclerosis rare Brown tumors and

chondrocalcinosis more common

Soft tissue and vasc calcification less common

Skeletal features with changes of renal osteodystrophy

More florid Sclerosis common Brown tumors and

chondrocalcinosis less common

Soft tissue and vasc calcification more common

PRIMARY HYPERPTH SECONDARY HYPERPTH

DIALYSIS ASSOCIATED ARTHROPATHY

Axial and appendicular skeleton destructive arthropathy due to long term dialysis

Chronic, progressive ,symmetric polyarthropathy involving large and small peripheral joints

Periarticular cysts , erosions , loss of joint space , loss of articular surface, osteopenia

SPINE DRSA usually after 3-5 years of dialysis,

cervical spine involved MC . Narrowing of disc height, subchondral

cysts, endplate erosions, collapse, erosion of contiguous vertebral bodies, facet erosion , spondylolisthesis, peridiscal calcification.

Calcification in subcutaneous regions, vascular, muscular , visceral organ .

RENAL OSTEODYSTROPHY

Bony changes seen in patients with chronic renal insufficiency

Children : structural abnormalities of urinary tract

Adults : chronic glomerulonephritis

RADIOLOGIC FEATURESSec hyperparathyroidism Bone resorption (subperiosteal,

intracortical , endosteal , subligamentous) Brown tumors Soft tissue and vascular calcification Osteosclerosis ( focal / diffuse ): rugger

jersey spine, pelvis , ribs , clavicles Osteopenia : end result of osteomalacia,

bone resorption, osteoporosis

RENAL OSTEODYSTROPHY

Deposition of bone in subchondral areas of vertebral bodies

Radiodense bands across superior and inferior vertebral margins

Rugger jersey spine

CALVARIAL THICKENING

HYPOPARATHYROIDISM

CAUSES OF HYPOPTH MCC : excision/ trauma to parathyroid

gland during thyroid surgery Idiopathic hypoparathyroidism due to

circulating antibodies to PTH , adrenal and thyroid glands

Radiation induced damage to the gland

Low serum calcium and PTH , high phosphate

RADIOLOGICAL FEATURES Focal or generalised bone sclerosis Pelvis, proximal femur , vertebral bodies Calvarial thickening Hypoplastic Dentition Band like areas of increased radiodensity in

metaphysis of long bones Calcifiction and ossification of anterior

longitudinal ligament and spinal osteophytes Calcification in basal ganglia, cerebrum,

cerebellum

 Mineralization of iliolumbar ligament (pink arrow), broad ossification at the lateral margin of acetabulum (white arrow), osseous proliferation and irregular bony excrescences above the acetabulum (arrowhead), and lesser and greater trochanters and ischial tuberosities (open arrows)

Capsular calcification of the hip joint (black arrow) and internal fixator for the right femoral shaft fracture.

Bilateral basal ganglia calcification

PSEUDOHYPOPARATHYROIDISM

Autosomal dominant Due to end organ resistance to

parathyroid hormone Due to defect in adenyl cyclase cyclic

AMP system in renal tubules and bones Second decade, F>M Short , obese , mentally retarded,

brachydactyly Low calcium, high PTH and phosphate

RADIOLOGICAL FEATURES Shortening of fourth

metacarpal Soft tissue calcification

and ossification, basal ganglia and calcification

Calvarial thickening Short metatarsals and

phalanges Premature closure of

epiphysis Exostoses projecting at

right angles to the bone Features of hypoPTH

Not seen Short first and fourth metacarpal

Exostosis perpendicular surface of bone

HYPOPARATHYROIDISM PSEUDOHYPOPARATHYROIDISM

PSUEDOPSEUDOHYPOPARATHYROIDISM

Result of incomplete genetic manifestation of PHP

Caused by end organ resistance to PTH Pts with PPHP have normal calcium Radiological features like PHP except

higher rate of short metacarpals in PPHP and short distal phalanges in PHP

HYPERCORTISOLISM

CAUSE Tumor of adrenal gland Ectopic ACTH production Iatrogenic Basophil pituitary adenoma

Inhibiton of bone formation Stimulation of bone resorption Decrease in intestinal absorption of

calcium Decrease in synthesis of collagen

Osteonecrosis, osteoporosis, muscle wasting

RADIOLOGICAL FINDINGS Generalized loss of bone density : spine, pelvis, ribs,

cranial vault (trebacular bone > cortical bone) Accentuation of primary trebaculae, with central

endplate depressions in the vertebral bodies (biconcave fish like appearance )

Increased radiodensity of superior and inferior margins of compressed / collapsed vertebrae (d/t exuberant callus formation )

Exuberant callus at fracture sites in long bones and ribs

Local regions of osteonecrosis esp after exogeneous steroids ( AVN at femoral and humeral heads)

Skeletally immature child Suppresses growth : short child Osteoporosis , truncal obesity , delayed

bone age Osteonecrosis at growing epiphysis may

lead to abnormal development at ends of long bones

Early development of osteoarthropathy

HYPOPITUITARISM

Delay in skeletal maturation : delay in appearance and closure of epiphysis

Retarded skeletal growth Overall loss of bone density

HYPOTHYROIDISM

Thyroid neoplasm Thyroiditis Thyroid ablation Disturbance in

iodine metabolism

Def of TSHPRIMARY SECONDARY

Infant : cretinism Child : juvenile myxedema Adult : myxedema

CONGENITAL HYPOTHYROIDISMXRAY WRIST AND XRAY KNEE Delay in skeletal maturation with bone age lagging

behind chronological age : short stature and late appearance of epiphyseal ossification centres

Normally , distal femoral epiphysis is ossified at 36 wks and proximal tibial epiphysis at 38 wks : dec size/ absence indicates hypothyroidism

Deformed , irregularly shaped epiphysis (EPIPHYSEAL DYSGENESIS ): bilateral and symmetrical

Delayed closure of epiphyseal plates

Skull : sutures may remain open and show wormian bones, small sella in young or large, rounded in old children

PNS are underdeveloped Pelvis : narrow with coxa vara deformity ,

inc incidence of SCFE Spine : bullet shaped VB , kyphosis

ADULT HYPOTHYROIDISM Mild skeletal manifestations Generalized osteoporosis

HYPERTHYROIDISM

Accelerated skeletal maturation therefore bone age ahead of chronological age

Osteoporosis with VB fracture and kyphosis

CHILD ADULT

RADIOLOGICAL FINDINGS Osteoporosis : spine, pelvis, skull, hands and feet Progression of thyrotoxic osteoporosis is faster than

post menopausal osteoporosis but same radiologically

DL vertebra more affected : Biconcave VB , wedge deformities , kyphosis, fractures

Tubular bones of hands, feet : cortical tunneling and striations due to inc osteoblastic and osteoclastic activity

Thyroid acropachy in treated pts : exophthalmos, soft tissue swelling of fingers and toes, pretibial myxedema or clubbing

Dense , solid, periosteal new bone formation with feathery margins

Asymmetric periosteitis : most prominent along the radial margin of metacarpals and phalanges in the diaphyseal region

Hands and feet Feathery contour

Long bones Absent

THYROID ACROPACHY HYPERTROPHIC OSTEOARTHROPATHY

TURNERS SYNDROME

Skeletal maturation is usually normal till 15 years of age following which delayed epiphyseal closure occurs esp apophysis of iliac crest

Depression or slanting of the medial tibial plateau with concomitant overgrowth of medial condyle of femur

Short fourth and fifth metacarpal Narrow ribs Small sella Android pelvis Hypertelorism

ACROMEGALY

Reactivation of enchondral bone formation

Stimulates periosteal bone formation Connective tissue proliferation

CLINICAL FEATURES 3-4 decade Coarse facial features Thick skin Dental occlusion Deepening of voice Prominent tongue Broad hands and feet Organomegaly

DEFINITIVE DIAGNOSIS 24 hours serum GH levels GH secretion not suppressed by oral

glucose Serum level of insulin like growth factors

RADIOLOGICAL FINDINGSSKULL

Cranial vault thickening Prominence of supraorbital ridges and zygomatic

arches Prominence of ext occipital protruberance Enlargement of sella Prominence and enlargement of maxillary and

frontal sinuses Excessive pneumatisation of mastoid Enlargement and elongation of mandible with

widening of mandibular angle

HANDS AND WRIST AND FEET Soft tissue thickening of fingers Thickening and squaring of phalanges and

metacarpals Overconstriction of shafts of phalanges Abn wide articular surfaces : MCP, MTP, IP Bony excrescences at site of tendon and ligament

attachment to bone Prominence of ungal tufts ( spade like ) Keel shaped deformity : resorption of cortex along

plantar aspect

INDICES Increased phalangeal soft tissue thickness at

prox mid phalanges > 27 mm (men) and > 26 mm (women)

Widening of second MCP joint > 2.5 mm in men and women

Bone excrescences and marginal spurs Inc width of phalages : spade like Large sesamoid index > 40 mm(M) and >

32mm (F) Inc interstyloid distance

HEAL PAD THICKNESS Shortest distance between calcaneum

and plantar surface of skin > 21.5 mm (f) and >23 mm (m) :

suggestive >23 mm (f) and > 25 mm (m) :

diagnostic

MALE FEMALE

HEEL PAD THICKNESS > 23 > 21.5

SESAMOID INDEX >40 >32

TUFTAL WIDTH >12 >10

PHALANGEAL SOFT TISSUE >27 >26

JOINT SPACE >2.5 >2.5

VERTEBRAL COLUMN Elongation and widening of vertebral

bodies Increase in vertebral height Ant and lat osteophytes Inc height of IVD Scalloping of post margins of VB Inc thorasic kyphosis Exagerrated lumbar lordosis

Enlarged thorax due to elongation of ribs and prominence of costochondral junction

Pelvis : enlargement and beaking of symphysis pubis

Feet : soft tissue enlargement , prominence of tufts and base of terminal phalanges, bone proliferation at sites of tendon and ligament attachment like undersurface of calcaneum

Articular abnormalities : knee, hips, glenohumeral joints. Widening of articular space seen at MCP, MTP and IP joints

ACROMEGALIC ARTHROPATHY

Hypertrophy causing Fissuring Ulceration Denudation

(Degenerative arthropathy , changes of OA )

Hypertrophy Brisk

regeneration : chronic > thickened cartilage > inc joint space > enlarged bones > hypertrophy of periarticular soft ts.

HYALINE CARTILAGE FIBROCARTILAGE

FIBROCARTILAGE HYPERTROPHY Calcification and ossification > calcinosis

+ osteophytes > at atypical sites like glenohumeral and elbow joint

Presence of beaklike osteophytes at inferior part of head of humerus , lateral aspect of acetabulum , medial part femoral head , sup margin pubic symphysis , radial head , tibia

GIGANTISM

Extreme height with normal body proportions

SCURVY

Due to long term vitamin c deficiency Infantile : due to pasteurised or boiled

milk formula 6 months – 2 years C/F : progressive irritability with tender

edematous limbs, subcutaneous / mucous membrane hemorrages, anaemia, bleeding gums, malena, bulging at costochondral junction

PATHOLOGY Vitamin C necessary for Endothelial

lining : deficiency causes increased vascular fragility

Decreased osteoblastic activity and cartilage proliferation resulting in decreased formation of bony matrix

Normal mineralisation Osteoporosis

WHITE LINE OF FRENKEL White line in the zone

of provisional calcification at the growing metaphysis

Cartilage proliferation decreased with normal mineralisation resulting in widened and dense zone of provisional calcification

TRUMMERFELD ZONE (SCORBUTIC ZONE)

Transverse radiolucent band adjacent to zone of provisonal calcification due to suppressed osteoblastic activity with normal mineralisation

Trabecular bone mass is decreased in zone of primary and secondary spongiosa.

WIMBERGER SIGN Epiphysis is small

sharply marginated by sclerotic rim with central portion more radiolucent.

Due to decrease cartilage proliferation and unimpaired mineralization (sclerosis)

CORNER (ANGLE) SIGN Irregularity of the

metaphyseal margins secondary to infractions of the epiphyseal-metaphyseal junction

PELKAN’S SPUR Zone of

provisional calcification extends beyond the margins of the metaphysis resulting in periosteal elevation and marginal spur formation

SUBPERIOSTEAL HEMORRAGES

Due to increased capillary permeability

Seen in ends of long bones(femur,tibia, humerus)

May cause periosteal elevation and new bone formation

On vitamin C therapy, all changes are reversible though single growth arrest line may remain in metaphysis as residual frenkel’s line.

FLUOROSIS

ETIOLOGY Chronic ingestion of flouride in excess of

8 ppm in drinking water Industrial expose to fluorine

compounds for many years In laboratory personnel due to

inhalation of fluorine vapors Agricultural fluoride contamination Habitual drinking of wine containg

fluorine i.e. wine fluorosis

PATHOLOGY Generalized increase in bone density due to

osteoclastic response to fluorine

Excess fluorine Osteoclastic activity increases, Disturbed normal collagen synthesis

Fluoride have strong affinity for bone salts replacing hydroxyl ion; Hydroxipatite converted into fluoropatite which is more resistant to dissolution

CLINCAL FEATURES Initially asymptomatic Rare in children because it takes 12 or

more years after exposure to develop changes

Polydipsia Anemia Mottling of enamel of teeth Crippling stiffness and pain Pathological fractures

RADIOLOGIC FEATURES Thickening of the

cortex of affected bones

Ribs : Inferior margin may show irregularity/fringed appearance (rose thorn appearance )

Osteosclerosis most marked in

spine, pelvis, ribs Skull and tubular

bones are spared Calvarium :

sclerosis of base of skull and posterior clenoid

Ossification and calcification of ligaments of sacrospinous, sacrotuberous

Ossification of interosseus membrane

Vertebral Osteophytes Paraspinal and

intraspinal ligament ossification

OSSIFICATION OF INTERROSEUS MEMBRANE

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