Calcium metabolism

CALCIUM METABOLISM
PRESENTED BY
B.RAVI
MDS 1ST
YEAR

CONTENTS
HISTORY
INTRODUCTION
DISTRIBUTION OF CALCIUM IN THE BODY
SOURCE , ABSORPTION AND EXCRETION
FUNCTIONS OF CALCIUM IN THE BODY
FACTORS AFFECTING THE CALCIUM LEVEL IN THE BODY
REGULATION OF BLOOD CALCIUM LEVEL
DISORDERS OF CALCIUM METABOLISM
CONCLUSION
REFERENCES

history
 Latin- calx or calcis meaning ”lime”
Known as early as first century when ancient Romans prepared lime as
calcium oxide.
 Isolated in 1808 by Englishman Sir Humphrey Davy through the
electrolysis of a mixture of lime (CaO) and mercuric oxide (HgO)..
In 1883 Sir Sydney Ringer demonstrated the biological significance of
calcium

INTRODUCTION
 Refers to the movements and regulation of calcium ions (Ca2+
) into and
out of various body compartments, such as the gastrointestinal tract,
the blood plasma, the extracellular and the intracellular fluid, and bone.
 An important aspect of calcium metabolism is plasma
calcium homeostasis, the regulation of calcium ions in the blood
plasma within narrow limits

In this process, bone tissue acts as a calcium storage center for deposits
and withdrawals as needed by the blood, via continual bone remodeling..
 Derangements of this mechanism lead to hypercalcemia or hypocalcemia,
both of which can have important consequences for health.

In humans, when the plasma calcium level rises above its set point,
the thyroid gland releases calcitonine, causing the plasma calcium
level to return to normal.
When it falls below that set point, the parathyroid gland
release parathyroid hormone (PTH), causing the plasma calcium
level to rise.

DISTRIBUTION OF BODY CALCIUM
Calcium is the most abundant mineral in the human body. The average adult
body contains in total approximately 1-1.5 kg, 99% in the skeleton in the
form of calcium phosphate salts, the remaining 1% is in the blood, body
fluids and soft tissues.
 Normal level of plasma calcium is 9-11gm/dl

calcium ions in plasm is of 3 types

SOURCES OF CALCIUM
The best source of Calcium rich foods, there is nothing that beats Milk, Milk
is a natural source of Calcium for both adults, Children and Calcium in it is
easly digested.

DAILY REQUIREMENT OF CALCIUM
It is most important to note that the body does not produce its own Calcium,
Adequate calcium intake is vital
The recommended amounts of calcium for adults and children

Absorption of calcium
Calcium absorption across the intestinal wall into the blood occurs by
two major mechanisms includes
Active transport (transcellularly)
Passive diffusion (paracellularly)

Active transport of calcium is dependent on the action of calcitriol and the
intestinal vitamin D receptor (VDR)
Passive diffusion or paracellular uptake involves the movement of calcium
between mucosal cells and is dependent on luminal:serosal electrochemical
gradients

FACTORS INCRESING THE CALCIUM ABSORPTION
 VitaminD –Calcitriol induces the synthesis of the carrier protein
(Calbindin) in the intestinal epithelial cells & so facilitates the absorption
of calcium.
Parathyroid hormones - Increases calcium transport from the intestinal
cells.
Amino acids - Especially lysine & arginine increase absorption.
Lactose :- Enhance passive Ca uptake; its effect is valuable because of it
presence in milk.

FACTORS THAT DECREASES CALCIUM ABSOPTION
 Phytates - Phytates are substances found in some plant foods that can bind
calcium in the intestine and decrease its absorption.
 Oxalates are present in some leafy vegetables which cause formation of
insoluble calcium oxalates .

In malabsorption syndromes , fatty acid is not absorbed , causing
formation of insoluble calcium salt of fatty acid .
High phosphate content will cause precipitation as calcium phosphate.
Absorption is also decreased with increase intake of protein & fiber in
diet.

Calcium Excretion
 Calcium leaves the body mainly in urine and feces, but also in
other body tissues and fluids, such as sweat.
 Calcium is excreted partly through the kidneys and mostly
through the intestine. The renal threshold for serum calcium is
10mg/dl. Calcium gets excreted into the urine beyond this
concentration

FUNCTIONS OF CALCIUM
1) Bone :Bone rigidity
2) ECF : Clotting of blood
3) ICF : Muscle contraction - Skeletal, Cardiac
. vasospasm of smooth
muscle
. Neurotransmission

BONE
Development of bones and teeth:
 Bone is regarded as a mineralized connective tissue
 Bones also act as reservoir for calcium
 The bulk quantity of calcium is used for bone and teeth formation
 Osteoblasts induce bone deposition and osteoclasts produce
demineralization

Calcium metabolism in bone has two divisions:
 Bone remodeling
 Calcium homeostasis
BONE REMODELLING
 Throughout life, small portions of bone is removed and replaced by new
bone deposition.

For bone remodeling - A set of locally acting chemicals like
interleukins, prostaglandins, estrogen and other hormones are necessary.
Calcium acts as second messenger for initiation of formation of bone
cells namely,
osteoclasts and osteoblasts which are responsible for bone remodeling.
Eg. ln orthodontic tooth movement.

CALCIUM HOMEOSTASIS
 Calcium homeostasis is the mechanism by
which the body maintains adequate calcium levels.
CALCIUM BALANCE
This term is used to describe the amount of Ca++ either stored or lost
by the body over a specific period of time.

 When the assimilation of calcium from dietary sources is less than the
metabolic requirements and the obligatory losses , then calcium is withdrawn
from the skeleton to maintain the critical concentration of the element in the
blood and tissue fluids.

Positive Ca2+ balance
 Is seen in growing children, where intestinal Ca2+ absorption exceeds
urinary excretion and the difference is deposited in the growing bones
Negative Ca2+ balance
Is seen in women during pregnancy or lactation, where intestinal Ca2+
absorption is less than urinary excretion and the difference comes from the
maternal bones.

The primary source of available calcium is trabecular bone, not cortical bone.
 The sites of trabecular bone which supply mobile calcium are the jaws, ribs,
bodies of the vertebrae, and the ends of the long bones.

 A significant finding from animal experimentation is that, when skeletal
depletion of calcium occurs as a result of stimulation of the parathyroid
gland, alveolar bone is affected first, the ribs and the vertebrae are affected
second, and the long bones third.
Prolonged depletion results in disorganization and loss of trabeculae,
followed by cortical remodeling or structural failure.

2) CLOTTING OF BLOOD:
Clotting of blood is an important haemostatic mechanism because the
clot formed
l) Prevents further bleeding.
2) Seals the wound against further infection.
Normally blood contains 2 sets of materials
1) Procoagulants - Help in clotting.
2) Inhibitors (anticoagulants) of coagulation- Oppose the clotting. Ex:
Heparin present in mast cells.

Mechanism of Coagulation
Fibrinogen is present in blood and it has to be converted to fibrin for blood
clot formation. For this conversion factor Xa is necessary.
Factor Xa can be produced by any of the 2 paths.
Intrinsic path
Extrinsic path

3) Muscle contraction
For muscle contraction  myosin filament should get attached with actin
muscle filament - for this calcium ions are required.

                 Action potential on Sarcolemma
                        Ca+ Channels open up
                         Ca release (from ECF to lCF)
Ca acts as a coupling agent between AP and contraction.

 Muscles are composed of two major protein filaments: a thick
filament composed of the protein myosin and a thin filament
composed of the protein actin.
 Muscle contraction occurs when these filaments slide over one
another in a series of repetitive events
Muscle contraction

Mechanism of Muscle contraction

Muscle contraction Mechanism of

Calcium play a vital roles in contraction of heart as well as skeletal and
smooth muscles.
 Therefore drugs affecting calcium ion metabolism can be used to treat
hypertension or cardiac contractility.

Activation of enzymes:
  Calmodulin is a calcium binding regulatory protein,
  Calmodulin can bind with 4 calcium ions
  Calcium binding leads to activation of enzymes
 Calmodulin is part of various regulatory kinases
  Enzymes activated by Ca2+ include pancreatic lipase, enzymes of
coagulation pathway, and rennin

Second messenger:
Calcium and cAMP are second messengers for hormones e.g. epinephrine in
liver glycogenolysis
 Calcium serves as a third messenger for some hormones e.g, ADH acts
through cAMP and then Ca2+
Myocardium:
 Ca2+ prolongs systole
 In hypercalcemia, cardiac arrest is seen in systole

Factors regulating calcium level
   3 HORMONES:
                                                VITAMIN-D
                                                 PARATHORMONE
                                                CALCITONIN
3 PRINCIPAL TISSUES:

l) Parathormone -
 is a protein hormone secreted by chief cells of the parathyroid gland
 Its main function is to increase the blood calcium level by mobilizing
calcium from bone
The rate of formation & secretion of PTH are promoted by low Ca2+
concentration

2).1,25-dihydroxy cholecalciferol – Calcitriol
 Calcitriol is a steroid hormone synthesized in kidney.
 It is the activated form of vitamin D.
Its main action is to increase the blood calcium level by increasing the
calcium absorption from the small intestine.

3).CALCITONIN
 Calcitonin secreted by parafollicular cells of thyroid gland.
 Calcitonin decreases serum calcium level
 It inhibits resorption of bone
 It decreases the activity of osteocalasts and increases that of osteoblasts
 PTH & CALCITONIN are directly antagonistic

Effects of other hormones
Growth hormone –
Growth hormone increases the blood calcium level by increasing the intestinal
calcium absorption.
 It is also suggested that it increases the urinary excretion of calcium.
Glucocorticoids -
 Decrease blood calcium by inhibiting intestinal absorption and increasing the renal
excretion of calcium

Disorders of calcium
HYPOCALCEMIA
A decrease in total plasma calcium concentration below
8.8 mg/dL (2.20 mmol/L) in the presence of normal plasma
protein concentration.

CLASSIFICATION
PARATHYROID HORMONE (PTH) absent
Hereditary hypoparathyroidism
Acquired hypoparathyroidism
PARATHYROID HOEMONE (PTH) ineffective
 Chronic renal failure
 Lack of Vit D

HYPOPARATHYOIDISM
Results from a deficiency or absence of PTH.
Hypocalcemia and Hyperphosphatemia and is often associated with
chronic tetany.
 Hypoparathyroidism usually results from the accidental removal of
or damage to several parathyroid glands during thyroidectomy.
Transient hypoparathyroidism is common after subtotal
thyroidectomy.
Permanent hypoparathyroidism occurs in fewer than 3% of expertly
performed thyroidectomies.

HYPOPARATHYOIDISM
CAUSES
Accidental removal of gland during surgery
occasionally from autoimmune destruction of the gland.
Congenital absence of the gland
 Atrophy of the gland-Idiopathetic
 Pseudohypoparathyroidism

Clinical Features and Developmenta Anomalies Includes-
 short stature
Short metacarpal or metatarsal bones
Mental retardation

ORAL MANIFESTATIONS:
 Enamel hypoplasia and dentine dysplasia
Dryness of the mucous membranes
 Angular cheilitis
Circumoral parasthesia

ORAL MANIFESTATIONS:
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

Radiographic features
• Enamel hypoplasia
• External root resorption
• Delayed eruption
• Root dilaceration

HYPOPARATHYOIDISM
MANAGEMENT
Administration of extremely large quantities ofvitamin 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.

PSEUDOHYPOPARATHYROIDISM
It 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.

CAUSES OF HYPOCALCEMIA
VITAMIN D DEFICIENCY
 It 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.

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 of endochondral
ossification at the epiphyseal plates.

TYPES OF RICKETS
Nutritional Rickets
 Vitamin D Resistant Rickets.
Vitamin Dependent Rickets.
Oncogenous Rickets.

NUTRITIONAL RICKETS
Primarily, Vitamin D deficiency due to poor dietary intake
                     -Vegetarian diet(cereals, vegetables, fruits).
    - Non-vit.D supplimented formulations for children.
 Children with chronic diarrhea or malabsorption disorders e.g cystic
fibrosis.
 Exclusive breastfed infants in mothers with poor uv light exposure
or mother with vit D deficiency
 Dark skin infants at higher risk.
 Premature infants on parenteral nutrition.

Cupping of proximal
tibia Bowing of lower
limbs
Flaring of metaphysis Cupping of metaphysis of
distal radius/ulna

VITAMIN D RESISTANT RICKETS
Also referred as X-linked hypophosphatemia.
 Non-nutritional rickets.
 Some mothers of affected siblings manifest the disease features.
Renal tubular disorder leading to excessive loss of phosphorus
Autosomal dominant and sporadic cases may occur

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.

Radiographic features:
- Metaphyseal widening and fraying.
- Cupping of metaphysis of proximal
and distal tibia,distal femur, radius and
ulna
Dental radiographs reveal
hypocalcification of teeth and the
presence of large pulp chambers and
alveolar bone loss.

Pathogenesis:
Defect in the proximal tubular reabsorption of phosphate.
Defect in conversion of 25-(OH)D to 1,25D(OH) .
Reduced activity of Na+ dependent phosphate transport resulting in excessive
PO4 excretion. Abnormal gene in this disorder is on X-chromosom
22p(PHEX) OR Phosphate regulating gene.
In autosomal dominant there’s mutation in Fibroblast Growth Factor ,FGF23
which impairs PO4 reabsorption.

VITAMIN D DEPENDENT RICKETS
Also known as Pseudo vitamin D deficiency OR Hypocalcimic
Vitamin D resistant Rickets.
Two types exist;
Type 1.( VDDR1)
Type 2.(VDDR2)

Oncogenous Rickets
(Primary hypophosphatemic Rickets)
 Rickets due to a mesenchymal tumor .
 Mostly benign.
 Occur in sites difficult to detect.e.g nasal antrum, pharynx,small bones of
the hands,etc.
May be associated with other syndromes like Neurofibromatosis.

RICKETS ORAL MANIFESTATIONS
•Developmental abnormalities of
dentin and enamel
•Delayed eruption
•Misalignment of teeth in the jaw
•High caries index
•Enamel hypoplasia

RICKETS
Treatment:
Oral therapy:
Vitamin D- 0.5-1g/24 hr for children 2-4 yrs
1-4g/24 hr for children > 4 yrs.
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 clinical manifestations.

With early diagnosis and compliance limb deformity Can be
minimized.
Corrective osteotomy for deformed limbs should be delayed till
radiological healed rickets is noted and serum alkaline phosphatase
levels are normal.

OSTEOMALACIA
• Softening of bones due to defective mineralization (Ca and PO4).
• Also due to excessive resorption of bones in hyperparathyroidism.
• Common cause is vit.D deficiency

OSTEOMALACIA
Main causes
• Inadequate Ca absorption
•Phosphate deficiency due to renal losses

OSTEOMALACIA
Other causes
 Renal tubular acidosis
 Malabsorption syndrome.
 Malnutrition during pregnancy.
 Hypophosphatemia.
 Tumor induced osteomalacia.
 Drugs-anticonvulsants, anti TB, Steroids, glucocorticoids

OSTEOMALACIA
Clinical features
 Pain and Chronic fatigue, starting insidiously.
 Proximal muscles weakness.
Waddling gait.
Deformed pelvis and exaggerated lordosis.
Bowing of Lower limbs
Biochemical features are similar to Rickets except in renal

OSTEOMALACIA
Radiographic features
• Pseudofractures-Common on scapula, medial
femoral cortex and pubic rami.
• Biconcave vertebral bodies.
•Femoral neck fractures.

IDIOPATHIC HYPOPARATHYROIDISM
It is an uncommon condition in which the parathyroid glands are absent or
atrophied. It may occur sporadically or as an inherited condition.
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.

MAGNESIUM DEPLETION
Occurring with intestinal malabsorption or dietary deficiency can
causes hypocalcemia. Relative PTH deficiency and end-organ
resistance to its action occur with magnesium depletion, resulting in
plasma concentrations of < 1.0 mEq/L (< 0.5 mmol/L); repletion of
magnesium improves PTH levels and renal Ca conservation

ACUTE PANCREATITIS
Causes hypocalcemia when Ca is chelated by lipolytic products released
from the inflamed pancreas

HYPOPROTEINEMIA
Can reduce the protein-bound fraction of plasma Ca. Hypocalcemia
due to diminished protein binding is asymptomatic. Since the ionized
Ca fraction is unaltered, this entity has been termed factitious
hypocalcemia.

HYPERPHOSPHATEMIA
Also causes hypocalcemia by one or a variety of poorly understood
mechanisms. Patients with renal failure and subsequent phosphate
retention are particularly prone to this form of hypocalcemia

SEPTIC SHOCK
May be associated with hypocalcemia due to suppression of PTH release
and conversion of 25(OH)D3 to 1,25(OH)2D3.
DRUGS
Associated with hypocalcemia include those generally used to treat hypercalcemia
anticonvulsants (phenytoin, phenobarbital) and rifampin, which alter vitamin D
metabolism.

TETANY
 A condition that is usually due to low blood calcium (hypocalcemia)
and is characterized by spasms of the hands and feet, cramps, spasm
of the voice box (larynx), and overactive neurological reflexes.
 Tetany is generally considered to result from very low calcium
levels in the blood. However, tetany can also result from reduction in
the ionized fraction of plasma calcium without marked
hypocalcemia, as is the case in severe alkalosis(when the blood is
highly alkaline).

CHVOSTEK’S SIGN
CARPOPEDAL SPASM

TROUSSEAU’S
SIGN
ACCOUCHER’S HAND

HYPOCALCEMIA Treatment
Severe symptomatic cases
Intravenous Calcium gluconate
Asymptomatic cases
Calcium carbonate
Vitamin D

HYPOCALCEMIA Treatment
Emergency treatment:
calcium gluconate inj 0.23 mmol Ca/ml
Dose : 10ml iv in first instance
Oral calcium tablets
- Calcium gluconate 54mg Ca/tab
- Calcium gluconate 90mg/tab
- Sandoz calcium 400mg /tab
- Sandoz calcium 135mg /tab
Long term treatment: vitamin D therapy

HYPERCALCEMIA
Elevated serum calcium level up to 12- 15 mg/dl
Conditions leading to hypercalcemia
 Hyperparathyroidism
 Acute osteoporosis
 Thyrotoxicosis
 Vitamin D intoxication

HYPERCALCEMIA
Classification of Causes of Hypercalcemia
A) PTH related
i) Primarily hyperparathyroidism
a) Solitary adenoma
b) Multiple endocrine neoplasia
ii) Lithium therapy
iii) Familial hypocalcuric hypercalcemia

HYPERCALCEMIA
B) Vit D related
i) Vit D intoxication
ii) Increased 1,25 DHCC, sarcoidosis.
iii) Idiopathic hypercalcemia of infancy
C) Malignancy related
i) Solid tumor with metastasis
ii) Solid tumor with humoral mediation of hypercalcemia

HYPERCALCEMIA
D) Associated with High bone turn over
i) Hyperthyroidism
ii) Immobilization
iii) Thiazide
E) Association with renal failure
i) Severe secondary hyperparathyroidism
ii) Milk alkali syndrome

HYPERPARATHYROIDISM
 Hyperparathyroidism 3rd most common endocrine disease after diabetes
and thyroid disease.
excessive secretion of Parathyroid hormone (PTH) extensively above the
normal level (12-70 pg/mL) ,
HPT can be characterized into primary, secondary, and tertiary forms

Primary
Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma
Secondary
Parathyroid hyperplasia
Tertiary
Autonomous nodule on top of hyperplasia

PRIMARY HYPERPARATHYROIDISM
Single adenoma
 80% of cases
 A rim of normal parathyroid tissue around the adenoma
distinguishes adenoma from hyperplasia
Hyperplasia
 15-20% of cases.
 No rim of normal parathyroid tissue and lack of stromal fats

All 4 glands are involved.
The hyperparathyroidism of MEN syndromes is due to hyperplasia.
Parathyroid carcinoma –
 <1% of cases.
 Exceptionally high calcium or palpable neck mass should raise suspicious.
 Excision with thyroid lobectomy is indicated.

 Radical neck dissection for recurrent disease.
 Recur locally 30%; distant metastasis to lung,liver and bone in 30%.
 Difficult to distinguish adenoma from hyperplasia histologically Primary
Hyperparathyroidism

MEN type I (MEN 1 gene) MEN type II
•Parathyroid adenoma,
•Pituitary adenoma
 •Pancreatic islet cell tumor
•Parathyroid adenoma,
•Thyroid medullary carcinoma &
•Pheochromocytoma

Oral Manifestations:
 Dehydration
 Mandibular or maxillary tumors of the bone, which on biopsy display a
brown tumor of von Recklinghausen
Increased incidence of tori;
Reduction in cortical bone content leading to osteoporosis

BROWN TUMOR
••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 inthe lesion.

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.
Normal trabecular pattern is lost & replaced by granular or ground glass
appearance.
Moth-eaten like appearance of jaw bones
Teeth are mobile and migrate.
 Lamina dura diminished or completely absent in 10% of cases

SECONDARY HYPERPARATHYROIDISM
Vitamin D deficiency
Chronic renal disease
 Hypocalcemia, hyperphosphatemia & increased serum alkaline
phosphatase

TERTIARY HYPERPARATHYROIDISM
Parathyroid tumor develop from long standing secondary
hyperparathyroidism.
Serum calcium is increased
 Phosphorus is normal to increased
Alkaline phosphatase is increased

TREATMENT OF HYPERCALCEAMIA
Emergency treatment:
The solution of IV infusion contains a mixture of mono and
dihydrogen phosphate so that pH is 7.4.
500ml of this solution should be infused over 4 to 6 hours
Long term phosphate treatment:
Oral phosphate is given as diphosphate. Choice depends upon serum
phosphate levels.
Dose 100 to 300ml per day in divided doses

TREATMENT OF HYPERCALCEAMIA
Phosphate sandoz tablet
Phosphorous :500mg
Na: 21 mmol
K : 3mmol
Dose: 1 to 6 tab daily

PATHOLOGICAL CALCIFICATIONS
 Calcifications if occurs in sites other than calcified structures are called
pathological calcifications.
Dystrophic calcification- it is the precipitation of calcium in
degenerating and dead tissues .
Metastatic calcification- occurs due to excess amount of calcium in the
blood which gets deposited in the previously undamaged tissues.
Calcinosis- it is the calcification occuring under the skin. can be
associated with scleroderma .

OSTEOPOROSIS
Defined as a condition characterized by a reduction in the total mass of
calcified bone at a point at which a markedly increased risk of fracture
develops.
Osteoporosis is thinning of bone tissue and loss of bone density over time.
Causes:
Estrogen deficiency in postmenopausal women.
Reduced intake of calcium rich food.
Decreased vitamin d synthesis.

Secondary to prolonged immobilization.
Chronic rheumatoid arthritis ,chronic kidney diseases eating disorders
Taking corticosteroid medications for longer periods.
Hyperparathyroidism

CLINICAL FEATURES:Resorption exceeds Formation

Sudden onset of back pain in thoracic or lumbar spine on physical
activity.
Radiographs may reveal fractures of vertebral bodies.
Multiple fractures over a period of several years.
Oral manifestations:
Fracture during dental treatment.

Treatement:
 No generally accepted specific treatment . Adequate intake of calcium ,
phosphorus and vitamin D (1,200 mg per day of calcium and 800 – 1000
international units of vitamin D3.
Hormone replacement therapy ,
Bisphosphonates
Calcitonin

Osteoporosis drugs used
Anabolic Agent Antiresorptive Agents
Function Forms new bone Suppresses bone
resorption
Mechanism ↑s osteoblast activity ↓ osteoclast activity
Bone
turnover
Accelerates turnover Slows turnover
Dual action bone agent :Strontium ranelate

PROSTHODONTIC CONSIDERATIONS:
Low calcium and vitamin D metabolism are one of the systemic
cofactors in Residual Ridge Resorption.
Denture wearing patients with excessive RRR report lower calcium
intake and poor calcium phosphorus ratio , along with less vitamin D.
Diet counseling for prosthodontic patients is necessary to correct
imbalances in nutrition intake.

• In Paget’s disease of the bone where the maxilla exhibits
progressive enlargement the dentures may be remade periodically to
accommodate the increase in size of the jaws.
• While fabricating the removable dentures the main area of focus
should be on reduction of the forces on residual ridge.

Mucostatic or open mouth impression techniques, selective
pressure impression technique, should be employed to reduce
mechanical forces while impression making, semi anatomic or non
anatomic teeth with narrow buccolingual width should be
selected.
Optimal use of soft liners, extended tissue intervals by keeping the
dentures out of mouth for 10 hours a day can be advised.

While fabricating fixed partial denture in periodontally
compromised abutments it may accelerate the bone loss in
osteoporotic patients.
So, the fabrication of FPD should follow treatment of
osteoporosis rather than preceding it.

osteoporosis affects trabecular bone more than cortical bone and the
maxilla has more trabecular bone content than the mandible, the
maxilla is more susceptible to the effects of systemic osteoporosis.
 During dental implant therapy, it may be wise to be cautious with
maxillary implant treatment planning

SUMMARY
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.

CONCLUSION
 As a dentists, it is vital for us to have a complete understanding of the
general metabolism of calcium and phosphorous as it is these minerals that
help in the formation and maintenance of the teeth and their supporting
bony structure .

Two points need to be kept in mind:
 An adequate calcium intake throughout life is essential for
maintenance of the skeleton, by far the largest body reservoir of
calcium.
The factors effecting calcium and phosphate metabolism in the
body as a whole and it should not be assumed that all these factors
necessarily affect the teeth

REFERENCES
PATHOLOGIC BASIS OF DISEASE– ROBBINS & COTRAN (8TH
EDITION)
TEXT BOOK OF BIOCHEMISTRY FOR MEDICAL STUDENTS-DM
VASUDEVAN(6TH
EDITION)
HARRISON’S PRINCIPLES OF GENERAL MEDICINE (19TH
EDITION)
TEXT BOOK OF HUMAN HISTOLOGY--INDERBIR SINGH (6TH
EDITION)
HUMAN EMBRYOLOGY– INDERBIR SINGH (9TH
EDITION)

REFERENCES
Cline J. Calcium and vitamin d metabolism, deficiency, and excess.
Topics in
companion animal medicine. 2012 Nov 30;27(4):159-64.
 Harrison MR, Edwards PP, Klinowski J, Thomas JM, Johnson DC,
Page CJ.Ionic and metallic clusters of the alkali metals in zeolite Y.
Journal of SolidState Chemistry. 1984 Oct 31;54(3):330-41.

Calcium metabolism

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