CALCIUM METABOLISM

PRESENTED BY
CH. LIKHITA
1ST YEAR P.G.
 CONTENTS
 HISTORY
 INTRODUCTION
 DISTRIBUTION OF CALCIUM IN THE BODY
 SOURCE , ABSORPTION AND EXCRETION
 CALCIUM BALANCE
 FUNCTIONS OF CALCIUM IN THE BODY
 FACTORS AFFECTING THE CALCIUM LEVEL IN THE BODY
 REGULATION OF BLOOD CALCIUM LEVEL
 DISORDERS OF CALCIUM METABOLISM
 ORTHODONTIC IMPORTANCE
 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.
 Calcium plays a vital role 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.
 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 9-11mg/dl

 calcium ions in plasma is of 3 types
SOURCES OF CALCIUM
 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)
 Uptake of calcium by active transport predominates in: duodenum jejunum;
 This transcellular mechanism accounts for most of the absorption calcium at low
and moderate intake
 ABSORPTION OF CALCIUM
 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
 Simple diffusion predominates in: ileum
 FACTORS INCREASING 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 faeces, 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

 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
 Calcium gives strength to bones.
 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.

 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
 Pro-covertin
Hageman Factor

Plasma Thromboplastin
Antecedent
Anti-
Christmas Factor hemophilic
Factor
Pro-accelerin

Stuart Factor

Fibrin Stabilising Factor

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)

 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
 Activation of enzymes:
 Calmodulin is a calcium binding regulatory protein, with a molecular
weight of 17,000 Daltons
 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
OTHER FUNCTIONS OF CALCIUM
 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-dihydroxycholecalciferol – 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 Developmental Anomalies Includes-
 short stature
 Short metacarpal or metatarsal bones

 Mental retardation
 ORAL MANIFESTATIONS:

 Enamel hypoplasia and dentin 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
 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.
 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.
 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.
 The latter is an important cause of acquired vitamin D deficiency in northern
climates among people wearing dress that covers them completely
 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.
RICKETS CLINICAL FEATURES
 RICKETS ORAL MANIFESTATIONS

•Developmental abnormalities of
dentin and enamel
•Delayed eruption
•Misalignment of teeth in the jaw
•High caries index
•Enamel hypoplasia
 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 Flaring of metaphysis Cupping of metaphysis of
tibia Bowing of lower distal radius/ulna
limbs
 VITAMIN D RESISTANT RICKETS

 Also referred as X-linked hypophosphatemia.

 Non-nutritional rickets.

 Some mothers of affected siblings manifest the disease features.

 Autosomal dominant and sporadic case may occur.

 Renal tubular disorder leading to excessive loss of phosphorus

 Manifestations:
 No profound myopathy, rachitic rosary, tetany,or enamel defects.

Radiographic findings :
- Metaphyseal widening and fraying.
- Cupping of metaphysis of proximal and distal tibia,distal femur, radius and
ulna
 VITAMIN D RESISTANT RICKETS

Radiographic features:
Dental radiographs reveal
hypocalcification of teeth and the
presence of large pulp chambers and
alveolar bone loss.
 VITAMIN D RESISTANT RICKETS

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.

 VITAMIN D DEPENDENT RICKETS

 Also known as Pseudo vitamin D deficiency OR Hypocalcemic Vitamin D

resistant Rickets.
Two types exist;
 Type 1.(VDDR1)

 Type 2.(VDDR2)
 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
 osteodystrophy where serum phosphate is high.
 OSTEOMALACIA

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

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.
 CAUSES OF HYPOCALCEMIA

MAGNESIUM DEPLETION
Occurring with intestinal malabsorption or dietary deficiency can causES
hypocalcemia. Relative PTH deficiency and end-organ resistance to itsaction
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
 CAUSES OF HYPOCALCEMIA

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

HYPOPROTEINEMIA
Can reduce the protein-bound fraction of plasma Ca. Hypocalcemia due to
diminished protein binding is asymptomatic. Since the ionized Cafraction is
unaltered, this entity has been termed factitioushypocalcemia.
 CAUSES OF 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
 CAUSES 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.
SYMPTOMS
 TETANY

It 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).
 CARPOPEDAL SPASM
CHVOSTEK’S SIGN
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
SIGNS AND
SYMPTOMS
 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
 VITAMIN D INTOXICATION

Ingestion of large doses of Vit D 50-100 times more is required to produce

hypercalcemia increased Vit D causes increased intestinal Ca absorption.

In the milk-alkali syndrome, excessive amounts of Ca and absorbabl alkali

are ingested, usually during peptic ulcer therapy, resulting in hypercalcemia,
renal insufficiency, and metabolic alkalosis. The availability of H2-blocker
therapy for peptic ulcer disease has greatly reduced the incidence of this
syndrome
 HYPERPARATHYROIDISM

Primary hyperparathyroidism

Secondary hyperparathyroidism

Tertiary hyperparathyroidism
 PRIMARY HYPERPARATHYROIDISM

 Tumor of one of PTH gland.-single adenoma

 Adenomas are located at inferior portion of parathyroid gland
 Mostly seen in women than men & children
 Extreme osteoclastic activity in bones
 Elevates Ca ion conc. in ECF which depresses phosphate ions
 PRIMARY HYPERPARATHYROIDISM

MEN I (Wermer's syndrome)

consists of hyperparathyroidism and tumors of pituitary and pancreatic islet
cells, often associated with peptic ulcer and gastric hypersecretion (Zollinger
– Ellison syndrome)

MEN II - carcinoma of the thyroid

is a hereditary condition associated with three primary types of tumors:
medullary thyroid cancer, parathyroid tumors, and pheochromocytoma.
MEN2 is classified into three subtypes based on clinical features.
 PRIMARY HYPERPARATHYROIDISM

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 in the lesion.
 PRIMARY HYPERPARATHYROIDISM

 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

PRIMARY HYPERPARATHYROIDISM
 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 EXCEEDES 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
DENTAL IMPLICATIONS
 the following anomalies are associated with the calcium phosphate imbalance:
developmental anomalies of enamel and dentin.
delayed eruption.
misalignment of teeth.
increased caries index.
wide predentin zone and more interglobular dentine.
 SUMMARY
Disturbances in calcium intake, excretion and trans cellular shift result in
deranged metabolism accounting for abnormal serum levels.

As a result of the essential role played by this mineral in intra and

extracellular metabolism, the clinical manifestations of related disease states
are extensive.
Thus, an understanding of the basic mechanism of calcium metabolism and
pathophysiology of various related disorders is helpful in guiding therapeutic
decisions.
 CONCLUSION

 As dentists, it is vital for us to have a complete understanding of

the general metabolism of calcium as it is the mineral that helps in
the formation and maintenance of the teeth and their supporting bony
structure .
 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)

 TEXTBOOK OF PHYSIOLOGY - VOL.II – A.K.JAIN (5TH EDITION)