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 body
Mechanical
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
osteoclasts
Half 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: Wolffs law
Bone structure adapts itself to
functional demands: it is thicker, where
weight bearing is larger

Metabolic disorders of bone

Definition:
Disturbance of
osteogenesis (bone formation),
bone mineralization
bone remodelling
2 main types:
Osteopenia (bone loss, lack of bone) osteoporosis, osteomalatia
Osteosclerosis (too much bone) Pagets 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 metabolism

1. Parathyroid (parathormone)
2. Thyroid (C-cells - Calcitonine )
3. Growth hormone
4. Oestrogens, androgens
5. Corticosteroids
6. Vitamine D
7. 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 loss

Osteopenia: 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 bone

Hormones:
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%/year
2. 35- 50 years: 0,3%/year (men) or 0,5%/year (women) reduction in bone
mass
3. 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 remodelling
2 main types:
osteopenia too few bone( osteoporosis, osteomalatia,
hyperparathyroidism etc.)
Osteosclerosis too much bone (Pagets disease, osteopetrosis)
Causes of Primary Osteoporosis:
Likely causes:
-Hormonal changes - oestrogens / androgens
-INACTIVITY
Unlikely:
-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 measured
Calculation of changes in bone density:
deviation from bone mass measured at young age (SD- standard deviation) so
called T-score
Pathological 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 bodies
Osteoporosis, 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) osteomalatia

Definition:
Different expressions of the same disease: incomplete mineralization of bone due
to inadequate absorption (malabsorption) or utilization of calcium
OSTEOMALATIA: bone softening at adult age
RICKETS: 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 bone
Causes:
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

Loosers zones in pubic rami

patient had gastrectomy (poor
absorption of Vit. D )

Osteomalacia:
clinical features are unexplained pain in hip, vertebrae, muscle weakness
XR- features: see below (Loosers zones!)

Fracture of radius osteomalatia

Wide 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 haemodyalisis
Aluminium 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/day
Surgical:
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)

Pagets 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)

Pagets disease see typical x-ray

features (abnormal structure coarse
bone, deformity)

Pagets disease of skull: increased

sclerosis
Chronic stage

Pagets disease: clinical course

Two 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 decompensation
Histology:

-Irregular structure of bone

Laboratory changes: Increased serum alkaline phosphatase
Increased urinary calcium excretion
Treatment:
Biphosphonates in early stage calcium deposition in bone
Surgical treatment: in fractures
Beware: MALIGNANT CHANGES osteosarcoma may develope!!
Endocrine disorders with skeletal abnormalities
Hyperparathyroidism
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 density
Subperiosteal erosion of phalanges
also typical in hyperparathyroidism

Typical sign in acute hypocalcaemia

spasm of finger flexors

Cystic lesion in proximal humerus:

hyperparathyroidism
In the cyst brownish material
brown tumor

Hyperparathyroidism: pepper-pot
skull multiple osteolytic areas in
the skull

Cyst in 4th metacarpal due to

hyperparathyroidism

Hyperparathyroidism
Osteodystrophia fibrosa cystica
generalisata (von
Recklinghausens disease)
Multiple bone involvement

Hypothyroidism : thyroid hormone deficiency

Cause may be low iodine intake cretinism
Skeletal changes: delayed ossification in the epiphyses (in femur mostly)
Kidney disorders with skeletal abnormalities
Renal osteodystrphy
Cause: renal failure glomerular diseases
Consequence on the skeleton due to decreased production of Vitamin D
provitamin (1,25 dihydroxycholecalcipherol) and phosphate retention
Decreased absorption of calcium from the intestines
Secondary parathyroidism- low calcium blood level continously stimulates
parathyroid gland
Skeletal 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 reduced
Deviced introduced through
the pedicles into vertebral
body
Balloon inflated
reduces collapsed
vertebral body
Reduction completed
Bone cement injected into
balloon
Balloon protects the spinal
cord!
Locking Screw
for osteoporotic fractures
smaller threads
larger core diameter
Head of the screw is
threaded too
Cortex
Screw

Locking

Screw
Locked
Plating

Generalized disorders of the bone:

Endocrine disorders with skeletal abnormalities

Metabolic disorders of the bone