Rickets and osteomalacia

1. RICKETS AND OSTEOMALACIA
PRESENTER : Dr JEEVAN
MODERATOR : Dr S NARASIMHA REEDY
CHAIRPERSON: Dr V SARATH

2. CALCIUM METABOLISM
Increase in calcium starts in 3rd trimester reaches a nadir in adulthood and then
declines at the rate of 1-2 % per year
Total body calcium- 1-2 kg , of which 99% lies in skeleton
Intracellular content – less (100 nmol /lt)
Extracellular content – 1000 times more (2.2- 2.6 mmol/lt ---- 8. 5 -10.5mg/dl)
leading to a steep extracellular to intracellular gradient
50 % ionized
( active form and major regulator)
50% unionized
(bound to albumin, Igs,
sulphate,phosphate ,
citrate)
Ionized calcium maintain calcium homeostasis by regulating PTH secretion
and 1,25 D production
In gut – absorbed in distal duodenum & proximal jejunum-paracellular
pathway( non saturable ) trans cellular pathway(vit D dependent).
Absorption favored by acidic PH,absence of chelators , presence of bile
which reduces formation of calcium fatty soaps and increase availability of
fat soluble Vit D.

3. EXCRETION- mainly by kidney- reabsorbed 65% in PCT concomitant with
Nacl absorption(passive) ; 20% in thick asc loh (passive) dependent on
level of ionized calcium through a protein paracellin 1; 10% in DCT
(actively) PTH, vit D dependent by using ca2+ATPase,ca2+ na+ exchanger.
Absorption decreased by high conc. Of Na+ in urine , increased by PTHand
Vit D.
Normally over 95 % of filtered calcium is reabsorbed
Fecal excretion is dependent on dietary intake and comes into significancein
renal diseases

4. PHOSPHOROUS METABOLISM
 Total body content- 600 mg ( 85% in bones)
 Intracellular & extracellular contents are almost equal( 1-2 mmol/l, 2.5 -4.5
mg/dl)reabsorbed in
 65% of phosphate can be reabsorbed in absence of vitamin D, inits
presence increases to 90%
 90% of phosphate is reabsorbed in proximal tubules(Na+Phosphate
cotransporter)
 Phosphate reabsorption has a Tm(2 -6 mg per minute)
 Reabsorption control- vit D increases, PTH & FGF 23 decreases
 For diagnosis best to use Basal fasting levels

5. VIT D METABOLISM
 Major dietary source – D2 (calciferol)- produced fromergosterol
 Formed in body – D3( cholecalciferol) produced from7-
dehydrocholesterol
 U.V radiation of 230-313 nm required for conversion of ergo &
dehydroch. to D2 & D3
 D2 absorbed in upper 2/3 rd part of intestine – goes to lymphatics (aided
by bile salt) & D3 endogenous synthesized form, both binds to globulin
and reaches liver- hydroxylation occours form 25 OH Vit D ( 25 OH
ergocalciferol & 25 OH cholecalciferol/calcifediol)
 25 OH Vit D is major circulating form- 0.03% free, rest bound to vit
D binding protein(mainly) and albumin.
 25 OH Vit D goes to kidney for second hydroxylation by 1α hydroxylasein
PCT to 1,25 OH Vit D( calcitriol)
 Other places of 1 α hydroxylase – keratinocytes, trophoblast of
placenta, macrophages of granuloma and lymphoma.

6.  1 α hydroxylase – induced by PTH , hyphophosphatemia
repressed by ↑ ca2+; 1,25 D; FGF 23
 Action- acts through nuclear receptor- ↑ ca2+ reabsorption in gut,
resorption of bone( receptors present on osteoblast which activate RANK
ligand expression which promotes osteoclast activity), reabsorption of
calcium in renal tubels , antiproliferative effect on parathyroid.
 For diagnosis 25 OH D is most appropriate ( bcoz its pool is large enough
to form sufficient 1,25 D even in deficient state so measuring 1,25 D can
be fallacious).
 Sufficient levels - > 50 nmol/lt(>20 ng/ ml)
 <37 nmol/lt(15 ng/ml) deficient

7. Adequate supplies of vitamin
D3 can be synthesized with
sufficient exposure to solar
ultraviolet B radiation
Melanin, clothing or
sunscreens that absorb UVB
will reduce cutaneous
production of vitamin D3

8. RDA According to NIN (2020)

11. PARATHORMONE
↑ ca2+ flow from bone to blood
↓ Renal clearance of calcium
↑ intestinal absorption of calcium by activating vit D
In kidney-In Proximal tubule- inhibit phosphate reabsorption, activate renal
1 α hydroxylase
In Distal tubules- ↑ calcium absorption
also inhibit bicarbonate reabsorption
Bones- acute- causes resorption
chronic- causes increase in both osteoblastic and osteoclastic activity
continuous- ↑ osteoclastic activity
intermittent- ↑ bone formation
Receptors are present on osteoblast which release cytokines toactivate
osteoclast.

12. RICKETS & OSTEOMALACIA
These are different expression of the same disease.
Lack of available calcium and phosphorus ( or both)
for mineralization of newly formed osteoid .
Called as English disease
Rickets-
 Occur in children
 Before fusion of epiphysis
 Leads to softening of bone & deformity
Osteomalacia- occur in adult
- softening of bone

13. GROUPS ATRISK
• Infants
• Elderly
• Dark skinned
• Covered women
• Kidney failure patients
• Patients with chronic liver disease
• Fat malabsorption disorders
• Genetic types of rickets
• Patients on anticonvulsant drugs

14. PATHOPHYSIOLOGY
Metabolic abnormality- ↓ vitamin D- ↓ ca2+ - feedback ↑ in PTH – lead
to overall increase calcium absorption , phosphate loss , increase
mobilization of ca2+ and po43- from bone – overall negative balance of
ca2+ & po43- for mineralization of bone.
Epiphysial plate abnormality
RESTING- cells sparse rounded randomly arranged
PROLIFERATIVE- cells regular flattened & arranged in column site of
DNA synthesis & mitotic activity and growth in length ofplate
MATURATION- columnar arrangement becomes large & more rounded,
contain glycogen→ lowermost part k/a ZONE OF HYPERTROPHY–
cells have ↑ lacunae shrunken nuclei, vascular buds grows from
metaphysis at the base of column towards lacunae whereas bars of
cartilage which are highly calcified lies in b/w columns – this entire
region k/a ZONE OF PROVISIONALCALCIFICATION.
ZONE OF PRIMARY SPONGIOSA – lower in metaphysis calcifiedbars
surrounded by osteoblast which produce seams of osteoid aroundbars.

16. CHANGES IN GROWTH PLATE
Resting & proliferative zones are normal
Maturation zones column of cells largely
elongated as irregular tongue of cartilage
sometimes extending to metaphysis→
increased height of cartilagenous plate as well
as width.
Hypertrophic zones column of bars cannot be
identified properly

17. CAUSES OF CHANGES
Normally in hypertrophic zone vascular
ingrowth occours from metaphysis towards
tunnels formed by calcified cartilage which
destroys the basilar cells of hypertrophic layer
along with intervening cartilage.
IN RICKETS- calcified tunnels not formed-
vascular in growth does not occour so basilar
layer cannot be destroyed leading to increased
proliferation without destruction.

19. CUPPING- normally epiphyseal plate growth push against
calcified lower zones, so opposite pressure from both sides
leads to push of epiphyseal nucleus farther from metaphysis
along the axis of bone leading to longitudinal growth.
IN RICKETS- cartilage softened--calcified zone & metaphysis
collapse and spread under applied external force & intrinsic
growth force.
BIOCHEMICAL- resting and proliferative zone are normal
with normal DNA synthesis , zone of maturation is selectively
targeted along with zone of hypertrophy – respiratory paralysis
& shift from aerobic to anaerobic & HMP shunt, ↓ high energy
phosphate molecules→ ↓ RNA, protein , glycogen,
proteoglycan, polysaccharide leading to maturation arrest.But
no change in lysosomal activity.

20. HISTOLOGICAL FEATURES
Thinned cortex, ↑ porosity , ↓ density
Irregular haversian system
Trabecular bone is thin & porous with diminished
total no of trabeculae.
Trabeculae shows osteoid seams (thin layer of
mineralized bone surrounded by unmineralized
osteoid synthesized in preparation of mineralization
but cannot be done due to deficiency). Osteoid seams
are cardinal features but not pathognomic, width &
total no of osteoid seams is a good index of severity of
disease.

21. Osteoid seams generally in relation to 1
trabeculae but in one or more bones due to
very poor mineralization contain very large
ribbion like radiolucent area of osteoid seams
k/a looser’s zone/ umbauzons/ milkman
pseudofracture (VIRTUALLYDIAGNOSTIC
of osteomalacic syndrome)

22. PARADOX OF RICKETS
As the rickets become more severe and patient
become systemically more sicker with greater
abberation of biochemical abnormality the
changes in growth plate become less severe or
even disappear( if child survives) bcoz rickets
is a disease of growing bones with severe
systemic illness growth is suppressed due to
decreased nutrition & hypoprotenemia&
epiphyseal manifestation of rickets fade away
as they are directly related to rapidity of
growth.

23. CLINICAL FEATURES
AGE OF PRESENTATION
VITAMIN D DEFICIENCYRICKETS –
6 to 18months.
NON NUTRITIONALRICKETS
Beyond this age group.

24. Stereotyped can rarely diffrentiate one form
from other, infants & young children with
florid rickets manifest by 6 months of age.
Failure to thrive
Listless, apathic , irritable, hypotonic,
underweight, anemic, ligamentous laxity,
sweating of face and forehead, hypocalcemic
features

25. Head
craniotabes(soft skull)
frontal bossing
Widening of suture,
persistent fontanelae
Delayed dentition, caries,
enamel hypoplasia
Caput quadratum/ hot cross bun
skull( cruciate pattern in skull
due to widened sutures &
thickening around sutures)

26. Chest
Rachitic rosary
Flattening of hemithorax
Harrison groove
Pigeon chest
Respiratory infection and
atelectasis

28. Protuberant abdomen

29. Widening of wrist, knee and ankle due to physeal
over growth

30. Deformity
Toddlers: Bowed
legs
(genu varum)

31. Deformity
Older children: Knock-
knees
(genu valgum)

32. Deformity
windswept knees

33. Rachitic cat back- thoracic khyphosis,
lumbar lordosis, scoliosis, waddling gait
Rachitic saber shin, coxavara
String of pearl deformity- enlarged ends of
phalanx and metacarpals with constricted
joints
Hypotonia
Pathological #-especially greenstick
Tetany, PEM
Bone pain or tenderness

34. Clinical evaluation
Dietary history
Maternal risk factors
Drugs
GI disease
Renal disease

35. Diagnosis
History & physical examination finding
Biochemical study
Radiographic abnormality
Special etiology confirmed with lab. test

36. Biochemical findings
Calcium - n/↑/↓, rarely fall below 7.5 to 8 mg/dl
Urinary calcium-↓ usually less than 3 mg/ kg / 24 hr(
below normal level of 5 mg / kg / 24 hr in children),
in adults on dietary intake of 750 to 1000 mg / day if
urinary excretion less than 200 mg/day – significant.
Fecal calcium - ↑ depends on dietary intake

37. Phosphate- ↓ in all cases(b/w 1- 3.5 mg/dl) except
renal osteodystrophy - ↑ due to inadequate filteration
from kidney. Best to measure basal fasting levels as
dependent on time of day, GH levels
Urinary phosphate- ↑ due to decreased tubular
reabsorption of phosphate but may be dependent on
dietary intake as well as serum levels( if high serum
conc. Excretion may be upto 300- 1000 mg/day, if low
serum conc.clearnce may be low despite ↓
reabsorption.

38. Better to measure % tubular reabsorption- <
85% significant, < 60% abnormal
Po43- creatinine clearance, max tubular
reabsorption, exogenous phosphate load
handling- done to diagnose hyperPTH
Alk. Phophatase - ↑(> 15 – 50 bodansky unit)
Bone biopsy
Hb, ESR
Other specefic tests

40. DISORD
ER
Ca2+ Po4
3- PTH 25 D 1,25D Alk.ph Urine
ca2+
Urine
po4
3-
Vit D def N/↓ ↓ ↑ ↓ ↓/N/↑ ↑ ↓ ↑
Ca2+ def N/↓ ↓ ↑ N ↑ ↑ ↓ ↑
Po4
3- def N ↓ N/↓ N ↑ ↑ ↑ ↓
VDDR 1 N/↓ ↓ ↑ N ↓ ↑ ↓ ↑
VDDR 2 N/↓ ↓ ↑ N ↑↑ ↑ ↓ ↑
VDRR N ↓ N N ↓ ↑ ↓ ↑
HHRH N ↓ N/↓ N ↓ ↑ ↑ ↑
RTA N ↓↓ N N ↓ ↑ ↑/↓ ↑
CRF N/↓ ↑ ↑ N ↓ ↑ N/↓ ↓

41. ETIOLOGICAL CLASSN
Nutritional deficiency
 Vit D def.
Decreaserd vit D - ↓ calcium -secondary hyperPTH- causes
phosphaturia & ↑ 1α hydroxylase: 1,25 D can be↑/N
(compensatory increase bcoz still 25 D pool is enough to
produce 1,25 D or ↓(in severe def of 25 D)
Metabolic acidosis – PTH induced HCO3- loss
DISO
RDER
Ca2+ Po4
3- PTH 25 D 1,25D Alk.ph Urine
ca2+
Urine
po4
3-
Vit D
def
N/↓ ↓ ↑ ↓ ↓/N/↑ ↑ ↓ ↑

42. Vitamin D deficiency Rickets
Most common cause of rickets globally.
Causes:
• vitamin D nutritional deficiency
• Fat Malabsorption
• Decreased exposure to sunlight
• Decreased 25-hydroxylase in liver
diseases
• Drugs like phenytoin.
• Chronic kidney failure
• Vitamin D–dependent rickets type 1
• Vitamin D–dependent rickets type 2

43. Etiology:
 Most common in infancy: Due to poor intake + inadequate cutaneous synthesis.
 Transplacental transport of vitamin D, mostly 25-D,provides vitamin D for 1st 2 months
of life unless there is severe maternal vitamin D deficiency.
 Breast-fed infants, because of low vitamin D content of breast milk, rely on cutaneous
synthesis or vitamin supplements.
 Infants who receive formula receive adequate vitamin D, even without cutaneous
synthesis
Clinical Manifestations:
The clinical features are typical of rickets with a significant minority
presenting with Symptoms of hypocalcemia.
 These children have an increased risk of pneumonia and muscle weakness, adding
to a delay in motor development.
NUTRITIONAL VITAMIN D DEFICIENCY

44. SECONDARY VITAMIN D DEFICIENCY.
Inadequate absorption :
- --cholestatic liver disease,
- defects in bile acid metabolism,
- cystic fibrosis
- other causes of pancreatic dysfunction,
- celiac disease & Crohn disease
- after intestinal resection

45. VITAMIN D–DEPENDENT RICKETS,
TYPE 1.
 Autosomal recessive disorder.
 Mutations in the gene encoding renal 1α
hydroxylase preventing conversion of 25-D into
1,25-D.
 Present during the 1st 2 yr of life
 Classic features of rickets including
symptomatic hypocalcemia.
 They have normal levels of 25-D, but low levels
of 1,25-D
VITAMIN D–DEPENDENT RICKETS, TYPE 2.
 Autosomal Recessive disorder.
 Mutations in gene encoding the vitamin D receptor.
 Prevents a normal physiologic response to 1,25-D.
 Levels of 1,25-D are extremely elevated.
 Less severe disease is associated with a partially
functional vitamin D receptor

46. Most patients present during infancy.
Less severely affected patients may not be diagnosed until adulthood.
50–70% of children have alopecia.
Treatment.
 Some patients, especially those without alopecia,
respond to extremely high doses of vitamin D2, 25-D, or
1,25-D.
 Due to partially functional vitamin D receptor,3–6 months
trial of high-dose vitamin D and oral calcium.

47. CALCIUM DEFICIENCY
Calcium chelators- phytate, oxalate , fatty acid( forms
insoluble soap with calcium) excessive phosphate
(forms insoluble salt with calcium)
DISO
RDER
Ca2+ Po4
3- PTH 25 D 1,25D Alk.ph Urine
ca2+
Urine
po4
3-
Ca2+
def
N/↓ ↓ ↑ N ↑ ↑ ↓ ↑

48. Phosphate def.
Rare (bcoz almost all food are sufficient enoughin
phosphate)
DISO
RDER
Ca2+ Po4
3- PTH 25 D 1,25D Alk.ph Urine
ca2+
Urine
po4
3-
Po4
3-
def
N ↓ N/↓ N ↑ ↑ ↑ ↓

49. • RICKETS OF PREMATURITY :
premature infants are more prouned .
Risk factors :
hepatobiliary diseases,
total parental nutrition,
diuretic theraphy ,
percussion theraphy .
Infants having this conditions have chances of pathological fractures which heals
readily as infants gain weight
DRUG INDUCED RICKETS :
Phenytoin – hepatic enzyme inducer
drug converts calcidiol into inactive
metabolite

50. VITAMIN D RESISTANT RICKETS :
also known as hereditary / familial hypophosphatemic rickets
inherited as X-linked dominant ( mc type of inheritance ) , Autosomal ressesive
,Autosomal dominant.
X-linked hypophosphatemia rickets :
X-linked dominant type (mc type)
Gene – PHEX gene ( phosphate regulating gene homologous to
endopeptidases on X chromosome ) location Xp22
fibroblast growth factor 23
inhibits resorbtion of phosphorus in kidney & inhibits 1 alpha hydroxylase
urinary phosphate & serum phosphate calcotriol

51. Conditions causing RENAL LOSSES of phosphate and calcitriol due to increased
level of FGF23
 X linked hypophosphatemic rickets[*]
 Overproduction of phosphatonin
 Tumor-induced rickets[*]
McCune-Albright syndrome[*]
 Epidermal nevus syndrome[*]
 Neurofibromatosis[*]
 Fanconi syndrome
 Dent disease
 DISTAL RENAL TUBULAR ACIDOSIS.
-

53. Investigations
 BASIC INVESTIGATIONS TO
CONFIRM RICKETS
 Serum Ca, P and SAP
 X rays of ends of long bones at knees or
wrists
 CLASSICAL RADIOLOGICAL
CHANGES

54. RADIOLOGY
 most easily visualized on posteroanterior
radiographs of the wrist ,knee ,chest
Decreased calcification leads to thickening of the
growth plate, and is most easily seen at the distal
ends of the radius, ulna, and fibula. There is
widening of the distal end of the metaphysis,
corresponding to the clinical observation of
thickened wrists and ankles, as well as the rachitic
rosary.
 The edge of the metaphysis loses its sharp border,
which is described as fraying.
 In addition, the edge of the metaphysis changes
from a convex or flat surface to a more concave
surface. This is termed cupping.
Other radiologic features include coarse
trabeculation of the diaphysis and generalized
rarefaction

57. Widening of space s
between epiphyses and
metaphysis &
decreased density of
bone
After treatment

58. Second level investigations
1. Blood urea, creatinine,
electrolytes, tubular reabsorption
of phosphate( Trp)
2. Urine analysis for specific gravity,
glucose, protein, amino acids,
potassium and calcium.
3. USG abdomen
4. LFT, malabsorption.

59. Tertiary level investigations
1. Estimation of vitamin D metabolites
to differentiate VDDR type 1 from
type 2
2. Receptor vitamin D interaction – in
vitro study to assess VDDR type 2
3. Bone mineral content
4. Bone densitometry

60. TREATMENT
 Vitamin D supplementation for 6-10 weeks.
 After 2-4weeks radiograhs show improvement in
mineralisation.
 If child doesn’t respond Vit D therapy then it is vit D
resistant rickets.
 Single dose 600,000 units/15000mcg is given or
divided into 4-6 oral dose.
 125-250mcg(5000-10000u)daily for 2-3 months is
given.
 As residual deformity is rare after medical
management there is no specific orthopaedic
treatment for nutritional rickets.
STOSS THERAPHY
Cholcalciferol 6lakh IU+Calicium given
check x ray for white line of calcification
present absent
healed rickets repeat the dose
check x ray
present absent
Healed rickets refractory rickets

61. ORTHOPAEDIC MANAGEMENT
• The orthotic management of vitamin D–resistant
rickets has not been efficacious.
• Indications such as-pain,difficulty in walking lead
to angular deformity corrections.
• Most common deformity seen is anterolateral
bowing of femur combined with Tibia vara.
• Multilevel osteotomy is generally required to
satisfactorily correct the mechanical axis of the
limb.

62. • Surgical correction/fixation varies.
• External fixation allows fine tuning of the
alignment postoperatively, when the patient is
able to stand.
• Some advise intramedullary fixation or
plating.
• Regardless of the type of fixation used, careful
preoperative planning of the surgical
treatment of these multiplanar deformities is
crucial to restoring alignment.

63. • Recurrent deformity is a common sequela of
osteotomies in patients with hypophosphatemic
rickets.
• Younger patients have a higher risk of
recurrence. So,milder deformities should not be
corrected in early childhood.
• Some children have severe varus at a very young
age that leads to thrust during gait.
• When gait is compromised or symptoms or pain
is present, osteotomy should be performed and
the alignment monitored for recurrent deformity.

64. • Spinal deformity may be seen in patients with
hypophosphatemic rickets.
• Kyphoscoliosis, Arnold-Chiari malformations,and
spinal stenosis have all been described in patients
with vitamin D–resistant rickets.
• Adults with hypophosphatemic rickets are prone to
the development of arthritis.

70. Post operative
Pre operative-
-genu valgum
-Corrected with an external fixator

71. INTRODUCTION
Osteomalacia is the softening of the bones caused
by defective bone mineralization secondary to
inadequate levels of available phosphate and
calcium, or because of overactive resorption of
calcium from the bone which can be caused by
hyperparathyroidism (which causes hypercalcemia).
Osteomalacia in children is known as rickets, and
because of this, use of the term "osteomalacia" is
often restricted to the milder, adult form of the
disease. Signs and symptoms can include diffuse
body pains, muscle weakness, and fragility of the
bones.

73. CAUSES
Osteomalacia is a generalized bone condition in
which there is inadequate mineralization of the
bone. Many of the effects of the disease overlap
with the more common osteoporosis, but the two
diseases are significantly different.
There are two main causes of osteomalacia:
1. insufficient calcium absorption from the intestine
because of lack of dietary calcium or a deficiency
of, or resistance to, the action of vitamin D; and
2. phosphate deficiency caused by increased renal
losses.

74. CAUSES
dietary deficiency of vitamin D + lack of solar
irradiation
deficiency of metabolism of vitamin D
chronic renal disease (most common cause)
1-hydroxylation of 25-vitamin D
renal tubular disorder (vitamin D resistant rickets): high level
of phosphorus in urine
X linked hypophosphatemia
chronic liver disease:
hepatocellular: 25-hydroxylation vitamin D
biliary: abnormal gut absorption
administration of phenobarbital (alternate liver pathway)

75. CAUSES
decreased absorption of vitamin D
malabsorption syndromes such as Crohn's
partial gastrectomy (self-restriction of fatty foods)
decreased deposition of calcium in bone
diphosphonates
Other causes
Tumour induced osteomalacia
Cadmium poisoning
Itai-itai disease

76. SIGNS AND SYMPTOMS
Diffuse joint and bone pain (especially of spine,
pelvis, and legs)
Muscle weakness
Difficulty walking, often with waddling gait
Hypocalcemia (positive Chvostek sign)
Compressed vertebrae and diminished stature
Pelvic flattening
Weak, soft bones
Easy fracturing
Bending of bones

78. SIGNS AND SYMPTOMS
Osteomalacia in adults starts insidiously as aches
and pains in the lumbar (lower back) region and
thighs before spreading to the arms and ribs. The
pain is symmetrical, non-radiating and accompanied
by sensitivity in the involved bones. Proximal
muscles are weak, and there is difficulty in climbing
up stairs and getting up from a squatting position.
As a result of demineralization, the bones become
less rigid. Physical signs include deformities like
triradiate pelvis and lordosis. The patient has a
typical "waddling" gait. However, these physical
signs may derive from a previous osteomalacial
state, since bones do not regain their original shape
after they become deformed.

79. LAB FINDINGS
Biochemical features are similar to those of rickets.
The major factor is an abnormally low vitamin D
concentration in blood serum.
Major typical biochemical findings include:
Low serum and urinary calcium
Low serum phosphate, except in cases of renal
osteodystrophy
Elevated serum alkaline phosphatase (due to an
increase in compensatory osteoblast activity)
Elevated parathyroid hormone (due to low calcium)
Furthermore, a technetium bone scan will show
increased activity (also due to increased osteoblasts).

80. Condition Calcium Phosphat
e
Alkaline
Phosphat
e
Parathyroid
hormone
Special
features
Osteopeni
a
Unaffecte
d
Unaffecte
d
Normal Unaffected Decrease
d bone
mass
Osteoporo
sis
Unaffecte
d
Unaffecte
d
Elevated Unaffected Thick
dense
bones
Osteomala
cia/Rickets
Decrease
d
Decrease
d
Elevated Elevated Soft
bones
Osteitis
fibrosa
cystica
Elevated Decrease
d
Elevated Elevated Brown
tumors
Paget’s
disease
unaffecte
d
decreased variable unaffected Abnormal
bone
structure
COMPARISION OF
CONDITIONS

81. RADIOLOGY
diffuse demineralization: osteoporotic-like pattern
may show a characteristic smudgy "erased" or
"fuzzy" type of demineralization
coarsened trabeculae
insufficiency fractures
Pseudofractures (looser’s zone)
articular manifestations (uncommon)
rheumatoid arthritis-like picture
osteogenic synovitis
ankylosing spondylitis-like picture

82. Looser’s Zone
( Milkman’s Pseudofractures )
Pathognomonic
Looser zones are
radiolucent lines that are
often penetrating through the
cortex perpendicular to the
shaft and are most often
seen in the medial cortices
of the femurs and in the
pelvis and ribs, neck of
scapula.
Caused by rapid resorption
and slow mineralisation

84. Biconcave
vertebrae
Compression
fractures

85. Trefoil Pelvis

86. TREATMENT
Nutritional osteomalacia responds well to
administration of 10,000 IU weekly of vitamin D
for four to six weeks.
Osteomalacia due to malabsorption may require
treatment by injection or daily oral dosing of
significant amounts of vitamin D.
Calcitriol supplement for CKD.

87. Treatment
Exercise
Exercise helps to strengthen the bones, especially weight-
bearing exercise (anything that involves walking or running).
However, you should avoid intensive exercise while any fractures
or cracks in the bones are healing.
Sunlight
Where possible, going outside and exposing your arms and face
to sunlight is the best way to get vitamin D. From June toAugust
just 15 minutes a day is generally enough. Don’t allow your skin
to go red and take care not to burn, particularly in strong
sunshine and if you have fair or sensitive skin.
Diet and nutrition
A diet that includes vitamin D and calcium can help, but this
won’t prevent the condition by itself. Nevertheless, a diet that
provides vitamin D is especially important if you don’t get enough
exposure to sunlight.