1. CALCIUM & PHOSPHATECALCIUM & PHOSPHATE
METABOLISMMETABOLISM
MadhuBilla
1st
M.D.S

2. Contents:Contents:
Introduction
Distribution
Daily requirements
Dietary sources
Functions
Factors controlling absorption
Hormonal control
Other hormones affecting metabolism
Clinical importance
Conclusion

3. DEFINITION OF METABOLISMDEFINITION OF METABOLISM
It is defined as the chemical and physical
process in an organism by which protoplasm
is produced , sustained , and then
decomposed to make energy available.
Metabolism: is the biochemical
modification of chemical compounds in living
organisms and cells that includes the
biosynthesis of complex organic molecules
(anabolism) and their breakdown
(catabolism).

4. INTRODUCTIONINTRODUCTION
The minerals in foods do not contribute directly
to energy needs but are important as body
regulators and as essential constituents in many
vital substances within the body.
About 25 elements have been found to be
essential, since a deficiency produces specific
deficiency symptoms.

5. Principal Minerals include - Calcium, Phosphorous,
Magnesium, Sodium, Potassium and Sulphur.
Calcium and phosphorous individually have their
own functions and together they are required for
the formation of hydroxyapatite and
physical strength of the skeletal tissue.

6. DISTRIBUTIONDISTRIBUTION
• Skeleton - 99%
• Muscle – 0.3%
• Other tissues – 0.7%
CALCIUM PHOSPAHATES
Skeleton – 90%
Intracellularly – 5%
Extracellularly - <0.03%

8. CALCIUM PHOSPHATE RATIOCALCIUM PHOSPHATE RATIO
Calcium : Phosphate ratio normally is 2:1.
Increase in plasma calcium levels causes
corresponding decrease in absorption of
phosphate.
This ratio is always constant.
The serum level of calcium is closely regulated
with normal total calcium of 9-10.5 mg/dL and
normal ionized calcium of 4.5-5.6 mg/dL.
Serum Phosphate levels
Children - 4 to 7 mg/dL
Adults - 3 to 4.5 mg/dL

9. Daily RequirementsDaily Requirements
Calcium:
Adults
Pregnancy
Lactating mother
Infants
Children
Phosphates:
Adults
Pregnancy, lactation
& children
Infants
500-800mg
1500mg
2000mg
360mg
800mg
1200mg
240mg
800mg

10. Dietary SourcesDietary Sources
 Calcium:
- milk and milk
products
- eggs
- fish
- vegetables
- fruits (oranges)
- fortified bread
- nuts
- hard water
 Phosphates:
- same as calcium
- present in high
amount
in cereals and pulses
- absent in hard water

11. Functions of CalciumFunctions of Calcium
 Muscle contraction
Formation of bone and teeth
 Coagulation of blood
Nerve transmission:Integrity of cell
membrane by maintaining the resting
membrane potential of the cells
Release of certain hormones

12. Major structural element in the
vertebrate skeleton (bones and teeth) in
the form of calcium phosphate
(Ca10(PO4)6(OH)2 known as
hydroxyapatatite
Key component in the maintenance of
the cell structure
Membrane rigidity, permeability and
viscosity are partly dependent on local
calcium concentrations

14. Functions of PhosphatesFunctions of Phosphates
Formation of bones.
Like calcium, important component of teeth.
Important constituent of cells.
Forms energy rich bonds in ATP.
Forms co-enzymes.
Regulates blood and urinary pH.
Forms organic molecules like DNA & RNA.

15. Absorption of CalciumAbsorption of Calcium
Calcium is taken through dietary sources as calcium
phosphate, carbonate, tartarate and oxalate. It is
absorbed from the gastrointestinal tract in to blood and
distributed to various parts of the body.
Two mechanisms have been proposed for the
absorption
of calcium by gut mucosa:
 Simple Diffusion.
 An active transport process, involving energy
and calcium pump.

16.  While passing through the kidney, large quantity of
calcium is filtered in the glomerulus. From the
filtrate, 98 to 99% of calcium is reabsorbed in the
renal tubules in to blood and only small quantity is
excreted through urine. In the bone, the calcium
may be deposited or resorbed depending upon the
level of calcium in the plasma.

17. Factors controlling absorptionFactors controlling absorption
Factors are classified into
1. Those acting on the mucosal cells
2. Those affecting the availability of
calcium and phosphates in the gut.

18. Factors acting on the mucosal cellsFactors acting on the mucosal cells
Vitamin D
Pregnancy and growth
PTH

19. VITAMIN-D
Calcitriol (1,25-DHCC) is the biologically
active form of vit-d
It regulates plasma levels of Ca and P
Calcitrial acts at 3 different levels intestine,kidney,
bones
Action on Intestines:
It increases the intestinal absorption of ca&p iin the
intestinal cells calcitriol binds with a cytosolic receptor
to form a calcitriol-receptor commplex
This complex then approaches the nucleus and
interacts with a specific dna leading to synthesis of
specific ca binding protein
This protein increases the ca uptake by intestine

20. Action on bone:
In the osteoblasts of bone calcitriol
stimulates ca uptake for deposition as
capo4
Action on kidney:
It is involved in minimizing the excretion of
ca&p through kidney by decreasing their
excretion and enhancing reabsorption

21. • During later stages of pregnancy, greater amount of calcium
absorption is seen.
• 50% of this calcium is used for the development of fetal
skeleton and the rest is stored in the bones to act as a reserve
for lactation.
• This is due to the increased level of placental lactogen and
estrogen which stimulates increased hydroxylation of vitamin
D.
• In growth there is a increased level of growth hormone.
GH acts by increasing calcium absorption. It also
increases the renal excretion of calcium and phosphates.
Pregnancy and growth:

22. • Parathyroid hormone is one of the main hormones
controlling Ca+2
absorption.
• It mainly acts by controlling the formation of
1,25 DHCC, which is active form of Vit. D, which is
responsible for, increased Ca+2
absorption.
Parathyroid Hormone:

23. Factors affecting availability ofFactors affecting availability of
Calcium and Phosphates in gut.Calcium and Phosphates in gut.
pH of the intestine
Amount of dietary calcium and phosphates
Phytic acid and Phytates
Oxalates
Fats
Proteins and amino acids
Carbohydrates
Bile salts

24. pH of intestine:
• Acidic pH in the upper intestine (deodenum) increases calcium
absorption by keeping calcium salts in a soluble state.
• In lower intestine since pH is more alkaline, calcium salts
undergoes precipitation

25. Amount of dietary calcium and
phosphates:
• Increased level of calcium and phosphate in diet increases
their absorption however up to a certain limit.
• This is because the active process of their absorption can
bear with certain amounts of load beyond which the excess
would pass out into faeces

26. Phytic acid and phytates:
• They are present in oatmeal, meat and cereals and are
considered anti-calcifying factors as they combine with calcium
in the diet thus forming insoluble salts of calcium
Oxalates:
• They are present in spinach and rhubarb leaves. They form
oxalate precipitates with calcium present in the diet thus
decreasing their availability.
Fats:
• They combines with calcium and form insoluble calcium ,
thus decreasing calcium absorption.

27. Bile salts:
• They increases calcium absorption by promoting metabolism
of lipids.
•
Protein and aminoacids:
• High protein diet increases calcium absorption as protein
forms soluble complexes with calcium and keeps calcium in a
form that is easily absorbable.
Carbohydrates:
• Certain carbohydrates like lactose promotes calcium
absorption by creating the acidity in the gut as they favours
the growth of acid producing bacteria.

28. Concept of Calcium BalanceConcept of Calcium Balance
Defined as the net gain or loss of calcium by the
body over a specified period of time
Calculated by deducting calcium in faeces and
urine from the calcium taken in diet.
Positive calcium balance in growing children
Negative calcium balance in aging adults.

29. Hormonal Control of Calcium &Hormonal Control of Calcium &
Phosphate metabolismPhosphate metabolism
Three hormones regulate calcium and phosphate
metabolism.
Vitamin D
PTH
Calcitonin

30. Vitamin DVitamin D
 Cholecalciferol / D3
 Ergocalciferol / D2
 Can be called as hormone as it is produced in the skin when
exposed to sunlight.
 Vitamin D has very little intrinsic biological activity.
Vitamin D itself is not a active substance, instead it must be first
converted through a succession of reaction in the liver and the
kidneys to the final active product 1, 25 di hydroxycholecalciferol,

31. Daily requirementDaily requirement
Adults – 2.5mg
Lactating mother
Pregnancy
Adolescents
Infants
5mg

32. Dietary sourcesDietary sources
Cod liver oil
Fish- Salmon
Egg, liver
• Mean action of vitamin D is to increase the plasma level of
calcium.
• Increases intestinal Ca&P absorption.
Increases renal reabsorption of Calcium and
phosphate.

33. Parathyroid HormoneParathyroid Hormone
(PTH)(PTH)
Secreted by parathyroid gland
Glands are four in number
Present posterior to the thyroid gland
Formed from third and fourth branchial pouches
Combined weight of 130mg with each gland weighing
between 30-50mg.
Histologically – two types of cells
Chief cells (forming PTH)
Oxyphilic cells (replaces the chief cells
stores hormone)

35. Parathyroid HormoneParathyroid Hormone
Single chain polypeptide
Molecular weight 9000
Consist of 84 amino acids
Plasma half life – 20-30 minutes
Plasma concentration – 10-50ug/ml
Measured by immunoassay .

36. Actions of PTHActions of PTH
 The main function is to increase the level of
Ca in plasma within the critical range of 9
to11 mg.
 Parathormone inhibits renal phosphate
reabsorption in the proximal tubule and
therefore increases phosphate excretion
 Parathormone increases renal Calcium
reabsorption in the distal tubule, which also
increases the serum calcium.
 Net effect of PTH  serum calcium↑
↓ serum phosphate

37. Stimulation for PTH secretionStimulation for PTH secretion
 The stimulatory effect for PTH secretion
is low level of calcium in plasma.
 Maximum secretion occurs when plasma
calcium level falls below 7mg/dl.
 When plasma calcium level increases to
11mg/dl there is decreased secretion of
PTH

38. CALCITONINCALCITONIN
 Minor regulator of calcium & phosphate
metabolism
 Secreted by parafollicular cells or C-cells of
thyroid gland.
 Also called as thyrocalcitonin.
 Single chain polypeptide
 Molecular weight 3400
 Plasma concentration – 10-20ug/ml

39. Action of CalcitoninAction of Calcitonin
Net effect of calcitonin  decreases Serum Ca
Target site
◦ Bone (osteoclasts)
decreased ability of osteoclasts to resorb bone
Osteoclasts cells
◦ Lose their ruffled borders
◦ Undergo cytoskeletal rearrangement
◦ Decreased mobility
◦ Detach from bone

40. Calcitonin is a Physiological Antagonist to
PTH with respect to Calcium.
With respect to Phosphate it has the same
effect as PTH i.e. ↓ Plasma Phosphate level

41. OTHER HORMONES on CALCIUMOTHER HORMONES on CALCIUM
METABOLISMMETABOLISM
GROWTH HORMONE
 INSULIN
 TESTOSTERONE & OTHER HORMONES
LACTOGEN & PROLACTIN
STEROIDS
THYROID HORMONES

42. Increases the intestinal absorption of calcium and increases its
excretion from urine
Stimulates production of insulin like growth factor in bone which
stimulates protein synthesis in bone
Stimulates stomatomedian C which acts on cartilage to increase
the length of bones
GROWTH HORMONE

43. TESTOSTERONE
Testosterone causes differential growth of
cartilage resulting to differential bone
development
Acts on cartilage & increase the bone growth.
INSULIN
• It is an anabolic hormone which favors bone formation

44. Thyroid HormoneThyroid Hormone
In infants  stimulation of bone growth
In adults
increased bone metabolism  increased
calcium mobilization

45. GlucocorticoidsGlucocorticoids
Anti vitamin D action, decrease
absorption of calcium in intestine
Inhibit protein synthesis and so decrease
bone formation
Inhibit new osteoclast formation &
decrease the activity of old osteoclasts.

46. Excretion of Calcium and PhosphorousExcretion of Calcium and Phosphorous
Calcium is excreted in the urine, bile, and digestive
secretions.
The renal threshold for serum ca is 10 mg/dl.
70-90% of the calcium eliminated from the
body is excreted in the feces.
The daily loss of calcium in sweat is about 15 mg.

47. Daily turnover rates of Ca in an adult are as follows:
Intake 1000mg.
Intestinal absorption 350mg
Secretion in GI juice 250mg
Net absorption over secretion 100mg
Loss in the faeces 200mg
Excretion in the urine 80-100mg

48. PhosphorousPhosphorous ExcretionExcretion
Phosphorous is excreted primarily through the urine.
Almost 2/3rd
of total phosphorous that is excreted is
found in the urine as phosphate of various cations
phosphorous found in the faeces is the non-absorbed
form of phosphorous.

49. Increased serum Ca:
 1) Hyperparathyroidism.
 2) Hypervitaminosis (Vit. D).
 3) Multiple myeloma.
 4) Sarcoidosis.
 5) Thyrotoxicosis.
 6) Milk alkali syndrome.
 7) Infantile hypercalcemia
Decreased serum Ca:
 1) Renal failure.
 2) Hypoparathyroidism.
 3) Vit. D deficiency.
 4) Tetany.
 5) Malabsorption syndrome.
SYMPTOMS OF CALCIUM -
PHOSPHORUS IMBALANCE

50. Frequent colds and 'flu
Sensitive to pain and noise
Signs of calcium deficiency
Tendency to low blood pressure
Blood is too acid
gingivitis
Red-rimmed eyes
Acute arthritic attacks
INCREASED SERUM PHOSPHATE LEVELS

51. Clinical ImportanceClinical Importance
 Hypercalcemia
Elevated serum calcium level up to 12- 15 mg/dl
 Conditions leading to hypercalcemia
Hyperparathyroidism
Acute osteoporosis
Thyrotoxicosis
Vitamin D intoxication

52. Symptoms:
Polyuria,
dehydration,
confusion,
depression,
fatigue,
nausea/vomiting,
anorexia,
abdominal pain, and
renal calculi
Signs:
Diminished reflexes,
short QT interval on
ECG.

53. Treatment
Parathyroidectomy
Hydration.
Furosemide, Bisphosphanate, Calcitonin,
Mithramycin, Gallium nitrate, Steroids.
IV Phosphate.
Dialysis.
Others- Glucocorticoids, phosphate, amifostine

54. Hypocalcaemia
Decreased level of calcium in the blood
(<4mg/dl)
Conditions leading to hypocalcaemia
Insufficient dietary calcium
Hypoparathyroidism
Insufficient vitamin D
↑ in calcitonin levels

55. Symptoms:
Irritability,
muscle cramps,
depression,
bronchospasm, and seizures.
Signs:
Increased reflexes, prolonged QT interval on ECG (the only
cause of a prolonged QT with a normal duration of the T wave
itself)

56. Treatment:
Asymptomatic
Oral calcium and vitamin D supplementation
Symptomatic
IV calcium gluconate (200mg IV over 10min,
then 50-150mg/hr for a total of 15mg/kg)

57. Tetany (Carpopedal spasm)
Basic feature of tetany is uncontrolled,
painful, prolonged contraction (spasm)
of the voluntary muscles.
Chvostek’s sign
Contraction of ipsilateral facial muscles
when tapping facial nerve over the
angle of the mandible.
Erbs sign
◦ Hyperexitability of muscles to electrical stimulation

58. • Trousseau’s sign
• Spasm of the muscles of the upper extremity causing
flexion of wrist and thumb and extension of fingers.
• Clinically can be produced by applying pressure with
sphygmomanometer cuff on the upper arm.

59. Vitamin D deficiencyVitamin D deficiency
Rickets
◦ Occurs in children between 6
months to 2 years of age.
◦ Affects long bones
◦ Lack of calcium causes failure of
mineralization resulting into
formation of cartilagenous form of
bone.
◦ Most critical area that gets affected
is the center endochondral
ossification at the epiphyseal plates.

60. Dental findings in RickettsDental findings in Ricketts
Developmental anomalies of enamel and dentin
Delayed eruption
Misalignment of teeth
Increase caries index
Wide predentin zone and more interglobular
dentin
Treatment
Daily administration of 1000 – 4000 units of vit.D.

61. ◦ Occurs in adults
◦ Flat bones affected
◦ Softening and distortion of skeletal bones
 Dental findings
◦ Severe periodontitis
Osteomalacia is softening of the bones, caused by not having
enough vitamin D, or by problems with the metabolism
(breakdown and use) of this vitamin. These softer bones have
a normal amount of collagen that gives the bones its structure,
but they are lacking in calcium
Osteomalacia

62. OsteoporosisOsteoporosis
It is the most common of all bone diseases in adults ,
especially in old age.
It is different from osteomalacia and rickets because
it results from diminished organic bone matrix rather
than from poor bone calcification.
Characterised by low bone mass, microarchitectural
deterioration of bone tissue.

63. Symptoms:
Fractures of brittle bones occur even after minor
accident
Pain due to fractures of vertebrae which may radiate
round the trunk , to the buttocks or down the legs
Oral manifestations include alveolar bone loss
resulting in ill- fitting dentures and periodontitis.

64. Prevention:
Physical activity
Androgen and Oestrogen
Increased calcium intake and strontium and sodium
flouride ingestion.

65. HyperparathyroidismHyperparathyroidism
May be Primary or Secondary.
Primary hyperparathyroidism
In Primary form, a primary abnormality of the
parathyroid glands causes inappropriate, excess
PTH secretion.
Caused mainly by an adenoma of parathyroid.

66. • Osteitis fibrosa cystica : Bone pain, joint
stiffness and pathological fracture are the early
symptoms.
• Parathyroid poisoning and Metastatic
calcification
• Hypercalcemia.
• Formation of Kidney stones.

67. Secondary Hyperparathyroidism
In Secondary form, high levels of PTH occur as a
compensation rather than as a primary abnormality
of the parathyroid glands.
It can be caused by Vitamin D deficiency or
chronic renal disease.

68. Oral Manifestations:
 Dehydration
 Mandibular or maxillary tumors of the bone,
which on biopsy display a brown tumor of von
Recklinghausen
Increasedincidence of tori;
Reduction in indices of cortical bone leading to
osteoporosis(lamina dura and gonial index);

69.  According to Schour and Massler, malocclusion
caused by a sudden drifting with definite spacing of
the teeth may be one of the first signs of the disease.
Radiological features include:
 Small cystic areas in the calvarium and large/ small
sharply defined radioluscencies may be present in the
maxilla/ mandible, typically described as having a
‘ground glass appearance’.
 Lamina dura around the teeth may be partially
lost
Management: involves excision of the parathyroid
tumour

71. HypoparathyroidismHypoparathyroidism
Decrease level of PTH
Due to
◦ Surgical removal of parathyroid gland
◦ Congenital absence of the gland
◦ Atrophy of the gland
Diagnosis
◦ Decrease plasma calcium level & increase plasma phosphate
level

72. Clinical signs & symptoms
◦ Hyperactive reflexive
◦ Spontaneous muscular contractions
◦ Convulsions
◦ Laryngeal spasm
Oral Manifestations:
Dryness of the mucous membranes,
Angular cheilitis
Circumoral parasthesia

73. •Enamel hypoplasia and dental dysplasia
•Disturbances in tooth eruption
•Root defects
•Hypodontia and impacted teeth
•Large pulp chambers were observed in the
deciduous teeth and the permanent teeth,
•Thickening of the lamina dura was
observed in the permanent teeth.

74. PseudohypoparathyroidismPseudohypoparathyroidism
is the result of defective G protein in kidney and
bone, which causes end-organ resistance to PTH.
there is hypocalcemia and hyperphosphatemia that is
not correctable by administration of exogenous
PTH.
circulating endogenous PTH levels are elevated.

75. Management
Administration of extremely large quantities of
vitamin D, to as high as 100,000 units per day,
along with intake of 1 to 2 grams of calcium,
keeps the calcium ion concentration in a normal
range.

76. • Increased intake Diet containing Vit-D
• Increased release of P from cells (DM, Acidaemia, Starvation)
• Increased release of P from bone (malignancy, Renal failure,
Increased PTH)
• Decreased excretion (Renal failure, Hyperparathyroidism,
Increased growth hormone)

77. • Phosphate trapping
• Respiratory insufficiency
• Erythrocyte dysfunction
• Nervous Dysfunction
• Leukocyte Dysfunction
• Metabolic acidosis

78. Treatment
Treat the underlying cause
In patients with hypoparathyroidism, calcium
and vitamin D supplementation are generally
prescribed to correct hypocalcemia.
In hyperphosphatemia due to chemotherapy for
leukemia or lymphoma, vigorous saline diuresis will
lead to increased phosphaturia. Alternatively, the
administration of acetazolamide, 500 mg every six
hours, will enhance renal phosphate excretion
through urinary alkalinization and natriuresis.

79. • Decreased Intake (Starvation, Malabsorption, Vomiting)
• Increased cell uptake (High dietary carbohydrate, Liver disease)
• Increased Excretion (Diuretics, Hypomagnesaemia, Increased
PTH)

81. Oral manifestations:
 Histological evidence of widespread formation of
globular,hypocalcified dentin, with clefts and tubular
defects occuring in the region of pulphorns.
Periapical involvement of grossly normal appearing
deciduous and permanent teeth, followed by the
development of multiple gingival fistulas.
Abnormal cementum and the alveolar bone pattern
Lamina dura is frequently absent or poorly defined.

82. Radiographic features:
Dental radiographs reveal hypocalcification of teeth
and the presence of large pulp chambers and alveolar
bone loss.
Histologic features:
Absence of cementum leading to a lack of sound
attachment of the tooth to the bone by
periodontal ligament. This lack of attachment accounts
for the early spontaneous exfoliation of the deciduous
teeth.

83. Treatment
Treat the underlying cause
A total daily amount of 2 to 3 grams of elemental
phosphorus may be given in two to four divided doses,
orally.
 For patients requiring parenteral administration of
phosphate, an initial phosphate dose of 0.08 mmol per
kg body weight may be given over six hours.The dose
may be increased to 0.16 mmol per kg if a patient has
serious life-threatening clinical manifestations.

84. HYPOPHOSPHATASIAHYPOPHOSPHATASIA
The basic disorder is a deficiency of the enzyme
alkaline phosphatase in serum or tissues and
excretion of phosphoethanolamine in the urine.
Clinical features:
Infantile- severe Rickets, Hypercalciemia, Bone
abnormalities and failure to thrive.

85. Childhood- Premature exfoliation of deciduous teeth,
increased infection, growth retardation,
rachitic like deformities, pulmonary, GIT
and renal abnormalities
Adult- spontaneous fractures, prior history of rickets
and osseous radiolucencies.
Oral manifestations:
Loosening and premature loss of deciduous teeth,
chiefly the incisors.

86. Radiographs show hypocalcification of teeth.
Histogically, the teeth present a unique appearance
characterised by the absence of cementum.
Treatment:
Administration of high oral doses of phosphate
results in moderate improvement in bone
calcification.

87. In pagets disease alk.phosphatase levels may
be elevated over 250 bodansky units
It is particularly increased in patients with
osteoblastic phase of disease where there is
Rapid formation of new bone and when there
is polyostotic involvement
Serum Ca & P levels are usually within normal
limits.

88. PSEUDOHYPOPHOSPHATASIA:PSEUDOHYPOPHOSPHATASIA:
A disease resembling classic hypophosphatasia but with
a normal serum alkaline phosphatase level.
Patients exhibit osteopathy of the long bones and skull,
premature loss of deciduous teeth, hypotonia,
hypercalcemia and phosphoethanolaminauria.

89. • It has often been supposed that a low intake of
calcium, or phosphorous, or both might lead to
poor calcification of teeth and possibly, therefore,
to an increased risk of dental caries.
• the calcification of the teeth could be affected if
calcium was very low in the diet.

90. • deficiencies in calcium and phosphate intake do
not affect tooth calcification they do reduce that
of bone, and they result in mobilization of
calcium from already formed bone.
• In pregnancy, when the dietary need of the
mother for calcium and phosphate are increased
by the demands imposed by the growing fetus,
there is mobilization of bone calcium if the
dietary supply is insufficient.

91. ConclusionConclusion
Disturbances in calcium and phosphate intake,
excretion and transcellular shift result in deranged
metabolism accounting for abnormal serum levels.
As a result of the essential role played by these
minerals in intra and extracellular metabolism, the
clinical manifestations of related disease states are
extensive.
Thus, an understanding of the basic mechanism of
calcium, phosphate metabolism and pathophysiology
of various related disorders is helpful in guiding
therapeutic decisions.

92. ReferencesReferences
Textbook of Biochemistry by U. Satyanarayana,
second edition.
Essentials of Medical Physiology by K. Sambulingam,
third edition.
Textbook of Medical Physiology by Guyton and
Hall, tenth edition.
Shafer’s textbook of oral pathology, Fifth edition
Burkets oral medicine 11th
edition
Clinical Disorders of Phosphorous Metabolism,
West J Med. 1987 November; 147(5): 569–576
Calcium and Phosphate Metabolism - Annual
Review of Physiology Vol. 36: 361-390 A B Borle