metabolic disorders of bone
TRANSCRIPT
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By
Dr Akkad Rafiq
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Bone Structure
Three main functions of bone support,
protection
leverage
Composition Type I collagen fibers,
mineral component
Other non-collagenous proteins Osteopontin
osteonectin
Osteocalcin
alkaline phosphatases
Bone morphogenetic protein
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Bone Minerals
Almost half the bone volume is mineral
matter
mainly calcium and phosphate in the
form of crystalline hydroxyapatite
‘demineralization’ of bone occurs only by
resorption of the entire matrix
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Bone Cells
Osteoblasts - concerned with bone
formation and osteoclast activation
Osteocytes -These cells can be
regarded as spent osteoblasts
Osteoclasts- These cells are the
principal mediators of bone resorption
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Bone structure
The mature tissue is lamellar
bone, in which the collagen
fibres are arranged parallel to
each other to form multiple
layers with the osteocytes
lying between the lamellae.
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Minerals of bone
Calcium
Magnesium
Vit D
Phosphorus
Calcitonin
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Osteoporosis
clinical disorder characterized by an
abnormally low bone mass and effects
in bone structure, which renders the
bone fragile and at greater risk of
fracture in a person of that age, sex and
race.
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Pathology:
• results from an unhealthy imbalance between two normal activities of bone: bone resorption and bone formation.
• The combined processes of bone resorption and bone formation allow the healthy skeleton to be maintained continually by the removal of old bone and its replacement with new bone.
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Pathology
the destruction of bone begins to exceed the formation of bone; this imbalance leads to a net loss of bone, and the beginnings of osteoporosis.
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PRIMERY RISK FACTORS
Caucasoid (white) or Asiatic ethnicity
Family history of osteoporosis
History of anorexia nervosa and/or amenorrhoea
Low peak bone mass in the third decade
Early onset of menopause
Unusually slim or emaciated build
Early hysterectomy
Nutritional insufficiency
Chronic lack of exercise
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Causes of secondary
osteoporosis Nutritional
Malabsorption
Malnutrition
Scurvy
Inflammatory disorders Rheumatoid disease
Ankylosing spondylitis
Tuberculosis
Drug induced Corticosteroids
Excessive alcohol consumption
Anticonvulsants
Heparin
Immunosuppressives
Endocrine disorders Gonadal insufficiency
Hyperparathyroidism
Thyrotoxicosis
Cushing’s disease
Malignant disease Carcinomatosis
Multiple myeloma
Leukaemia
Other Smoking
Chronic obstructive
pulmonary disease
Osteogenesis imperfecta
Chronic renal disease
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Investigations
X-ray findings are generally insufficient
• cannot reliably measure bone density
• useful to identify spinal factures, explains back pain, height loss or kyphosis.
• X-rays may detect osteopenia only when bone loss is > 30%.
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Patient who had a severe fracture and a moderate fracture in her spine. Three years later a second xray revealed a new fracture. These fractures were in the lower spine.
Radiographic Fracture Assessment
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DEXADual energy x-ray absorptiometry (DEXA)
• This is the most popular and accurate test to date
• non-invasive
• involves no special preparation.
• Radiation exposure is minimal,
• Can be used to measure bone mineral density in the spine, hip, wrist, or total body.
•expensive
•not portable.
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Screening- Ultrasound Densitometry
inexpensive,
portable\
no radiation
can be used only in peripheral
sites (eg, the heel),
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Fracture Reduction
Goal: prevent fracture, not just treat
BMD
Osteoporosis treatment options
Calcium and vitamin D
Calcitonin
Bisphosphonates
Selective Estrogen Receptor Modulators
Parathyroid Hormone
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Osteoporosis Treatment: Calcium and Vit
D Calcium and Vit D supplementation shown
to decrease risk of hip fracture in older adults 1000 mg/day standard;
1500 mg/day in postmenopausal women/osteoporosis
Vitamin D (25 and 1,25): 400 IU/Day
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Osteoporosis Treatment:
Bisphosphonates Decrease bone resorption
decrease hip and vertebral fractures
Alendronate, risodronate PO
IV: pamidronate, zolendronate
Ibandronate : once/month
Calcetonin not as effective as Bisphosphonates
200 IU nasally/day
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Osteoporosis Treatment:
Selective Estrogen Receptor Modulators
Raloxifene
Decrease bone resorption like estrogen
No increased risk cancer (decrease risk
breast cancer)
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Osteoporosis Treatment:
PTH
Teriparatide
INTERMITTENT PTH: overall improvement
in bone density
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Current Guidelines
US Preventive Task Force
Test Bone Mineral Density in all women over
age 65, younger postmenopausal women
with at least one risk factor, and
postmenopausal women with a history of
fracture
Treat patients with T score <-2 and no risk
factors, T score <1.5 if any risk factors, and
anyone with prior vertebral/hip fracture
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Rickets:
Etiology, pathogenesis, clinical
features, diagnostics, treatment and
prevention
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Rickets is a childhood disorder
involving softening and
weakening of the bones.
It is primarily caused by lack of
vitamin D, calcium, or
phosphate.
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Etiology
1. Lack of sunshine due to:
1) Lack of outdoor activities
2) Lack of ultraviolet light in fall and winter
3) Too much cloud, dust, vapour and smoke
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Etiology
2. Improper feeding:
1) Inadequate intake of Vitamin D
Breast milk 0-10IU/100ml
Cow’s milk 0.3-4IU/100ml
Egg yolk 25IU/average yolk
Herring 1500IU/100g
2) Improper Ca and P ratio
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Etiology
3. Fast growth, increased requirement
(relative deficiency)
4. Diseases and drug:
Liver diseases, renal diseases
Gastrointestinal diseases
Antiepileptic
Glucocorticosteroid
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The history in patients with rickets may include the following:
The infant's gestational age, diet and degree of sunlight exposure should be noted.
A detailed dietary history should include specifics of vitamin D and calcium intake.
A family history of short stature, orthopedic abnormalities, poor dentition, alopecia, parental consanguinity may signify inherited rickets.
Evaluation
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Clinical signs
Rickets
is a systematic disease with
skeletons involved most, but the
nervous system, muscular system
and other system are also involved.
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• Skeletal deformities
1. Bow legs
2. pigeon chest 3. Bumps" in the rib
cage
4. odd-shaped skull;
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Generalized muscular hypotonia is observed in the
most patients with clinical signs of rickets.
Clinical signs
• If rickets occurs at a later age,
thickening of the skull
develops. This produces
frontal bossing and delays
the closure of the anterior
fontanelle.
Frontal bossing
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Protruding foreheadasymmetrical or odd-shaped skull
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Chest deformity
Funnel chest – pectus
excavatum
Pigeon chest
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Clinical signs In the chest, knobby deformities results in the rachitic rosary along the costochondral junctions.
Rib beading
(rachitic rosary)
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Bowlegs and
knock-knees.
Clinical signs
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Knock knee deformity
(genu valgum)Bowleg deformity
(genu varum)
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A teenage male with rickets.
Note deformities of legs (bow legs)
and compromised height.
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The ends of the long bones demonstrate that same
knobby thickening. At the ankle, palpation of the tibial
Clinical signs
malleolus gives
the impression
of a double
epiphysis
(Marfan sign).
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Pain in the bones of Arms, Legs, Spine, Pelvis.
Dental deformities
Delayed formation of teeth
Defects in the structure of teeth
Holes in the enamel
Increased incidence of cavities in the teeth (dental
caries)
Clinical signs
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Progressive weakness
Decreased muscle tone (loss of muscle strength)
Muscle cramps
Impaired growth
Short stature (adults less than 5 feet tall)
Fever or restlessness, especially at night
Clinical signs
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The entire skeletal system must be palpated to search for tenderness and bony abnormalities.
Rickets should be suspected in older bowlegged children and in cases associated with asymmetry, pain, or progression in severity.
Physical examination
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Gait disturbances and neurologic abnormalities (such as hyperreflexia) in
all children should be sought.
muscle cramps, numbness, paresthesias,
tetany and seizures.
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Decreases
in serum calcium,
serum phosphorus,
calcidiol, calcitriol,
urinary calcium.
The most common laboratory findings in
nutritional rickets are:
Parathyroid hormone,
alkaline phosphatase,
urinary phosphorus
levels are elevated.
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Classic radiographic findings
include:
widening of the distal epyphysis, fraying
and widening of the metaphysis, and
angular deformities of the arm and leg
bones.
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Classic radiographic findings include
Anteroposterior and lateral radiographs of the wrist of an 8-year-
old boy with rickets demonstrates cupping and fraying of the
metaphyseal region
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Classic radiographic findings include:
Radiographs of the knee of a 3-year-old girl with hypophosphatemia
depict severe fraying of the metaphysis.
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Rickets in wrist - uncalcified lower ends of bones
are porous, ragged, and saucer-shaped
(A) Rickets in 3 month old infant
(B) Healing after 28 days of
treatment
(C) After 41 days of
treatment
A
B C
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Radiographic image of wrist and
forearm showing pathologic
fractures of radius and ulna with
rachitic changes of distal end of
radius and ulna.
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X-ray in rickets
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Clinical manifestation
Stages Early stage
Usually begin at 3 months old
Symptoms: mental psychiatric symptoms
Irritability, sleepless, hidrosis
Signs: occipital bald
Laboratory findings: Serum Ca, P normal or
decreased slightly, AKP normal or elevated
slightly, 25(OH)D3 decreased
Roentgen-graphic changes: normal or
slightly changed
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Clinical manifestation
Advanced stage
On the base of early rickets, osseous changes become marked and motor development becomes delayed.
1. Osseous changes:
1) Head: craniotabes, frontal bossing, boxlike appearance of skull, delayed closure of anterior fontanelle
2) Teeth: delayed dentition with abnormal order, defects
3) Chest: rachitic rosary, Harrison’s groove, pigeon chest, funnel-shaped chest, flaring of ribs
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Clinical manifestation
4) Spinal column: scoliosis, kyphosis, lordosis
5) Extremities: bowlegs, knock knee, greenstick fracture
6) Rachitic dwarfism
2. Muscular system: potbelly, late in standing and walking
3. Motor development: delayed
4. Other nervous and mental symptoms
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Clinical manifestation
Laboratory findings: Serum Ca and P decreased
Ca and P product decreased
AKP elevated
Roentgen-graphic changes: Wrist is the best site for watching the changes
Widening of the epiphyseal cartilage
Blurring of the cup-shape metaphyses of long bone
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I Mild form: small changes of nervous system, changes of one part of the skeleton;
II Moderate form: changes of all organs and systems, changes of two parts of the skeleton;
III Severe form: damaging function of all organs and systems, changes of three parts of the skeleton;
Classification
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Types of Rickets
Nutritional
Nutritional rickets results from inadequate
sunlight exposure or inadequate intake of
dietary vitamin D, calcium, or phosphorus.
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Vitamin D dependent
Vitamin D-dependent rickets, type I is secondary to a defect in the gene that codes for the production of renal 25(OH)D3-1-alpha-hydroxylase.
Vitamin D-dependent rickets, type II is a rare autosomal disorder caused by mutations in the vitamin D receptor. Type II does not respond to vitamin D treatment; elevated levels of circulating calcitriol differentiate this type from type I.
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Vitamin D resistant
Rickets refractory to vitamin D treatment may be
caused by the most common heritable form,
known as vitamin D-resistant rickets or familial
hypophosphatemic rickets.
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Other Conditions That Can Cause Rickets Medications
Antacids Anticonvulsants Corticosteroids Loop diuretics
Malignancy Prematurity Diseases of organs associated with vitamin D and
calcium metabolism Kidney disease Liver and biliary tract disease
Malabsorption syndromes Celiac disease Cystic fibrosis (rare)
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Diagnosis
Assessed according to the followings:
1. History
2. Physical examination
3. Laboratory findings
4. Roentgen-graphic changes
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Treatment for rickets The replacement of Vitamin D may correct rickets
using these methods of
ultraviolet light and medicine.
4000 IU of oral vitamin D per day for one month.
Parents are instructed to take their infants outdoors
for approximately 20 minutes per day with their faces
exposed.
Foods that are good sources of vitamin D include
cod liver oil,
egg yolks,
butter
oily fish.
Some foods, including milk and breakfast cereals, are also
fortified with synthetic vitamin D.
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Treatment
1. Special therapy: Vitamin D therapy
A. General method: Vitamin D 2000-4000 IU/day
for 2-4 weeks, then change to
preventive dosage – 400 IU.
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TREATMENT
1 STAGE
VITAMINE D – - 2000 IU 1 TIME\DAY 30 DAYS
2 STAGE
VITAMINE D – - 3500 IU 1 TIME\DAY 40 DAYS
3 STAGE
VITAMINE D – - 5000 IU 1 TIME\DAY 45 DAYS
Then profilactic dose – 500 iu till the end of the second – third year of life
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Vitamin D
Fat-soluble vitamin used to treat vitamin D
deficiency or for prophylaxis of deficiency.
Cholecalciferol (Delta-D)
Vitamin D-3 1 mg provides 40000 IU vitamin D
activity
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Treatment
4. Calcium supplementation: Dosage: 1-3
g/day
only used for special cases, such as baby
fed mainly with cereal or infants under 3
months of age and those who have already
developed tetany.
5. Plastic therapy:
In children with bone deformities after 4
years old plastic surgery may be useful.
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Prevention
Vitamin D supplements
Because of human milk contains only a small amount
of vitamin D, the American Academy of Pediatrics
(AAP) recommends that all breast-fed infants receive
400 IU of oral vitamin D daily beginning during the
first two months of life and continuing until the daily
consumption of vitamin D-fortified formula or milk
is two to three glasses, or 500 mL.
AAP also recommends that all children and
adolescents should receive 400 IU a day of vitamin D.
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Prevention
Vitamin D supplementation:
In prematures, twins and weak babies, give Vitamin D 800IU per day,
For term babies and infants the demand of Vitamin D is 400IU per day,
For those babies who can’t maintain a daily supplementation, inject muscularly
Vitamin D3 100000-200000 IU.
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Prevention
Calcium supplementation:
0.5-1gm/day, for premature, weak babies and babies fed mainly with
cereal
Recommended daily intake of calcium is as follows: 1 to 3 years of age. 500 mg (two servings of dairy products a day)
4 to 8 years of age. 800 mg (two to three servings of dairy products a day)
9 to 18 years of age. 1,300 mg (four servings of dairy products a day)
19 to 50 years of age. 1,000 mg a day (three servings of dairy products a day)
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Sources of Vitamin D
Sunlight is the most important source
Fish liver oil
Fish & sea food (herring & salmon)
Eggs
Plants do not contain vitamin D3