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Osteomalacia
Present by
Sajjad Moradi
PhDstudentofnutritionalsciences
SchoolofNutrition&Foodsciences
IsfahanUniversityofMedicalSciences(IUMS)
1
Preface
Introduction
Risk Factors
Pathophysiology
Symptoms
Diagnosis
Treatment
2
Introduction Osteomalacia is the general
term for the softening of the
bones due to defective bone
mineralization
In children is known as rickets
It is often restricted to the
milder, adult form of the
disease
3
Nicholas et al 1963, Osteoporosis,
osteomalacia, and the skeletal system. JBJS
45 (2):391-405
Introduction Rickets refers to the changes caused
by deficient mineralization at the
growth plate
Osteomalacia refers to impaired
mineralization of the bone matrix
Rickets & osteomalacia usually occur
together as long as the growth plates
are open; only osteomalacia occurs
after the growth plates have fused.
4Whyte MP,Thakker RV (2005) Rickets and
osteomalacia. Medicine 33 (12):70-74
Risk
Factors
Malnutrition
Malabsorption / Postgastrectomy
Darker skin more susceptible
Renal defects
Decreased solar exposure
Geriatric patients
Medications
5
Hazzazi et al(2013) Clinical presentation and etiology of
osteomalacia/rickets in adolescents. Saudi journal of kidney
diseases and transplantation : an official publication of the Saudi
Center for OrganTransplantation,SaudiArabia 24 (5):938-941
Pathophysiology
6
Aworski Z (1972) Pathophysiology, diagnosis
and treatment of osteomalacia.The Orthopedic
Clinics of North America 3 (3):623
Symptoms
Bone pain , backache
Muscle weakness
Vertebral collapse: kyphosis
loss of height
Deformities & stress fractures
7
Osteomalacia in adults starts
insidiously as aches and pains in the
lumbar region, spreading later to the
arms and ribs
 Pain is non-radiating, symmetrical,
and accompanied by tenderness in the
involved bones
 Proximal muscles are weak
8
Symptoms
9
Symptoms
Physical signs include deformities like
lordosis
Looser zone
Biconcave vertebra
Spontaneous fractures
Symptoms
10
Symptoms
Rickets
Tetanus , convulsions, failure
to thrive
Muscular flaccidity
Flattening of skull
Thickening of wrists from
epiphyseal overgrowth,
Stunted growth, Rickety
rosary, spinal curvature, Coxa
vara, bowing
11
Glorieux FH, Chabot G,Tau C Familial hypophosphatemic
rickets: pathophysiology and medical management. In:
Rickets. Nestle NutritionWorkshop Series, 1991. pp 185-199
Diagnosis
Comparison of bone pathology
Condition Calcium Phosphate Alkaline
phosphatase
Parathyroid
hormone
Comments
Osteopenia unaffected unaffected normal unaffected decreased
bone mass
Osteoporosis unaffected unaffected elevated unaffected
thick dense
bones also
known as
marble bone
Osteomalacia
and rickets
decreased decreased elevated elevated soft bones
12
YasudaY, Kaleta J, Brömme D (2005). "The role of cathepsins in osteoporosis and arthritis: rationale for the design of new
therapeutics". Adv. Drug Deliv. Rev. 57 (7): 973–93. doi:10.1016/j.addr.2004.12.013. PMID
Meunier, Pierre (1998). Osteoporosis: Diagnosis and Management. London:Taylor and Francis. ISBN 1-85317-412-2.
Diagnosis
13
Diagnosis
14
Diagnosis
15
Biconcave vertebra
Diagnosis
16
Coxa vara Rickety rosary
Muscular flaccidity Flattening of skull
Treatment
17
 Type I – active vitamin D metabolites, 1-
alpha hydroxyvitamin D (1-2 microgram
daily) or 1,25(OH)2D (0.25-1.5 microgram
daily orally), with or without calcium
supplements
 Type II – sometimes responds partially to
very high doses of active vitamin D
metabolites & calcium and phosphate
supplements.
Treatment
18
 Renal rickets and osteomalacia
They occur in patients with chronic renal failure
due to:
Defects in synthesis of 1,25(OH)2D3
Over treatment with oral phosphate binders
Treatment
1-alpha hydroxylated vitamin D
Dietary restriction of foods with high
phosphate content (milk, cheese, eggs)
Phosphate-binding drugs (calcium
carbonate, aluminum hydroxide)
Pathogenesis, diagnosis and management of osteomalacia
Jennie Walker. doi: 10.7748/nop.26.6.32.e593
Treatment
19
Hypophosphatemic rickets and osteomalacia
Causes
 Inherited or acquired defects in renal tubular
phosphate reabsorption
 Tumours that secrete phosphaturic substance
Clinical features & diagnosis
 Hereditary disorders present as rickets. The diagnosis
is made on the basis of the presence of
hypophosphatemia with renal phosphate wasting in
the absence of vitamin D deficiency.
 Tumour-induced disorder presents with severe ,
rapidly progressive symptoms in patients with no
obvious predisposing factor for osteomalacia.
Pathogenesis, diagnosis and management of osteomalacia
Jennie Walker. doi: 10.7748/nop.26.6.32.e593
Phosphate supplements (1-4g daily) +
active metabolites of vitamin D (to
promote intestinal calcium and phosphate
absorption)
Tumour-induced osteomalacia is treated
in the same way + surgical excision of the
tumour
20
Treatment
Pathogenesis, diagnosis and management of osteomalacia
Jennie Walker. doi: 10.7748/nop.26.6.32.e593
21

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Osteomalacia Diagnosis and Treatment

  • 3. Introduction Osteomalacia is the general term for the softening of the bones due to defective bone mineralization In children is known as rickets It is often restricted to the milder, adult form of the disease 3 Nicholas et al 1963, Osteoporosis, osteomalacia, and the skeletal system. JBJS 45 (2):391-405
  • 4. Introduction Rickets refers to the changes caused by deficient mineralization at the growth plate Osteomalacia refers to impaired mineralization of the bone matrix Rickets & osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused. 4Whyte MP,Thakker RV (2005) Rickets and osteomalacia. Medicine 33 (12):70-74
  • 5. Risk Factors Malnutrition Malabsorption / Postgastrectomy Darker skin more susceptible Renal defects Decreased solar exposure Geriatric patients Medications 5 Hazzazi et al(2013) Clinical presentation and etiology of osteomalacia/rickets in adolescents. Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for OrganTransplantation,SaudiArabia 24 (5):938-941
  • 6. Pathophysiology 6 Aworski Z (1972) Pathophysiology, diagnosis and treatment of osteomalacia.The Orthopedic Clinics of North America 3 (3):623
  • 7. Symptoms Bone pain , backache Muscle weakness Vertebral collapse: kyphosis loss of height Deformities & stress fractures 7
  • 8. Osteomalacia in adults starts insidiously as aches and pains in the lumbar region, spreading later to the arms and ribs  Pain is non-radiating, symmetrical, and accompanied by tenderness in the involved bones  Proximal muscles are weak 8 Symptoms
  • 9. 9 Symptoms Physical signs include deformities like lordosis Looser zone Biconcave vertebra Spontaneous fractures
  • 11. Symptoms Rickets Tetanus , convulsions, failure to thrive Muscular flaccidity Flattening of skull Thickening of wrists from epiphyseal overgrowth, Stunted growth, Rickety rosary, spinal curvature, Coxa vara, bowing 11 Glorieux FH, Chabot G,Tau C Familial hypophosphatemic rickets: pathophysiology and medical management. In: Rickets. Nestle NutritionWorkshop Series, 1991. pp 185-199
  • 12. Diagnosis Comparison of bone pathology Condition Calcium Phosphate Alkaline phosphatase Parathyroid hormone Comments Osteopenia unaffected unaffected normal unaffected decreased bone mass Osteoporosis unaffected unaffected elevated unaffected thick dense bones also known as marble bone Osteomalacia and rickets decreased decreased elevated elevated soft bones 12 YasudaY, Kaleta J, Brömme D (2005). "The role of cathepsins in osteoporosis and arthritis: rationale for the design of new therapeutics". Adv. Drug Deliv. Rev. 57 (7): 973–93. doi:10.1016/j.addr.2004.12.013. PMID Meunier, Pierre (1998). Osteoporosis: Diagnosis and Management. London:Taylor and Francis. ISBN 1-85317-412-2.
  • 16. Diagnosis 16 Coxa vara Rickety rosary Muscular flaccidity Flattening of skull
  • 17. Treatment 17  Type I – active vitamin D metabolites, 1- alpha hydroxyvitamin D (1-2 microgram daily) or 1,25(OH)2D (0.25-1.5 microgram daily orally), with or without calcium supplements  Type II – sometimes responds partially to very high doses of active vitamin D metabolites & calcium and phosphate supplements.
  • 18. Treatment 18  Renal rickets and osteomalacia They occur in patients with chronic renal failure due to: Defects in synthesis of 1,25(OH)2D3 Over treatment with oral phosphate binders Treatment 1-alpha hydroxylated vitamin D Dietary restriction of foods with high phosphate content (milk, cheese, eggs) Phosphate-binding drugs (calcium carbonate, aluminum hydroxide) Pathogenesis, diagnosis and management of osteomalacia Jennie Walker. doi: 10.7748/nop.26.6.32.e593
  • 19. Treatment 19 Hypophosphatemic rickets and osteomalacia Causes  Inherited or acquired defects in renal tubular phosphate reabsorption  Tumours that secrete phosphaturic substance Clinical features & diagnosis  Hereditary disorders present as rickets. The diagnosis is made on the basis of the presence of hypophosphatemia with renal phosphate wasting in the absence of vitamin D deficiency.  Tumour-induced disorder presents with severe , rapidly progressive symptoms in patients with no obvious predisposing factor for osteomalacia. Pathogenesis, diagnosis and management of osteomalacia Jennie Walker. doi: 10.7748/nop.26.6.32.e593
  • 20. Phosphate supplements (1-4g daily) + active metabolites of vitamin D (to promote intestinal calcium and phosphate absorption) Tumour-induced osteomalacia is treated in the same way + surgical excision of the tumour 20 Treatment Pathogenesis, diagnosis and management of osteomalacia Jennie Walker. doi: 10.7748/nop.26.6.32.e593
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