orthopedics bonedisorders
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Orthopedics BoneDisordersTRANSCRIPT
Orthopedic disorders classification• Injuries • Deformities (congenital, acquired)• Joint disorders (infection, degeneration, subluxation - derangement)• Bone disorders (infection, tumour, generalized disorders)• Soft tissue disorders (inflammation, infection, tumor)• Neurological disorder (eg. poliomyelitis, cerebral palsy, peripheral nerve lesions)
Generalized disorders of the bone: • Endocrine disorders with skeletal abnormalities • Metabolic disorders of the bone• Bone dysplasias
Functions of bone in the human bodyMechanical • Support, protect soft tissues• Transmit force, mediate movement, locomotion
Biological – metabolic:• Mineral reservoir of clacium +phosphate: regulates calcium + phosphate concentration in the
body fluids Bone composition and structure:Largely collagenous matrix which is impregnated with mineral salts and filled up with cells – osteoblasts and osteoclastsHalf of bone volume is mineral material – calcium and phosphate in the form of crystalline hydroxyapatite
Bone mass: the amount of osseous tissue in any unit volume of bone (eg. Ccm)
Effect of mechanical stress on bone: Wolff’s lawBone structure adapts itself to functional demands: it is thicker, where weight bearing is larger
Metabolic disorders of boneDefinition: Disturbance of • osteogenesis (bone formation),• bone mineralization• bone remodelling
2 main types:• Osteopenia (bone loss, lack of bone) – osteoporosis, osteomalatia • Osteosclerosis (too much bone)– Paget’s disease, osteopetrosis
Basic metabolic element of bone biology: Calcium metabolism , calcium turnover– absorption and reabsorption from intestine, excretion through urine, integration into bone and resorption from bone
Regulation of bone metabolism1. Parathyroid (parathormone)2. Thyroid (C-cells - Calcitonine )3. Growth hormone4. Oestrogens, androgens5. Corticosteroids6. Vitamine D7. Vitamin C
• Parathyroid (PTH): increased calcium resorption and phosphate excretion in kidney• Calcitonine (thyroid C-cells): inhibits osteoclast activity• Growth hormone: acts on growth plate (physis)
• Oestrogens, androgens: in puberty they act on growth plate, in menopause, lack of oestrogen leads to osteoporosis
• Corticosteroids: inhibit calcium resorption from intestine, decrease bone mass• Vitamine D: increases calcium and phosphate resorption from kidney and intestine• Vitamin C: increases collagen synthesis in bone matrix
Calcium:• Serum level: 2,2 – 2,6 mmol/L• Daily intake of calcium: 800-1000mg ( 1500 mg during pregnancy)• Absorption of calcium from intestine, excretion through kidneys, and reabsorption from renal
tubules• Vitamin D: essential in calcium absorption from the bowel
• Calcium metabolism – absorption and reabsorption from intestine, excretion through urine, integration into bone and resorption from bone
Vitamin D:Main role: • calcium absorption from small intestine• Mineralization of bone
Source of vitamin D: • Direct source - diet (food)• Indirect: ultraviolet light converting the precursor (7-dihydrocholesterol) in the skin to vitaminD
Requirement of vitamin D: 400 IU (international unit) per day (exposure to sunlight may be sufficient in many countries)
Forms of bone lossOsteopenia: general term = diminished amount of calcified bone, due to any cause (with or without normal bony structure)Osteoporosis: Bone loss with normal microscopic bony structure and normal mineralization
Osteoporotic fracture- compression of thoracic vertebral bodies – increased kyphosis
Fracture of femoral neck due to simple fall – osteoporosis of femoral neck
Osteoporosis:Typical manifestations:• Increased thoracic kyphosis• Pain (mostly back pain)• Frequent fractures :- femoral neck- distal radius- proximal humerus
Regulation of calcium (and phosphate) metabolism of boneHormones:• Parathyroid: acting on renal tubules, increases phosphate excretion and calcium reabsorption• Calcitonin: thyroid C hormone – suppresses osteoclastic activity• Oestrogen: stimulates calcium absorption• Steroids (cortisone etc.): increased intake leads to massive osteoporosis
1. adolescence to 35 years: bone mass increases with 3%/year2. 35- 50 years: 0,3%/year (men) or 0,5%/year (women) reduction in bone mass3. Menopause and the next 10 yrs: 3%/year bone loss 4. From 65 or 70 yrs: rapid bone loss - 0,5%/year bone loss in women (in men 15 years later)
Metabolic Disorders of bone:Definition: Disturbance of osteogenesis (bone formation), bone mineralization and bone remodelling2 main types:• osteopenia – too few bone( osteoporosis, osteomalatia, hyperparathyroidism etc.) • Osteosclerosis – too much bone (Paget’s disease, osteopetrosis)
Causes of Primary Osteoporosis:Likely causes:-Hormonal changes - oestrogens / androgens-INACTIVITYUnlikely:-Low calcium intake? -Protein deficiency?-Vitamin -D deficiency – it may contribute to primary osteoporosis
Cause of Osteopenia:1./ Osteoporosis• Primary, age related (eg. postmenopausal)• Secondary
- steroid therapy- alcoholism + smoking- immobilization – following trauma (localized osteoporosis!!)- lack of gravity - space flight- malabsorption
2./ Osteopenia with abnormal bone structure:• Hyperparathyroidism• Regular haemodyalisis (uraemia)• Osteomalacia
3./ Ostopenia due to inherited disorders:• Osteogenesis imperfecta• Chromosome disorders
Clinical features in osteoporosis symptoms and signs• Back pain – later with kyphosis (collapsed vertebrae)• Shortening of trunk height• Generalized pain• Pathological fractures (radius, proximal humerus, hip Fxs)
Radiological features in osteoporosis• Generalized lack of bone density• In advanced cases, collapsed vertebral bodies
Diagnosis in Osteoporosis:Imaging – densitometry• Ultrasound• Single x-ray „absorptiometry”• Dual x-ray absorptiometry: x-rays from two sources – (eg. in examination of vertebral bone
density) – degree of absorption of radiation is being measuredCalculation of changes in bone density:deviation from bone mass measured at young age (SD- standard deviation) so called T-scorePathological value: T-score -2,5
Bone mass: amount of osseous tissue in any unit volume of bone.Bone mass decreases with advancing years above a certain age
Histological diagnosis of metabolic bone disease (osteoporosis): bone biopsy from iliac crest
(continue of diagnosis in osteoporosis)Laboratory:• Serum calcium level• Serum phosphor• Alkaline phosphatase
These values show no or minimal changes in primary osteoporosis, but may be of diagnostic value in secondary osteoporosis
Treatment of Osteoporosis:Drugs:• Calcium – supplementation 1000 – 1500 mg/day• Vitamin D - 800- 1000 U/day (intestinal calcium absorption increased, improves osteoblast
activity • Hormones – oestrogens, only for a limited time (<5yrs)- risk of breast cc, stroke, DVT
Drugs:• Biphosphonates: inhibit bone resorption, inhibit osteoclast activity (ALEDRONAT 70mg once a
week)• Calcitonin: Thyreoid- 3 hormone, reduces osteoclast activity
Osteoporosis of spine: „thinning” of bone in the vertebral bodiesOsteoporosis, that is visible on x-ray means 30%- 60% bone loss
Severe osteoporosis:Pathological fracture of vertebra (collapse of vertebral body) „fish vertebra”
Rickets (rachitis) – osteomalatiaDefinition:Different expressions of the same disease: incomplete mineralization of bone due to inadequate absorption (malabsorption) or utilization of calciumOSTEOMALATIA: bone softening at adult ageRICKETS: bone softening in children (with defective bone growth)Cause: lack of vitamin D (mostly) or hypophosphataemia, or severe calcium deficiency
Osteomalatia Definition: osteopenia caused by disturbed mineralization of boneCauses:• Lack of Vitamin D (malnutrition, malabsorption, lack of sunshine)• Disturbed synthesis of vitamin D (liver and kidney disorders – haemodyalisis)
X-ray features: 1. „Looser” – zones: radiolucent areas of bone (decreased density) - unhealed fractures that are
the result of repeated stress (incomplete or complete Fxs)2. Softening of acetabular floor - protrusion
Looser’s zones in pubic rami – patient had gastrectomy (poor absorption of Vit. D )
Osteomalacia: clinical features are „unexplained” pain in hip, vertebrae, muscle weaknessXR- features: see below (Looser’s zones!)
Fracture of radius – osteomalatiaWide fracture zone, looking like pseudarthrosis
Osteomalatia in kidney disease• Renal osteodystrophy:• Disturbed calcium- phosphorus metabolism – disturbed parathyroid function• Calcium deposits in soft tissues
These are typical features in chronic kidney failure (especially in juveniles)
Osteomalatia in chronic haemodyalisisAluminium intoxication through dialysis fluid • chemical binding to phosphate (phosphate is a basic mineral in bone)• increased blood level of phosphate • decreased serum calcium level –• increased parathyroid function (hyperparathyroidism) –• increased osteoclast activity
Calcium deposits in cornea – renal osteodystrophy
Rickets (rachitis)Features:Softening of bone with resultant bending• Swellings in the vicinity of joints• Tenderness around joints• Bowing at lower 1/3 of tibia
• Dietary rickets – disease of the past in Europe and N-America („English disease”)Still a problem in developing countries
• Renal rickets – due to diseases of kidney
Radiological features:• expansion of the metaphyseal regions –
trumpet mouth shaped expansion of metaphysis
• Bowing of tibiae• changes at the ribs: swelling (expansion) at
the anterior edge of ribs (at the costo-chondral junction) – „rickety rosary)
Rickets – typical features
Rickets – features: skull is square-shaped, short stature, severely curved long bones, widened epiphyses
Treatment:Medical:Vitamin D - prolonged administration, 50.000 Unit/week+1,5g Calcium/daySurgical:Correction of deformities (at present corrective osteotomy, in the old days OSTEOCLASIS – fracturing of bones)
58 year old woman – abnormal proprotions due to osteomalatia (coeliac disease – poor enteral absorption of calcium)
Paget’s disease of bones (osteitis deformans)• Aetiology : unknown• Manifestation : middle-aged or elderly patient, deformity of one or several bones (long tubular
bones and/or skull)
• Typical feature : „too much bone” – enlargement and thickening of bone (with abnormal architecture and altered mechanical characteristics – weak, brittle bone)
• X-ray features: bone becomes larger, texture of bone becomes coarse• Affected bone (long tubular bone) becomes curved – bowing („osteitis deformans”)
Paget’s disease – see typical x-ray features (abnormal structure – „coarse” bone, deformity)
Paget’s disease of skull: increased sclerosisChronic stage
Paget’s disease: clinical courseTwo stages:
1. Hyperaemic phase – bone becomes soft (bowing occurs at this stage)2. Chronic phase – bone becomes increasingly hard and brittle – fractures (stress- fractures) may
occur
Clinical features:-Pain in early stages-Deformity of femur or tibia-Skull involvement: cranial circumference increases, each year a larger hat is necessary-In hyperaemic phase: cardiac decompensationHistology:-Irregular structure of boneLaboratory changes: Increased serum alkaline phosphatase
Increased urinary calcium excretion
Treatment:Biphosphonates in early stage – calcium deposition in boneSurgical treatment: in fracturesBeware: MALIGNANT CHANGES – osteosarcoma –may develope!!
Endocrine disorders with skeletal abnormalitiesHyperparathyroidism Cause: tumors of parathyroid glands (adenoma)Consequence: • Hypercalcaemia – increased osteoclast activity• Calcium deposits in kidneys – nephrolithiasis• Calcium deposits in the soft tissues or in the cornea• Osseous changes
Osseous changes:• „osteitis fibrosa cystica” – subperiosteal bone resorption in the middle phalanges• Large cysts in bones – „brown tumours” – hemosiderin deposits• „molttled” appearance of the skull – spots of reduced bone density alternating with bone of
normal densitySubperiosteal erosion of phalanges – also typical in hyperparathyroidism
Typical sign in acute hypocalcaemia – spasm of finger flexors
Cystic lesion in proximal humerus: hyperparathyroidismIn the cyst brownish material„brown tumor”
Hyperparathyroidism: „pepper-pot skull” – multiple osteolytic areas in the skull
Cyst in 4th metacarpal due to hyperparathyroidism
HyperparathyroidismOsteodystrophia fibrosa cystica generalisata (von Recklinghausen’s disease)Multiple bone involvement
Hypothyroidism : thyroid hormone deficiencyCause may be low iodine intake – „cretinism”Skeletal changes: delayed ossification in the epiphyses (in femur mostly)
Kidney disorders with skeletal abnormalitiesRenal osteodystrphyCause: renal failure – glomerular diseasesConsequence on the skeleton due to decreased production of Vitamin –D provitamin (1,25 dihydroxycholecalcipherol) and phosphate retentionDecreased absorption of calcium from the intestines„Secondary” parathyroidism- low calcium blood level continously stimulates parathyroid glandSkeletal changes: like in hyperparathyroidism• in skull• in long bones (cysts)• osteomalatia – „renal rickets”• soft tissue calcification
Renal osteodysprophy: „rugger jersey” effect in vertebral bodies- alternating bands of increased bone density and less density
Treatment of osteoporotic fractures: New generation of implants – safer fixation of screws even in osteoporotic bones
Operative treatment of collapsed osteoporotic vertebrae:„balloon kyphoplasty”Collapsed vertebra reducedDeviced introduced through the pedicles into vertebral body
Balloon inflated – reduces collapsed vertebral bodyReduction completedBone cement injected into balloonBalloon protects the spinal cord!
Cortex Screw
Locking Screwfor osteoporotic fractures
smaller threadslarger core diameter
Head of the screw is threaded too
Locking ScrewLocked Plating
Generalized disorders of the bone: • Endocrine disorders with skeletal abnormalities • Metabolic disorders of the bone