slides contains information on calcium homeostasis and its clinical implications.

1. REGULATION OF BLOOD CALCIUM LEVEL
Dr. Arya S Kumar
JR 1
Dept . Of Pedodontics & Preventive
Dentistry

2. CONTENTS
1. Introduction
2. Distribution Of Calcium
3. Types Of Calcium in Plasma
4. Storage of Calcium
5. Calcium in Bone
6. Biochemical Function
7. Other functions of Calcium
8. Calcium in teeth
9. Sources of Calcium
10. Daily Requirement
11. Absorption & Excretion of Calcium
12. Regulation Of blood Calcium level
13. Calcitriol
14. PTH
15. Calcitonin
16. Calcium & Oral Health : A Review
17. Disorders of Ca Homeostasis
18. Conclusion
19. References

3. INTRODUCTON
 Calcium is the 5th most abundant elements in the earth’s crust.
 Calcium and phosphorous are amongst the most abundant elements
in the body.
 Minerals perform several vital functions which are absolutely essential for the
very existence of the organism. These minerals are classified as principal and
trace elements.
 The 7 principal elements constitute 60-80% of the body’s inorganic material.
They include calcium, phosphorous, magnesium, sodium , potassium, chlorine
and sulphur.
 The trace elements include iron, copper, manganese, zinc, molybdenum,
cobalt, selenium, nickel, chromium, cadmium, aluminium and mercury.

4. DISTRIBUTION OF CALCIUM
 Human body contains approx. 1 kg of calcium with 99 % deposited in the bone in the form
of hydroxyapatite, an inorganic crystal made up of calcium & phosphorus , 1 % in the cells,
0.1 % in the extra cellular fluids.

5.  Calcium is involved in a large amount of aspects of life, such as muscle
contraction, enzyme activation, cell differentiation, immune response, programmed
cell death and neuronal activity
 Such broad functions are maintained by tightly controlled calcium
concentration in extracellular fluid and cellular compartments.
 The concentrations of calcium in blood and extracellular fluid are usually
maintained at 1–2 mmol/L
 While the concentration of intracellular calcium at resting state is maintained
at 100 nmol/L or less by calcium ATPase channels, and exchangers located in
plasma membrane and endoplasmic reticulum (ER) membrane

6. TYPES OF CALCIUM
CALCIUM IN PLASMA
Most of the blood Ca is present in plasma, since blood cells contain
little of it. Its normal concentration in plasma is 9 – 11 mg/dl
It is present in 3 forms :
I. Ionized or diffusible calcium : Found freely in plasma & forms
about 50 % of plasma calcium. It is essential for vital functions
such as neuronal activity, muscle contraction, cardiac activity,
secretions in the glands, blood coagulation etc.
II. About 9 percent of the calcium (0.2 mmol/L) is diffusible
through the capillary membrane but is combined with anionic
substances of the plasma and interstitial fluids (citrate and
phosphate,) in such a manner that it is not ionized
III. About 41 percent (1 mmol/L) of the calcium is combined with the
plasma proteins and in this form is non diffusible through the
capillary membrane.

7. Storage of Calcium
• The primary site of storage is our bones (about 1000
grams)
• Some calcium is stored within cells (endoplasmic
reticulum and mitochondria).

8. CALCIUM IN BONE
Calcium is constantly removed from the bone and deposited in the bone.
Bone calcium is present in two forms :
I. Rapidly exchangeable calcium or exchangeable calcium : Available in small
quantity in bone & help to maintain plasma calcium level.
II. Slowly exchangeable calcium or stable calcium : Available in large quantity in
bones & helps in bone remodeling

9. Can be described under two heading.
1. Due to calcium in bone and ECF.
2. Due to calcium in cytosol (intra cellular calcium).
BIOCHEMICAL FUNCTIONS

10. 1) Bone formation & :
Teeth formation
 Calcium is essential for bone growth as it is composed of tough organic matrix that is
greatly strengthened by Ca salts deposition. Average compact bone contains by weight
about 30 % matrix & 70 % salts.
 An intake of calcium in adequate amount is one of the important factors which are
essential for acquiring bone mass and attaining Peak Bone Mass (PBM). Diet
containing insufficient amount of calcium may lead to a low bone mineral density that
may adversely affect bone health.
 Bone is in a dynamic state, where there is constant exchange of ca between ECF &
bone.
 If large quantities of calcium ions are removed from the circulating body fluids
or vice versa , the calcium ion concentration returns to normal within 30 minutes
to about 1 hour : these results from the exchangeable Ca in the bone that is always
in equilibrium with Ca ions in the ECF.

11. ECF calcium function:
1. Coagulation of blood.
2. It plays an important role in the transmission of nerve impulse at the neuromuscular junction.
The amount of acetyl choline (neurotransmitters) released is directly proportional to ionic
calcium level.

12. Functions of calcium within
the cells:
1. For muscular contractions;
cardiac and skeletal muscles.
2. Vasospasm of vascular smooth
muscles.
(e.g.: Calcium channel blocking
drugs mefedipine/felodipine
reduces rise of calcium in the
vascular smooth muscles, reduces
hypertension).
3. Calcium ions act as second
messengers.
4. Calcium entry into the
myocardial cells causes the
phase two of action
potential of ventricular
muscle.

13. OTHER FUNCTIONS OF CALCIUM
Action on the cells:
 The permeability between the adjacent cell membranes depends on calcium.
 The rate of mitosis both in whole animals and in cultures is raised by increasing and
reduced by lowering the calcium concentration of the environment.
 Calcium stimulates mitosis via cyclic AMP therefore growth increases and so is more
rapid utilization of nutrients and also stimulates appetite.
 Activation of enzymes : Calcium is needed for direct activation of enzymes
such as lipase, ATPase & succinate dehydrogenase.
 Release of certain hormones : release of Insulin , PTH , Calcitonin fom the
endocrine glands

14.  CALCIUM IN TEETH
Enamel
Organic component - protein
Inorganic component - apatite calcium phosphate
Calcium - 33.6 to 39.4 wt%
phosphorus – 16.1 to 18.0 wt%
Conc of ca and p decreases from surface to DEJ
Ca/P ratio is constant - 1.92-2.17
Dentin
Calcium-26-28wg%
Phosphate-12.2-13.2wg%
Ca/P ratio - 2.10-2.20
CEMENTUM
Calcium -26%
Phosphorus -13%
 CALCIUM IN SALIVA -5.8MG/100ML

15. SOURCES OF CALCIUM
 Milk : Good source
 Egg, Fish & Vegetables
 Cereals
 Percentage of calcium in various food substances :
 Whole milk = 10 %
 Low fat milk = 18 %
 Cheese = 27 %
 Other dairy products = 17 %
 Vegetables = 7 %

16.  Other substances such as meat, egg, grains, sugar, coffee, tea, chocolate,
etc. = 21%.
 Besides dietary calcium, blood also gets calcium from bone by resorption.

17. DAILY REQUIREMENT
Adult
800mg/day
Infants
300 – 500 mg/
day
After the age of 50 there is general tendency of osteoporosis that can be prevented by
increased calcium intake with vitamin D.
Pregnancy &
lactation
1500mg/day
Children (1
to 18 years)
1200mg/day
The Food & Nutrition Board Of National academy Of Sciences, National Research Council

18. ABSORPTION & EXCRETION OF CALCIUM
 Calcium taken through dietary sources are absorbed through GIT into the blood & distributed to
various parts of the body.
 Depending on the blood level calcium is either deposited in the bone or removed from the bone.
 Calcium is exrceted from body through urine & feces.
Absorption from GIT
 Calcium is absorbed from the duodenum by transcellular active transport process & a
paracellular, passive process that functions throughout rest of the intestine.
 Vit- D is essential for absorption of calcium from the GI tract.

19. Factors promoting Ca absorption:
Vitamin D ( through its active form calcitriol )
Parathyroid hormones : though increased synthesis of
calcitriol
Acidity ( low pH )
Lactose
Lysine & Arginine

20. Factors that inhibit Ca absoption:
Phytates and oxalates forms insoluble salts
Dietary phosphate insoluble calcium phosphate
( Ca:P = 1:2 & 2:1 )
Free fatty acids insoluble calcium soaps
Alkaline condition
High content of dietary fiber

21. Excretion
 About 1000 mg of calcium is excreted daily. While passing through kidney large quantity of
calcium is filtered in the glomerulus.
 From the filterate 98 – 99 % of calcium is reabsorbed from the renal tubules into the blood and
only small quantity is excreted in urine.

22. About 90 percent (900 mg/day) of the daily intake
of calcium is excreted in the feces.
Approximately 10 percent (100 mg/day) of the
ingested calcium is excreted in the urine.

23. Regulation of blood calcium level
( Homeostasis of Ca )
Mainly by three hormones :
Prathormone
Calcitonin
1,25 -
dihydroxy
cholecalciferol
(calcitriol )

24. CALCITRIOL
In calcium metabolism

25.  Calcitriol or 1,25 – dihydroxy cholecalciferol is a steroid hormone produced by the kidney . It is the
physiologically active form of Vit . D
 Cholecalceferol is derived from two sources.
 D3 → from action of UV light on 7 dehydro-cholesterol in the skin.
 D2 → arises from fat fish, eggs and diary products.
DAILY DIETARY REQUIREMENTS (VITAMIN D)
• Birth to 12 months – 10 mcg
• Children from 1 years & adults
up to70 years – 15 mcg
• Adults bove 71 years – 20 mcg
• Pregnancy & lactation – 15 mcg

26. 25 hydroxylase
1 alpha
hydroxylase
 Vitamin D is not the active substance but is converted in two stages to active form.
PTH

27.  When the plasma calcium concentration is already too high, the formation of
calcitriol is greatly depressed.
 Lack of this in turn decreases the absorption of calcium from the intestines, the
bones, and the renal tubules, thus causing the calcium ion concentration to fall
back toward its normal level.

28. Functions of calcitriol
 Action on intestinal epithelium
• Two routes exist for the absorption of Ca across the
intestinal epithelium: the paracellular pathway and the
transcellular route.
• Calcitriol primarily controls the active absorption of Ca.
• Ca moves down into the apical section of the microvillae
through a Ca channel or Ca transporter.
• Under the influence of calcitriol, intestinal epithelial cells
increase their synthesis of calbindin.
• As the calbindin-Ca complex dissociates, the free
intracellular Ca is actively extruded from the cell by either
the Ca- ATPase or Na-Ca exchanger.

29. • The rate of calcium absorption is directly proportional to the
quantity of calcium binding protein.
• This protein remains in the cells for several weeks after the 1, 25
DHCC has been removed from the body.
• Calcitriol may also increase the synthesis of the plasma
membrane Ca-ATPase, thereby aiding in the active extrusion of
Ca into the lamina propria

30. Action on kidneys
 Vitamin D increases calcium and phosphate reabsorption by the epithelial cells of the
renal tubules, thereby tending to decrease excretion of these substances in the urine.
 However, this is a weak effect and probably not of major importance in regulating the
extracellular fluid concentration of these substances.

31.  Effect of Vitamin D on Bone and Its Relation to Parathyroid Hormone
Activity.
 Vitamin D plays important roles in both bone resorption and bone deposition.
 The administration of extreme quantities of vitamin D causes resorption of bone.
This is because the active form of vitamin D called calcitriol increases the
production of osteoclasts which enhance bone resorption.
 Vitamin D in smaller quantities promotes bone calcification : It results from the ability
of 1,25-dihydroxycholecalciferol to cause transport of calcium ions through cell
membranes.
 PTH and Vitamin D form a tightly controlled feedback cycle, PTH is a major
stimulator of vitamin D synthesis in the kidney while vitamin D exerts negative
feedback on PTH secretion.
 In the absence of Vit D, bone resoptive action of PTH is greatly reduced.

32. Hypervitaminosis D
• It is a rare but potentially serious condition
• It is usually due to taking more than the recommended daily value of vitamin D.
• This can lead to a condition called hypercalcemia (too much calcium in your
blood).
•Fatigue , loss of appetite, weight loss, excessive thirst, excessive urination, dehydration, constipation,
irritability, nervousness, ringing in the ear (tinnitus), muscle weakness, nausea, vomiting, dizziness,
confusion, disorientation, high blood pressure
• Long-term complications of untreated hypervitaminosis D include:
• kidney stones, kidney failure, excess bone loss
• calcification (hardening) of arteries and soft tissues
• in addition increased blood calcium can cause abnormal heart rhythms.

33. PARATHORMONE
In calcium metabolism

34.  Human beings have four parathyroid glands, which
are situated on the posterior surface of upper and
lower poles of thyroid gland .
 Sandstrom (1880) – discovered the parathyroid
gland.
 Macroscopically it appears as a dark brown fat.
 Microscopically : Chief cells & oxyphil cells

35. ACTIONS OF PARATHORMONE ON BLOOD CALCIUM LEVEL
PTH maintains blood calcium level by acting on:
1. Bones
2. Kidney
3. Gastrointestinal tract.
 Maintenance of blood calcium level is necessary
because for many physiological functions
 It is a polypeptide hormone with 84 amino acids
 Primary action of PTH is to maintain the blood calcium
level within the critical range of 9 to 11 mg/dL.

36. On Bone
 Parathormone stimulate bone remodelling, which is an on going process in which bone tissue is
alternatively resorbed & rebuilt over time
 It has two effects on bone in causing resorption of calcium and
phosphate.
 One is a rapid phase that begins in minutes and increases
progressively for several hours ,
 This phase results from activation of the already existing bone cells
(mainly the osteocytes) to promote calcium and phosphate
resorption.
when large quantities of PTH are injected
 The second phase is a much slower one, requiring several days or even
weeks to become fully developed; it results from proliferation of the
osteoclasts, followed by greatly increased osteoclastic reabsorption of the
bone itself.

37. On Kidney
• PTH increases the reabsorption of calcium from the renal tubules along with
magnesium ions and hydrogen ions.
• PTH also increases the formation of 1,25-dihydroxycholecalciferol (activated
form of vitamin D) from 25-hydroxycholecalciferol in kidneys.

38. • PTH stimulates the production of 1 alpha-hydroxylase in the PCT.
On Intestine
• PTH greatly enhances both calcium and phosphate absorption from the
intestines by increasing the formation of calcitriol in kidneys.

39. Role of PTH on Blood Level of Calcium
 Blood level of calcium is the main factor regulating the secretion of PTH.
 If the decrease in the calcium concentration persists, the glands will
hypertrophy, sometimes fivefold or more. Eg : in rickets , pregnancy &
lactation where there is increased Ca demand even slight decrease in
Ca level leads to gland enlargement.
Causes the parathyroid glands to
increase their rate of secretion
within minutes.
The slightest decrease in
calcium ion concentration in the
extracellular fluid.

40.  Conversely, conditions that increase the calcium ion concentration in ECF
cause decreased activity and reduced size of the parathyroid glands
 Eg : (1) excess quantities of calcium in the diet, (2) increased vitamin
D in the diet, and (3) bone resorption caused by factors other than
PTH (e.g., bone resorption caused by disuse of the bones).
 Changes in extracellular fluid calcium ion concentration are detected by a calcium-
sensing receptor (CaSR) in parathyroid cell membranes

41. Calcium Sensing Receptors
• The calcium-sensing receptor (CaSR) is a G-protein coupled
receptor which senses extracellular levels of calcium ions.
• It is primarily expressed in the parathyroid gland and
the renal tubules of the kidney.
• In the parathyroid gland, it controls calcium homeostasis by
regulating the release of parathyroid hormone (PTH).
• In the kidney it has an inhibitory effect on the reabsorption
of calcium depending on which segment of the tubule is
being activated.

42. Summary of Effects of Parathyroid Hormone.
(1) PTH stimulates bone resorption, causing release of calcium into the extracellular fluid.
1) 2) 3)
(2) PTH increases reabsorption of calcium in the renal tubules.
(3) PTH is necessary for formation of active vit . D increased absorption.

43. Calcitonin

44.  Calcitonin, a peptide hormone secreted by the thyroid
gland, tends to decrease plasma calcium concentration
and, in general, has effects opposite to those of PTH.
 Synthesis and secretion of calcitonin occur in the
parafollicular cells, or C cells, lying in the interstitial
fluid between the follicles of the thyroid gland.

45.  Calcitonin is a 32-amino acid peptide with a molecular weight of about
3400
 Increased Plasma Calcium Concentration is the primary Stimulates for Calcitonin Secretion

46. On bone
 Calcitonin decreases blood calcium ion concentration rapidly , beginning within minutes in at least 2 ways :
1. The immediate effect is to decrease the resorptive activities of the osteoclasts.
2. The second and more prolonged effect is to decrease the formation of new osteoclasts.

47. On kidney
Calcitonin increases excretion of calcium through urine, by inhibiting the reabsorption from
the renal tubules.
On intestine
Calcitonin prevents the absorption of calcium from intestine into the blood.
• In patients with medullary thyroid carcinoma, on the other hand, cancerous C cells secrete
large amounts of calcitonin. These patients have a high level of serum calcitonin but a
normal level of serum calcium.
• Other conditions where the calcitonin concentration may also be increased include lung
cancer and some pancreatic tumors.

48. Effects of Other
Hormones
In addition to the above
mentioned three hormones,
growth hormone and
glucocorticoids also
influence the calcium level Glucocorticoids decrease
calcium level by inhibiting
intestinal absorption &
increasing renal excretion of
calcium.
Growth hormone increases blood
calcium level by increasing
intestinal calcium absorption

50. OTHER FACTORS
In blood calcium regulation

51. Phosphorus:
•There is a reciprocal relationship of calcium with phosphorus.
•Ionic products of calcium and phosphrous in the serum is kept as a constant i.e, Calcium=
10mg/dL and Phosohorus = 4mg/dL.
•When phosphorus content in the blood is increased the calcium content is lowered (tetany)
Serum proteins:
•In hypoalbuminemia the total calcium is decreased.

52. Alkalosis and acidosis:
•Alkalosis favors binding of more calcium with proteins
with constant lowering of ionised calcium in the serum
so calcium deficiency may be manifested
•Acidosis favors ionisation of calcium.

53. Calcium and Oral Health : a Review
Mineralized Tooth Structure
 Diet can influence teeth after eruption through local effects.
 The greater the concentration of calcium, the lower is the rate of
demineralization and risk of dental decay.
 The presence of calcium in foods can help protect against dental caries
as this increases the concentration of calcium in plaque & saliva & thus
helps remineralise teeth & prevent dental caries formation.
Dr. Manu Rathee et al , 2013
 Enamel demineralisation takes place below a pH of about 5.5 (the
critical pH). The critical pH is inversely related to both the calcium and
phosphate concentration of plaque and saliva, which are influenced by
diet.

54. Pre-eruptive Effects of Calcium
 Mineralization of primary teeth : 4 months in uetro
 Permanent teeth : birth & continues up to 6 to 13 years of age
 During formation, the enamel , dentin & cementum have vascular system
to supply nutrients for mineralization, which is severed at the time of
eruption.
 As a result, the time when an imbalance in calcium homeostasis will have
its major effect on tooth structure is during gestation and childhood.

55. Role of Calcium deficiency in the progress of periodontal diseases and osteoporosis
 Decline in dietary intake of calcium and calcium phosphorus ratio may enhance the
appearance of both these conditions by increasing bone resorption.
 This type of bone loss affects the bones in descending order-
1. Jaw bones (mainly alveolar bones)
2. Cranial bones
3. Ribs
4. Vertebrae
5. Long bones.
 Studies have shown that increased calcium intake improves the suffering of inflammatory
processes and tooth mobility in patients having periodontal diseases.

56. DISORDERS OF CALCIUM HOMEOSTASIS

57. • HYPOCALCEMIA
• Hypocalcaemia occurs when serum calcium is less than 8.5 mg/dl.
• Hypocalcemia causes nervous system excitement and tetany because of Increased
permeability of neurons to sodium ions.
1.Hypocalcemic Tetany is an abnormal condition characterized by violent and painful muscular
spasm (spasm = involuntary muscular contraction), particularly in feet and hand. It is because
of hyperexcitability of nerves and skeletal muscles due to calcium deficiency.
• Hypercalcaemia occurs when serum calcium exceeds 11.0 mg/dl.
• Hypercalcemia depresses nervous system and muscle activity.

58. HYPOPARATHYROIDISM
• It is a disorder of mineral metabolism caused by insufficient activity of parathyroid glands
Etiology: -
1. Inadvertent removal of Para thyroid gland (during removal
of thyroid).
2. Auto immune destruction of parathyroid tissue.
• This leads to reduced osteocytic resorption of exchangeable calcium and the osteoclasts become
almost totally inactive.
• As a result, calcium reabsorption from the bones is so depressed that the level of calcium in the
body fluids decreases

59. Clinical features:
• Usually is asymptomatic unless situation like metabolic alkalosis further reduces the calcium
level leading to tetany.
• Paresthesia of fingers, toes and perioral region
• “Chvostek’s sign” is an oral finding of
significance characterized by twitching of upper
lip when facial nerve is tapped just below the
zygomatic process.
Oral manifestation

60. • Aberrant developmental patterns may occur if
hypoparathyroidism occurs during tooth
development. Parathormone influences the
eruption rate and affects matrix formation
and calcification, these may present as
• Malformed teeth
• Anodontia
• Enamel hypoplasia
• Short blunt root apices
• Elongated pulp chambers
• Multiple impacted teeth
• Mandibular exostosis
• Persistent oral candidiasis in young patients

61. Treatment
• In most patients with hypoparathyroidism, the 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.
Primary Hyperparathyroidism
• In primary hyperparathyroidism, an abnormality of the parathyroid
glands causes inappropriate, excess PTH secretion.
• The cause of primary hyperparathyroidism ordinarily is a tumor of
one of the parathyroid glands
• This causes extreme osteoclastic activity in the bones thus
elevating the calcium ion concentration in the extracellular fluid .

62. Secondary Hyperparathyroidism
• In secondary hyperparathyroidism, high levels of PTH occur as a
compensation for hypocalcemia rather than as a primary abnormality of
the parathyroid glands.
• This contrasts with primary hyperparathyroidism, which is associated
with hypercalcemia.
• Secondary hyperparathyroidism can be caused by vitamin D deficiency or
chronic renal disease

63. • In severe hyperparathyroidism the osteoclastic
absorption soon far outstrips osteoblastic deposition
• Radiographs of the bone typically show extensive
decalcification and, occasionally, large punched out
cystic areas of the bone that are filled with
osteoclasts in the form of so-called giant cell
osteoclast “tumors.”
• The cystic bone disease of hyperparathyroidism is
called osteitis fibrosa cystica
• Multiple fractures of the weakened bones

64. Oral manifestations
• brown tumor
• loss of bone density
• mobile teeth
• drifting of teeth
• complaint of vague jaw bone pain
• sensitive teeth in mastication and percussion
• soft tissue calcifications and dental abnormalities such as development defects, alterations in dental
eruption.
• Malocclusion due to drifting of teeth, with definite spacing of the teeth may be one of the first signs
of the disease.
• Pseudocystic lesion can also be presents, radiolucent lesion at the apex of tooth misdiagnosed as
periapical cyst or granuloma.

65. Brown tumor
• May be the earliest manifestation of the undiagnosed
HPT in 6% of the cases.
• Brown tumor presents as osteolytic lesion (which may be
associated with pain and swelling) that develops due to
changes in bone metabolism caused by high serum
concentration of PTH.
• It is an erosive bony lesions caused by rapid osteolysis
and peritrabecular fibrosis resulting in a local destructive
phenomenon.

66. Rickets Caused by Vitamin D Deficiency
• Rickets occurs mainly in children.
• It results from calcium or phosphate deficiency in the extracellular
fluid, usually caused by lack of vitamin D : thus leading to poor bone
calcification.
• The parathyroid glands prevent the calcium level from falling by
promoting bone resorption every time the calcium level begins to fall.
• Rickets Weakens the Bones : During prolonged rickets, the marked
compensatory increase in PTH secretion causes extreme osteoclastic
absorption of the bone.
• Symptoms include delayed growth, bow legs, weakness and pain in
the spine, pelvis and legs.

67. Oral manifestations
• Abnormal tooth morphology such as thin globular
dentin and enlarged pulp horns that extend into the
dentino-enamel junction.
• Spontaneous gingival and dental abscesses occurring
without history of trauma or caries
• These abscesses are due to deficiencies of dentine
mineralization which result in large pulp chambers and
physical defects within dentine.
• In many teeth, there are channels connecting the pulp
horns to the dentino-enamel junction, and, therefore,
when the enamel is lost through attrition, oral
microorganisms enter the pulp through these channels

68. • Supplying adequate calcium and phosphate in the diet and administering large amounts of
vitamin D.
Treatment of Rickets
• Radiographic examinations revealed large pulp chambers, short roots, poorly defined
lamina dura and hypoplastic alveolar ridge.

69. Osteomalacia—“Adult Rickets.”
• Serious deficiencies of both vitamin D and
calcium occasionally occur as a result of
steatorrhea (failure to absorb fat), because vitamin
D is fat-soluble and calcium tends to form
insoluble soaps with fat; consequently, in
steatorrhea, both vitamin D and calcium tend to
pass into the feces.
• “Renal rickets” is a type of osteomalacia that results from prolonged kidney damage
• Only flat bones and diaphyses of long bones are
affected.
• Severe periodontitis in some cases.
Vit. D deficiency leads to impairment of the mineralisation phase of bone remodeling and thus an
increasing amount of the skeleton being replaced by unmineralized osteoid.

70. Osteoporosis—Decreased Bone Matrix
• It is different from osteomalacia and rickets because it results from
diminished organic bone matrix rather than from poor bone
calcification
• In osteoporosis the osteoblastic activity in the bone is usually less
than normal, and consequently the rate of bone osteoid deposition
is depressed
• Manifestations of osteoporosis :
• Loss of bone matrix and minerals leads to loss of bone strength,
associated with architectural deterioration of bone tissue, more
tooth loss, periodontitis, and decrease in alveolar crestal height.
• Ultimately, the bones become fragile with high risk of fracture.
Commonly affected bones are vertebrae and hip.

71. • Other conditions related to calcium:
• Osteo petrosis
• Hyper thyroidism
• Hypo thyroidism
• Kidney stones
• Gall stones (Cholelithiasis)
• Hyper-reflexia and convulsions

72. CONCLUSION
• Disturbances in calcium and phosphate intake, excretion and trans
cellular 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.

73. REFERENCES
• Guyton and Hall Textbook of Medical Physiology (Guyton Physiology) 13th
Edition
• Text book of biochemistry : by Satyaarayana; 5th edition
• Text book of Physiology : A.K. Jain
• Calcium Homeostasis – Calcium Transport – Parathyroid Action : Roy V.
Talmage
• Theobald HE. Dietary Calcium and Health. Nutrition Bulletin 2005; 30:
237–77
• Calcium intake, calcium homeostasis and health : FanPu , NingChen ,
ShenghuiXue
• Calcium homeostasis : A . M Parfitt