Calcium and phosphorous

CALCIUM AND PHOSPHOROUS
Dr P MIKITHA
Post Graduate
AECS Maaruti College Of Dental Sciences And Research centre

CONTENTS
• Introduction
• Minerals
• Calcium and phosphorous metabolism:
sources and requirements
functions
absorption and excretion
regulation
• Hormones involved in calcium and phosphate homeostasis
• Disorders of calcium and phosphate metabolism
• Periodontal considerations
• Summary
• References

INTRODUCTION
The rigidity of the skeleton which provides support and
protection for the soft tissues, muscle contraction, the
hardness and fitness of the teeth, the stability of the cell
membranes, activation of many hormones and last but not the
least the heart beat itself is dependent on the twin minerals of
the body- Calcium and Phosphorus. Together whether in
ionized or in unionized form, they are arguably two of the
most important body components.

MINERALS
• Inorganic elements essential to the nutrition of the body.
• Minerals perform several vital functions:
1. Calcification of bone
2. Blood coagulation
3. Neuromuscular irritability
4. Acid-base equilibrium
5. Fluid balance
6. Osmotic regulation
U. Satyanarayana, Textbook of Biochemistry ,Second edition, Uppala-Author-Publisher Interlinks, 2004, Chapter 19.449-
469.

U. Satyanarayana, Textbook of Biochemistry ,Second edition, Uppala-Author-Publisher Interlinks ,2004 ,Chapter 19.449-
469.

CALCIUM
• Most abundant among the minerals in the body.
• Ancient romans prepared lime-calcium oxide. 975 AD plaster
of Paris was used for setting broken bones.
• Sir Humphry Davy isolated calcium (1808).
469.

PHOSPHORUS
• Due to its use in explosives, poisons- “ The Devil’s element.”
• In human body phosphorus is present as phosphates
(compounds containing the phosphate ion)
• The first form of elemental phosphorus to be produced (white
phosphorus in 1669) by Greek.
• Henning brand 1669 discovered it.
469.

FUNCTIONS
 Bone and teeth formation
 Neuromuscular impulse
transmission
 Regulate normal muscle
contraction
 Blood clotting
 Excitation of cardiac and
skeletal muscles
 Synthesis and regulation of
endocrine and exocrine glands
 Mineralization of bones
teeth
 Part of every cell
 Genetic material
 Part of phospholipids
 Energy transfer
 Acid-base balance
 Required for formation of
phospholipids
CALCIUM PHOSPHORUS

ABSORPTION OF CALCIUM AND PHOSPHORUS
CALCIUM:
• Absorbed from the GI tract
into blood.
• Two mechanisms have
been proposed for the
absorption of calcium by
gut mucosa:
1. simple diffusion
2. An active transport process
involving energy and
calcium pump.
PHOSPHORUS:
• Absorbed in duodenum and
other parts of small
intestine by active transport
and passive diffusion.
469.

FACTORS CONTROLLING ABSORPTION
Those acting on mucosal
cells:
1. Vitamin D and Calcium
absorption
2. Effect of previous calcium
intake and of increased
calcium need.
3. Effect of pregnancy and
growth.
Those affecting the availability of
calcium and phosphate in the
gut:
1. PTH harmone
2. Effect of pH of the intestine
3. Amount of dietery calcium and
phosphorus and Ca:P ratio
4. Phytic acid and phylates
5. Effect of oxalates
6. Influence of fat on calcium
absorption
7. Effect of carbohydrates,
proteins and amino acids.
Arthur C. Guyton , John E. Hall. Text book of Medical Physiology . 11th edition, Elsevier Saunders; 2006. chapter 29. 365-

372.

EXCRETION OF CALCIUM AND PHOSPHORUS
 Calcium is excreted in urine,
bile and digestive secretions.
 The renal threshold for serum
ca-10mg/dl.
 70-90% of the calcium
eliminated from the body is
excreted in the feces.
 The daily loss of calcium in
sweat is about 15mg.
 Phosphorus is excreted
primarily through urine.
 Almost 2/3rd of total
phosphorus that is excreted
is found in the urine as
phosphate of various
cations.
 Phosphorus found in the
faeces is the non-absorbed
form of phosphorus.
469.

SYMPTOMS OF CALCIUM AND PHOSPHORUS
IMBALANCE
INCREASED SERUM Ca
 Hyperparathyroidism
 Hypervitaminosis
 Multiple myeloma
 Sarcoidosis
 Thyrotoxicosis
 Milk alkali syndrome
 Infantile hypercalcemia
DECREASED SERUM Ca
 Renal failure
 Hypoparathyroidism
 vit. D deficiency
 Tetany
 Malabsorption syndrome
372.

Increased phosphate level:
 Frequents cold and flu
 Sensitive to pain and noise
 Gingivitis
 Signs of calcium defiency
 Tendency to low blood pressure
 Blood is too acid
 Red-rimmed eyes
 Acute arthritic attack
372.

Bone structure, Formation and Turnover
 Human body contains 206 bones whose size and shape are
highly diverse, which contains joints at their ends that connect
them to adjacent bones.
 Functions of bone include maintenance of external form,
structural framework for attachment of muscles, weight-
bearing support , and protection of internal organs.
 The cells involved in bone formation and resorption arise in
the hematopoietic system.
Shafer, Hine, Levy, Textbook of Oral Pathology, Sixth edition, Elsevier;2009. Chapter 15. 613-623

 There are two basic types of bone:
 Compact(or cortical) and Cancellous (or trabecular).
 The outer layer is a compact bone, it is dense, solid and
responsible for mechanical and protective functions.
 The interior part contains the cancellous bone, which has the
appearance of sponge-like or honeycombed structures.
 Because of its larger surface area, cancellous bone contains
bone-forming cells and is the site of mineral requiring bone
formation.

 The skeleton is the body’s principal reservoir of calcium and
phosphorus. Bone is a dynamic tissue, calcium phosphates
are continuously deposited and released.
 Bone is a modified connective tissue consisting of a cellular
component, an organic matrix and an inorganic phase.
 Its cells are osteoblasts, osteoclasts, osteocytes and
osteoprogenitor cells.

Bone formation
 During bone formation, osteoblasts secrete tropocollagen,
mucopolysaccharides, sialoproteins and lipids to form the
organic matrix. This matrix matures into an insoluble, fibrillar
network(osteoid), mineralization begins with a nucleation
step, followed by precipitation of calcium and phosphate from
the surrounding interstitial fluid.
 The initial deposits are amorphous and have the composition
of brushite. This mineral changes to hydroxyapatite, a hard,
crystalline compound.

 The calcium phosphates are quite insoluble, their precipitation
may be enhanced by an increase in the calcium phosphate ion
product, by the action of Alkaline phosphatase on sugar
phosphates and pyrophosphates in the bone matrix.
 Alkaline phosphatase may regulate bone mineralization by
hydrolysis of pyrophosphate, which is a potent inhibitor of
mineralization in vitro.
 As mineralization progresses, osteoblasts become surrounded
by growing bone and differentiate into osteocytes which
reside in individual lacunae in the bone.

 These lacunae communicate with each other via canaliculi,
exchanging substrates and metabolites.
 Osteocytes nourish the bone, which is a living, highly
vascularized tissue.
 The bone cells account for 2-3% of mature bone volume.
 Bone mass is about 65% minerals and 35% organic matrix

Bone turnover
 Bone (remodelling) turnover is a dynamic, continuous
process. The adult skeleton is renewed about every ten years.
 The remodelling is accomplished by the formation of
temporary anatomical structures known as basic multicellular
units.
 In these units, multinucleated osteoclasts located in the front,
resorbs the existing bone whereas osteoblasts carried out bone
formation.

 Osteoclasts attachment is mediated by mechanical stimuli or
release of chemotactic substances from the damaged bone.
 Resorption of the bone requires hydrogen ions, lysosomal
enzymes and collagenase, which are secreted through the
ruffled borders containing microvilli of osteoclasts.
 The low pH is responsible for the solubilization of the mineral
component of the bone.
 Osteoblasts recruited to the site of the erosion cavity carry out
bone formation. During bone matrix synthesis, osteoblasts
becomes lining cells or osteocytes and some undergo
apoptosis.

Thus, in bone remodelling, regulators of apoptosis of
osteoclasts and osteoblasts play a major role.
Osteocytes compose more than 90% of the bone cells. The
osteocytes-canaliculi system plays an important role in
activating the bone remodelling process by functioning as a
transduces that detects microfractures or other flaws in the
bone formation.
Both osteoblasts and osteoclasts are derived from
osteoprogenitor cells originating in the bone marrow.
Osteoblasts precursors are pluripotent mesenchymal stem cells.

Osteoclasts precursors are hemotopoietic cells of the monocyte-
macrophage lineage.
The transformation of precursor cells to osteoclasts is stimulated
by Parathyroid hormones, Thyroxine, Growth hormones and Vit D
metabolites.
Calcitonin ,estrogens and glucocorticoids inhibits the formation of
osteoclasts.
Osteoblasts formation is promoted by calcitonin, estrogen, growth
hormones, inorganic phosphates and mechanical stress. It is
antagonized by PTH, Vit D metabolites.

REGULATION OF CALCIUM AND PHOSPHATE
METABOLISM
• Calcium and phosphate levels are mainly regulated by three
hormones, which are:
1. Vitamin D
2. PTH
3. Calcitonin
372.

VITAMIN D
Vitamin D is a steroid hormone involved in the intestinal
absorption of calcium and the regulation of calcium
homeostasis, bone differentiation and immune response.
 There are two major types of vitamin D:
1. Vitamin D2 (ergocalciferol) – which is synthesized by plants
and is not produced by the human body.
2. Vitamin D3 (cholecalciferol) – which is made in large
quantities in the skin when sunlight strikes bare skin. It can
also be ingested from animal sources.

The new 2010 Recommended Dietery
Allowance of Vitamin D:
1. children: 10mug/d
2. Adults: 5-10mug/d
3. Pregnency and lactation: 10mug/d
4. Elderly: 600iud

Studies conducted by Cheng et al. 2003 and
Strushkevich et al . 2008 suggested that
vitamin D is converted in the liver to
25(OH)D, a process carried out by CYP2R1.
The crystal structure of CYP2R1 has been
determined with vitamin D in the active site,
and the enzyme has been to shown to
metabolize both vitamin D2 and D3 equally
efficiently.

PARATHYROID HORMONE
• There are 4 parathyroid glands located behind the thyroid
gland at the upper and lower poles.
• Small in size, measures 6mm long, 3mm wide, 2mm thick.
• HISTOLOGY: each parathyroid gland is made up of 2 cells:
1. chief cells- secrete parathormone.
2. oxyphil cells- they are believed to be the degenerated chief
cells.
469.

ACTIONS OF PTH
On blood calcium level:
1. Increases resorption/absorption of calcium from the bones.
2. Increases renal calcium absorption in the distal tubules.
3. Increases absorption of intestinal calcium.
On blood phosphate level:
 Stimulates resorption of phosphate from the bone.
 Increases urinary excretion.
 Increases absorption of phosphate from GIT through
calcitrol.
372.

CALCITONIN
 Secreted by the parafollicular cells or C cells of throid gland.
 Also known as thyrocalcitonin.
 Polypeptide chain with 32 amino acids.
 Molecular weight 3400
 Plasma level of calcitonin- 1-2ng/l.
 It is not secreted until the plasma calcium level exceeds
9.5mg/dl.
 Minor regulator of calium and phosphate.
469.

APPLIED ASPECTS
 HYPERCALCEMIA
 HYPOCALCEMIA
 HYPERPARATHYROIDISM
 HYPOPARATHYROIDISM
 RICKETS
 OSTEOMALACIA
 OSTEOPOROSIS
 RENAL OSTEODYSTROPHY

HYPERCALCEMIA
•An increase in total serum calcium concentration
above 10.4 mg/dl bet 11.5 -12mg/dl.
•Hypercalcemia can be manifestation of serious illness –
malignancy can be detected coincidentally by lab testing.
•Whenever hypercalcemia is confirmed definite
treatment must be given.
•Hypercalcemia can also be the earliest clue to presence
of malignancy.
469.

PRIMARY HYPERPARATHYROIDISM
•Primary hyperparathyroidism (1o HPT) is the most common
cause of hypercalcemia in the healthy outpatient setting
•Results from an adenoma, multiple adenomas, or
hyperplasia of the parathyroids. Malignancy is fortunately
very rare.The defect lies with the parathyroid tissue.
White, Pharoah , Oral radiology, fifth edition, An imprint of Elsevier; 2008,Chapter 24. 516-535.

•Primary hyperparathyroidism is characterized by
•Hypercalcemia
•PTH above the normal range
•Hypercalciuria
•Increased risk of fractures
•Increased risk of kidney stones
•Seldom causes extreme hypercalcemia unless
confounded by renal failure, dehydration, etc

CAUSES OF PRIMARY HYPERPARATHYROIDISM
•Sporadic adenoma(s) most common cause
•Multiple endocrine neoplasia type 1 (MEN-1): Parathyroid tumors (and
pituitary and pancreas). Loss of activity of tumor suppressor gene (the
menin gene) found on human chromosome 11.
•MEN-2A: parathyroid tumors, medullary thyroid cancer (or
hyperplasia), and pheochromocytoma. Activating Mutation of ret
Proto-oncogene on human chromosome 10. This is rare.
• Familial benign hypocalciuric hypercalcemia: An inactivating
mutation in the calcium sensing receptor found in the parathyroids and
kidneys, and results in hypercalcemia and hyperparathyroidism, but
with low urinary calcium.

TREATMENT OF PRIMARY HYPERPARATHYROIDISM
•Surgical parathyroidectomy is curative
•There are no medications yet available to treat the
disease
•Some patients can be watched
•No clinical consequences of hypercalcemia (fracture,
stones, etc.)
•Mild hypercalcemia
•Older age groups
•Avoid dehydration
•Avoid excessive dietary calcium

HYPERVITAMINOSIS D
•Excessive intake of vitamin D
•Relatively hard to do if all relevant organ systems are
functioning properly; generally requires prescription
strength vitamin d, particularly 1,25(OH)2 D3 (calcitriol)
•Excessive production of 1,25(OH)2D3
•Extra-renal 1-hydroxylation of 25(OH)D3 by an enzyme
with 1-hydroxylase activity, but which is distinct from the
renal enzyme
•Usually associated with granulomas (macrophages)
or abnormal lymphoid tissue (b cell lymphoma)
•Not regulated by PTH

Clinical characteristics:
I. Hypercalcemia
II. Suppressed PTH
III. Increased 1,25(OH)2D3
Effects are mainly due to induced hypercalcaemia
• Immediate effects includes anorexia, thirst, lassitude,
constipation and polyuria.
Followed by nausea, vomiting and diarrhoea.
Delayed effects: persistent hypercalcaemia and
hyperphosphataemia produce:-
• Urinary lithiasis.
• Metastatic calcification.
• Renal failure may develop and leads to death.

NON HORMONAL HYPERCALCEMIA
•Milk-alkali syndrome:
•Intake of high doses of calcium and absorbable antacid
(such as NaCO3)
•Rare cause of hypercalcemia
• Increased intestinal absorption
Decreased renal clearance
•PTH Suppressed, PTHrP Normal, 1,25(OH)2D Normal

RENAL FAILURE ASSOCIATED WITH
HYPERCALCEMIA
•Renal failure may cause either hypercalcemia or
hypocalcemia
•Hypercalcemia usually results from a combination of
factors including decreased calcium clearance and
increased bone resorption,
•PTH elevation
•Low endogenous 1,25(OH)2D
•Exogenous 1,25(OH)2D may contribute to
hypercalcemia
•Calcium and phosphate renal clearance is abolished,
and dialysis does a relatively poor job at clearance
(compared to potassium)

DRUG INDUCED HYPERCALCEMIA
•Thiazide diuretic-induced hypercalcemia:
•Stimulate renal tubular calcium reabsorption
•Decrease urinary loss of calcium
•Uncommon cause of hypercalcemia at doses used to
treat hypertension
•More likely in combination with renal disease, 1o
HPT, etc.

•Lithium-induced hypercalcemia:
•Lithium may be associated with hypercalcemia at doses
routinely used to treat bipolar affective disorder (duration of
therapy is a factor)
•Augments PTH effect at target tissues (bone and kidney)

•High doses of vitamin A, or retinoic acid-induced
hypercalcemia:
•Various retinoids are used in treatment of acne, and certain
hematologic malignancies
•Bind to receptors in the supergene family of nuclear
receptors which includes steroid hormone, thyroid, vitamin
D receptors, etc.
•Appear to directly activate osteoclasts and mediate bone
resorption
•Hypercalcemia is associated with suppressed PTH, Normal
PTHrP, Normal 1,25(OH)2D

HYPOCALCEMIA
< 8.8 mg/dl
< 8.5mg/dl- mild tremors
< 7.5mg/dl- life threatening conditions-
tetany.
Symptoms:
1. Muscle cramps
2. Parasthesia
3. Neuromuscular irritatability
4. Muscle twitching
5. Seizures
6. Tetany
7. Bradycardia
Causes:
1. Hypoparathyroidism
2. Vitamin D deficiency
3. Increased calcitonin
4. Deficiency of calcium and
magnesium
5. hypoalbunemia
469.

TETANY
Tetany is characterized by sensory symptoms consisting of
paresthesias of the lips, tongue, fingers and feet; carpopedal
spasm, which may be prolonged and painful; generalized muscle
aching; and spasm of facial musculature. Tetany may be overt
with spontaneous symptoms or latent and requiring provocative
tests to elicit. Latent tetany generally occurs at less severely
decreased plasma Ca concentrations: 7 to 8 mg/dL (1.75 to 2.20
mmol/L).

TETANY
 Carpopedal spasm: basic feature of tetany is uncontrolled,
prolonged painful contraction of voluntary muscle.
 Chvostek’s sign: contraction of ipsilateral facial muscles when
tapping facial nerve over the angle of mandible.
 Erbs sign: hyperexcitability of muscles to electrical
stimulation.
 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
sphygnomanometer cuff on the upper arm.

PSEUDOHYPOPARATHYROIDISM
Biological active PTH is produced in this inherited
disorder but there is end organ resistance to its effects.
Clinical features are developmental anomalies includes
 Short stature
 Short metacarpal or
 Metatarsal bones
 Mental retardation

Hypoplasia of dentin or enamel and
delay or absence of eruption
Characteristic physical
appearance: short stature, round
face, short thick neck, obesity,
shortening of the metacarpals

Renal tubular disease
•Including Fanconi's syndrome due to nephrotoxins such as
heavy metals and distal renal tubular acidosis, can cause
severe hypocalcemia due to abnormal renal loss of Ca and
decreasing renal conversion to active vitamin D.
•Vitamin D deficiency is an important cause of hypocalcemia.
Vitamin D deficiency may result from inadequate dietary intake
or decreased absorption due to hepatobiliary disease or intestinal
malabsorption. It can also occur because of alterations in vitamin
D metabolism as occurs with certain drugs (phenytoin,
phenobarbital, and rifampin) or lack of skin exposure to sunlight.
The latter is an important cause of acquired vitamin D deficiency.

•Septic shock
May be associated with hypocalcemia due to suppression of
PTH release and conversion of 25(OH)D3 to 1,25(OH)2D3.
• Hyperphosphatemia
Also causes hypocalcemia. Patients with renal failure and
subsequent phosphate retention are particularly prone to this
form of hypocalcemia.
• Drugs
Associated with hypocalcemia include those generally used to
treat hypercalcemia anticonvulsants (phenytoin, phenobarbital)
and rifampin, which alter vitamin D metabolism.

TREATMENT OF HYPOCALCEMIA
•Emergency treatment: calcium gluconate inj 0.23
mmol Ca/ml
•Dose : 10ml iv in first instance
•Long term treatment: vitamin D therapy
•Oral calcium tablets
I. Calcium gluconate 54mg Ca/tab
II. Calcium gluconate 90mg/tab
III. Sandoz calcium 400mg /tab
IV. Sandoz calcium 135mg /tab

PARATHYROID HORMONE
Hyperparathyroidism :
•It is an endocrine abnormality in which there is an
excess of circulating parathyroid hormone.
•An excess of serum PTH increases bone remodeling in
preference of osteoclastic resorption, which mobilizes
calcium from the skeleton.
•PTH increases renal tubular reabsorption of calcium and
renal production of the active vit D metabolite.
•The net result of these function is in an increase in
serum calcium.

Clinical features:
•Women are more affected.
•Renal calculi, peptic ulcers, psychiatric problems, bone
or joint pain.
•Gradual loosening, drifting, and loss of teeth may occur.
•Serum alk.phosphatase level, a reliable indicator of
bone turnover, also elevated in hyperparathyroidism

Radiographic features
•Erosion of bone from subperiosteal surfaces of the phalanges of
the hands.
•Osteitis fibrosa cystica are localized regions of bone loss
produced by osteoclastic activity, resulting in loss of all apparent
bone structure.
•Brown tumors occurs in late stage of disease and in 10% of
cases. Gross specimen has a brown or reddish-brown color.

•Pathologic calcifications in soft tissues have nodular
appearance occurs in kidneys.
•Entire calvaria has a granular appearance caused by loss
of central trabeculae and thinning of the cortical tables.

Hypoparathyroidism:
•It is an uncommon condition in which insufficient secretion of
PTH occurs.
•It develops due to excision of parathyroid glands.
•Characterized by a fall in the serum calcium levels and an
increase in the serum inorganic phosphate levels.
White, Pharoah, Oral radiology, fifth edition, An imprint of Elsevier; 2008,Chapter 24. 516-535.

•Clinical features:
• Tingling and numbness in the fingers, face and
toes.
• Carpopedal spasm.
• Spasm of muscles of respiration resulting in the
dread of suffocation.

Dental findings:
•Hypoplasia of teeth,
•External root resorption
•Delayed eruption
•Root dilacerations

OSTEOMALCIA
•It is the adult equivalent of juvenile (Vitamin D- deficient)
rickets.
•Mainly affects the flat bones in the body and diaphyses of the
long bones .
•Most commonly seen in postmenopausal females with low
dietary calcium intake .
•And in little exposure to the sun resulting in increased removal
of calcium from the bone causing softening of the skeleton and its
distoration.
469.

•Dental findings:- severe periodontitis
•Radiographic features:
•Severe asymmetric deformities of all stress bearing bones,
e.g. pelvis, spine, long bones of the legs.
•Longitudinal hairline fractures are seen in the long bones.
469.
•In periodontitis:
•With regards to periodontitis, in year 1940, Taylor and Day have
reported that a 50% incidence of severe periodontitis in a series of 22
Indian women with osteomalacia.

 Glickman in the early 1950s considered that there is a role of
systemic component in all cases of periodontitis. The nature of
the systemic component whether its presence or absence has
influence on the severity of periodontal destruction and coined
as “bone factors” concept.
 periodontitis is an inflammatory condition of the supporting
structure of tooth (Cementum, Alveolar bone) the severity of
periodontitis may aggravate more rapidly due to influence of
systemic condition (osteomalacia) on alveolar bone and
cementum.

 In patients of osteomalacia, tooth histopathology shows
aplasia or hypoplasia of cementum and enlarged pulp
chambers.
 The principal function of cementum is to provide anchorage
of the tooth in its alveolus which is accomplished through the
collagen fiber bundles of the periodontal ligament whose
terminations (Sharpey's fibers) become firmly embedded in
cementum during the process of cementogenesis, thus, it could
be one of the reason why the exfoliation of permanent teeth
occurred in the patient.
Parfitt AM, Gallagher JC, Heaney RP, Johnston CC, Neer R, Whedon GD. Vitamin D and bone health in the elderly. Am
J Clin Nutr. 1982;36:1014–31.

OSTEOPOROSIS
•It is the commonest generalized disorder of the bone due to
decreased bone matrix rather than poor bone calcification.
•From age of 40years, there is normally a progressive loss of skeletal
mass, leading finally to senile osteoporosis with a liability to
fractures mainly neck of the femur.
•In women osteoporosis occurs particularly after the menopause and
other predisposing factors are adrenal cortex hyperfunction,
hyperparathyroidism, hyperthyroidism, prolonged calcium deficiency
and prolonged physical immobilization.

Clinical features:
•Most common feature is fracture.
•Most common locations are distal radius, proximal
femur, ribs, and vertebrae.
•Patient may have severe bone pain.
•Most at risk is postmenopausal women.

Radiographic features:
-Overall reduction in the density of
bone.
-Thinning of cortical boundaries in
the inferior mandibular cortex is
usually seen.
-Occassionally lamina dura may
appear thinner than normal.

RENAL OSTEODYSTROPHY
•When renal parenchyma is lost or diseased quite
significantly, it is unable to form calcitriol and calcium
absorption is impaired.
•Hypocalcemia leads to increase in PTH which acts on bone
to increase calcium.
•Consequently there is excessive bone turnover and structural
changes. This condition is known as Renal Osteodystrophy.
•Clinical features:
•Seen in chronic renal failure.
•In children, growth retardation, frequent bone fractures
occurs.

Radiographic features:
-Generalized loss of bone density and
thinning of bony cortices.
-Decrease or an increase in the number
of internal trabeculae, and trabecular
bone pattern may be granular.
-Hypoplasia,and hypocalcification of
teeth is seen
Lamina dura may be absent or less
apparent.

PERIODONTAL CONSIDERATIONS
 HENRICKSON suggested higher incidence of periodontal
disease in native of india attributed in part to their low dietery
calcium intake.
 Labile for resorption: alveolar bone, vertebrae, ribs, long
bones.
 LUTWAK et al. demineralization of alveolar bone in humans
was reversed by daily dietery calcium supplements over a
period of year.
 Hypothesized: periodontal bone loss was a direct result of
calcium deficient diet leading to secondary
hyperparathyroidismm and the reversal of this condition is by
dietary calcium supplements.

 Osteoporosis and periodontal diseases: Osteoporosis and
periodontitis are both diseases characterized by bone
resorption. Osteoporosis features systemic degenerative bone
loss that leads to loss of skeletal cancellous microstructure and
subsequent fracture, whereas periodontitis involves local
inflammatory bone loss, following an infectious breach of the
alveolar cortical bone, and it may result in tooth loss.
 Both diseases could also be risk factors for each other and
have a mutual impact that requires concomitant management.
Chin-Wei (Jeff) Wang and Laurie K. McCauley; osteoporosis and periodontitis; Current Osteoporos Rep. 2016 Dec;
14(6): 284-291.

SUMMARY
 Calcium and phosphate are important minerals
that required in minimal amount for basic
activities in the body like the normal ionic
calcium levels in the plasma is required for
proper bone mineralization and maintenance
of cell membrane integrity. The plasma
calcium levels need to be regulated within a
very narrow range because of its marked
effects on neuromuscular and cardiac
excitability.

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