3. CONTENTS
• INTRODUCTION
• CALCIUM METABOLISM
FUNCTIONS
NORMAL VALUES AND TYPES
SOURCES AND REQUIREMENTS
ABSORPTION AND EXCRETION
REGULATION
• PHOSPHORUS METABOLISM
FUNCTIONS
NORMAL VALUES AND SOURCES
ABSORPTION AND EXCRETION
REGULATION
• APPLIED ASPECTS
3
7. DAILY REQUIREMENTS OF
CALCIUM
• Adult men and women :- 800 mg/day
• Pregnant ladies and lactating mothers :- 1500 mg/day
• Children 1-8 years :– 800 mg -1200mg/day
• Infant<1 year:- 300- 500 mg/ day
7
9. FUNCTIONS OF CALCIUM
• 1. development of bone and teeth
• 2. Muscle contraction
• 3. Blood Coagulation
• 4. Membrane integrity & stabilization of cell Membrane
• 5. Release of Neurotransmitters from synaptic vesicles
• 6. Release of hormone
• 7. Synthesis of Nucleic acids & proteins
• 8. Activation of enzymes
• 9. calcium as intracellular messanger
• 10. Secretory processes
• 11. Contact inhibition
• 12. action on heart
9
10. ABSORPTION & EXCRETION OF
CALCIUM
10
Mostly occur in duodenum by an energy dependent active process
Calcium excreted partly through kidney mostly through the intestine
Renal threshold for serum calcium is 10 mgdl
11. FACTOR AFFECTING CALCIUM
ABSORPTION IN GUT
INCREASED
• Vitamin D
• Parathyroid hormone
• Acidity
• Lactose
• Amino acid Lysine & Arginine
• High protein diet
DECREASED
• Phylates & Oxlates
• High content of dietry
phosphate
• Free fatty acid
• Alkaline condition
• High content of dietary fiber
• High magnesium intake
• Coticosteroid therapy
• Renal failure
11
12. CALCIUM METABOLISM
• A complex regulatory system maintains the normal amounts of Ca,
phosphate in the body.
• Key hormone to regulate the amounts of Ca & phosphate are
1. 1,25 – dihydroxycholecalciferol(calcitriol)
2. Parathormone,
3. calcitonin
These hormones act on 3 organ system
Intestinal tract
The bone
Kidney
12
15. PARATHYROID HORMONE
15
Normal plasma level : 1.5-5.5 ng/dL
60-70% - degraded by kupffer cells of liver by proteolysis
20-30% - occurs in kidneys
16. CONTROL OF PARATHYROID
SECRETION BY CALCIUM ION
CONCENTRATION
16
Stimulate increased activity
pyrophosphate collagenase
Action is indirect on
kidney and intestine
17. EFFECT OF PTH ON CALCIUM AND
PHOSPHATE CONCENTRATIONS
17
18. CALCITONIN
• Parafollicular cells or clear cells ( C cells ) – follicles in thyroid
• Polypeptide chain- 32 aminoacids
• Plasma level : 1-2ng/dL
• Half life : 5-10 mins
• Degraded and excreted by liver and kidney
18
19. FUNCTION OF CALCITONIN
• Decreases blood calcium levels by acting on bones, kidneys and
intestine
• Facilitates deposition of calcium on bones
• Increases excretion of calcium through urine
• Prevents absorption of calcium from intestine
19
24. FUNCTIONS
• Formation of bone & teeth
• Important constituent of high energy phosphate compound(ATP, GTP)
• Helps in regulation of glycolysis
• Phosphorylation of lipids & sugar
• Urinary buffer, which regulates urinary pH.
• Required for the formation of phospholipids, nucleic acids (DNA , RNA)
• Essential component of several nucleotide coenzymes(NAD+, NADP+,
Pyroxidal phosphate, ADP , AMP)
24
25. ABSORPTION & EXCREATION
• Absorption occurs from jejnum
• Apsorption is optimum when dietary Ca:P is between 1:2
• Acidity increses absorption
• Phylates decreses uptakes by intestinal cells
• Renal threshold is 2 mgdl
• 500mg phosphate excreated in urine per day
• Calcitriol increses phosphate uptake along with calcium
• Parathyroid decreases phosphate uptake
25
26. DEPLETION OF PHOSPHATE
• Skeletal muscle weakness
• Cardiac & respiratory muscle dysfunction
• Loss of red blood cell membrane integrity
• Abnormal formation of bone
26
32. ACCOUCHER’S HAND
• Muscular spasm leading to uncontrolled prolonged flexion of
metacarpophalangeal joints while the fingers remain extended.
32
33. CAUSES OF HYPOCALCEMIA
• Hypoparathyroidism
• Accidentally sugical removal of parathyroid gland during
autoimmune disease
• Characterized by decrease of seum calcium & increase in serum
phosphate
• Reduced urinary excreation of both calcium & phosphate
• Psudohypoparathyroidism
33
34. HYPERCALCEMIA
• Level above 12mg/dl & become marked at 15mg/dl
• Depresses nervous system & muscle activity
• Decreases the QT interval of heart causes constipation & lack of
appetite.
• Polyuria, nausea, tiredness
• Impaired mentation
• Coma
• Parathyroid poisoning (>17mg/dl)
34
36. PARATHYROID POISONING
• Ca level must rise above 17 mg/dl
• CaHPO4 crystals deposit
Alveoli of lungs
Tubules of kidney
Thyroid gland
Wall of arteries throughout the body
• Death occurs in few days
36
38. TERTIARY
HYPERPARATHYROIDISM
• Parathyroid tumor develop from long standing secondary
hyperparathyroidism.
• Serum calcium is increased
• Phosphorus is normal to increased
• Alkaline phosphatase is increased
38
39. OSTEOPOROSIS
• Demineralization of bone resulting in progressive loss of bone
mass
• ETIOLOGY :
• Decrease ability to produce calcitriol from vit D in old age
• In postmenopausal females
• In immobilized and sedentary individuals
39
40. RICKETS
• Defective calcification of
bone due to low level of Vit
D in the body
• Due to a dietary deficiency
of Ca and Phosphate both
• Increase activity of alkaline
phosphatase
• Serum conc. Of calcium and
phosphate may be normal
40
41. OSTEOMALACIA
• Accumulation of osteoid in place of
mineralized bone after epiphysal closure
• Etiology
Vitamin D deficiency
Calcium mal-absorption
Liver & renal disorders
Prolonged anticonvulsive drugs
Hypophosphatemic rickets
41
42. CLINICAL FEATURES
• Weakness & generalized bone pain
• Pseudofracture
• Partial or complete fracture without
displacement
42
45. HYPERPHOSPHATEMIA
• Occurs due to
1. Increased phosphate load due to endogenous and exogenous
sources – exceeds – renal excretory ability
2. Decreased urinary excretion
45
46. CLINICAL MANIFESTATIONS
• Tetany and seizures due to hypocalcemia
• Elevation of calcium x phosphate product – soft tissue
calcification
• Nephrocalcinosis, cardiac and pulmonary calcification
46
48. BROWN TUMOR
48
Hyperparathyroidism results in disorders of
bone and mineral metabolism.
Diffuse and focal lesions may arise in
multiple bones.
On occasion, a patient with undiagnosed
hyperparathyroidism presents with a lytic
lesion that may be mistaken for a tumor.
These lesions are termed "Brown Tumors"
due to the presence of old hemorrhage in
the lesion.
49. OSTEITIS DEFORMANS
o Also called as PAGET ds
• These patients have an
excessive amount of bone
resorption (removal) followed by
an even more excessive
amount of new bone formation.
• Unfortunately, this increased
rate of bone remodeling leads to
new bone that is not as strong
as normal bone.
• This abnormal bone is weaker,
has more blood vessels, and is
larger in size than normal bone.
49
50. CLINICAL FEATURES
• Non specific headaches
• Impaired hearing
• Involved bone become warm
to touch
• Maxilla involved more
Alveolar ridge becomes
widened & the palate is
flattened
Teeth become loose &
migrate, producing spacing
Mouth may remain open,
exposing the teeth (lips are too
small)
50
52. DENTINAL SCLEROSIS
Sclerosis of primary dentin is a regressive alteration in tooth
substance that is characterised by calcification of the dentinal
tubules
52
53. DEAD TRACTS
• dead tracts in dentin are seen in ground sections of teeth and are
manifested as a black zone by transmitted light
53
54. SECONDARY DENTIN
• secondary dentin , which is formed after deposition of the primary
dentin has been completed , is characterised by its irregular
morphological pattern
54
55. HETEROTOPIC CALCIFICATION
• it is defined as deposition of calcium salts in tissue other than
osteoid or enamel
• it is of 2 types
1.METASTATIC CALCIFICATION :
calcium salts are precipitated in undamaged tissue
it is commonly seen in kidney
55
56. • CAUSES OF METASTATIC CALCIFICATION :
hyperparathyroidism
hypervitaminosis D
excessive absorption of calcium
56
57. • DYSTROPHIC CALCIFICATION
• it is deposition of calcium salts in dead or degenerating tissues
• Pathogenesis : related to change in local condition of the tissues
• Clinical features :
it is found intraorally in gingiva , tongue , pulp of the teeth.
57
60. • FALSE DENTICLES : do not exhibits dentinal tubules
• FREE & ATTACHED DENTICLES
FREE DENTICLES : lying entirely within pulp tissue
ATTACHED DENTICLES : continuous with dentinal walls
60
61. DIFFUSE CALCIFICATION
61
• Most common – root canals
• Resembles calcifications seen in other tissues
following degeneration
• Calcific degeneration
• Amorphous unorganized linear strands paralleling
blood vessels and nerves
62. HYPERCEMENTOSIS
• It may be regarded as a regressive change of teeth characterised
by the deposition of excessive amounts of secondary cementum
on root surface
62
63. REFERENCES
• Textbook of Medical physiology – Guyton & Hall (10th edition)
• Anthony’s textbook of anatomy & physiology – Gary.A.Thibodeau
(14th edition)
• Textbook of physiology – Robert.M.Beene
• Differential diagnosis of Oral & Maxillofacial lesions – Woods &
Goaz.
• Applied Oral physiology ( 2nd edition) – Christopher L.B Lavelle
• JAPI - Vol 56 – Aug 2008 - Disorders of Calcium, Phosphorus and
Magnesium Metabolism – Amit K Ghosh , Shashank R Joshi
• ATLAS OF DISEASES OF KIDNEY - Robert W. Schrier VOL 1
• Textbook of biochemistry by U. Satyanarayna
63
Most of the blood calcium present in the plasma, since the blood cell contain very little of it. Normal conc. Of plasma ca or serum conc is 9-11 mg/dl
About half of this 5 mg/dl is in the ionized form which is functionally is most active. At least 1mg/dlseum calcium is found in association with citrate or phosphate. The other half of serum calcium (4to 5 mg/dl) is bound to protein mostly albumin and to a lesser extent globulin. Ionized and citrate or phosphate bound calcium is diffusable from blood to the tissue while protein bound is non diffusable