DEVELOPMENTAL DISTURBANCES IN MINERAL METABOLISMCALCIUM&PHOSPHOROUS

MINERALS PERFORM SEVERAL VITAL FUNCTIONS WHICH ARE ABSOLUTELY FOR VERY EXISTENCE OF ORGANISM

MINERALS ARE OF 2 TYPES-1)PRINCIPAL ELEMENTS

2)TRACE ELEMENTS AMONG THE MINERALS

CALCIUM&PHOSPHOROUS ARE IMPORTANT BECAUSE THEY CONSTITUTE 60-80%OF BODY’S INORGANIC MATERIAL

CALCIUM

IT IS THE 5TH MOST ABUNDANT ELEMENTS AMONG THE MINERALS IN THE BODY

NORMAL SERUM Ca IS - 9-11mg/dlTOTAL Ca IN THE BODY IS 100-170gm99% - PRESENT IN BONES&TEETH0.5-1%-OUTSIDE THE SKELETAL TISSUE0.1%IS IN EXTRA CELLULAR FLUID

DIETARY REQUIREMENTS

ADULT MEN&WOMEN – 800mg/dayWOMEN DURING

PREGNANCY,LACTATION&POST MENOPAUSE – 1500mg/day

CHILDREN (1-18yrs) – 800-1200mg/day

INFANTS LESS THAN 1YEAR – 300-500mg/day

SOURCE

BEST-MILK&IT’S PRODUCTSGOOD SOURCES-BEANS,LEAFY

VEGETABLES,FISH,CABBAGE,E-GG YOLK

TYPES OF CALCIUM

CALCIUM IN PLASMA

IONIZED FORM50%

TO REGULATE VITAL FUNCTIONS

NONIONIZED FORM8-10%

PRESENT IN THEFORM OF

Ca-BICORBONATE

BOUND FORM40-42%

CALCIUM IN BONES

EXCHANGEBLE FORMTO MAINTAIN

THE PLASMA Ca LEVEL

STABLE FORMHELPS IN REMODELLING

FUNCTIONS

DEVELOPMENT OF BONES&TEETHMUSCLE CONTRACTIONBLOOD COAGULATIONNERVE TRANSMMISSIONMEMBRANE INTEGRITYACTIVATION OF ENZYMES

CALMODULIN MEDIATED ACTION OF Ca

CALCIUM AS INTRACELLULAR MESSENGER

RELEASE OF HORMONES

ABSORPTION

40%OF DAILY DIETARY INTAKE OF Ca IS ABSORBED FROM THE GUT,MAINLY IN THE DUODENUM&JEJUNUM BY ENERGY DEPENDENT ACTIVE PROCESS INFLUENCED BY SEVERAL FACTORS

FACTORS PROMOTING Ca ABSORPTIONVIT DPARATHARMONEACIDITYLACTOSECITRATESAMINOACIDS LIKE

LYSINE&ARGININE

FACTORS INHIBITING Ca ABSORPTION

PHYTATES&OXALATESHIGH CONTENT OF DIETARY

PHOSPHATEFREE FATTY ACIDSAKALINE CONDITIONHIGH CONTENT OF DIETARY FIBRE

EXCRETION

Ca is excreted in both feaces(80%)&urine

Renal threshold for Ca is 7mg/dlSmall intestine is the predominant

site in which Ca is reexcreted

CONDITIONS IN WHICH URINARY EXCRETION OF Ca IS INCREASED

Increased plasma CaDeprivation of phosphateExcessive vitDCorticosteroid administrationMetabolic acidosisHyperthyroidismIdiopathicimmobilisation

CONDITIONS IN WHICH URINARY EXCRETION OF Ca IS DECREASED

Decreased unfilterable plasma CaDec GFRIncreased dietary phosphateDec dietary CaInc utilisation as in

growth,pregnancy,lactationparatharmone

DISEASE STATES

HYPOCALCEMIA HYPERCALCEMIA

HYPOCALCEMIA

Hypoparathyroidism: Amount of parathyroidism is reduced Serum Ca level is 8mg/dlCAUSE:surgical removal of parathyroid

glands,autoimmune destruction of parathyroid tissue

CLINICAL FEATURES:metabolic acidosis-tetany,carpopedal spasm,hyperirritability

ORAL MANIFESTATIONS

CHVOSTEK’S SIGN – IT IS CHARACTERIZED BY TWITCHING OF THE UPPER LIP

THIS SUGGESTS A LATENT DEGREE OF TETANY

PITTING ENAMEL HYPOPLASIAFAILURE OF TOOTH ERUPTION

TREATMENT

Oral dosage of vitD precursor(ergocalciferol)

Additional supplementation of dietary Ca

HYPERCALCEMIA

Hyper parathyroidism – increased production of paratharmone

SERUM Ca levels exceed to 11mg/dlCAUSE:PRIMARY HYPERPARATHYROIDISM –

MALIGNANCYSECONDARY PARATHYROIDISM –

CHRONIC RENAL DISEASE

CLINICAL FEATURES

Renal stones,renal calculi Metastatic calcifications in blood

vessel,sclera,dura around the joints Genralised loss of lamina dura surrounding the

roots of teeth in early stage Alterations in trabecular pattern - -ground

glass appearance Striking enlargement of the jaws Renal osteodystrophy – palatal enlargement is

the characteristic feature

TREATMENT

PRIMARY HYPERPARATHYROIDISM: REMOVAL OF HYPERPLASTIC TISSUESECONDARY HYPERPARATHYROIDISM: RESTRICTION OF DIETARY PHOSPHATE PARATHYROIDECTOMY AN ACTIVE METABOLITE(CALCITRIOL)

OSTEOPOROSIS

Common in women after 60yrsETIOLOGY:lack of adequate bone matrix long term negative Ca balanceOCCURENCE:excess of bone

resorption,decreased bone deposition in old age people

EFFECTS:bones become fragile with high risk of fracture

TREATMENT

Supplementation of Ca ,strontium&ingestion of NaF

PHOSPOROUS

TOTAL BODY PHOSPOROUS 500-800gm

NORMAL PHOSPATE LEVEL OF BLOOD IN ADULTS- 2-4mg/dl

CHILDREN- 3-5mg/dlMAJOR PORTION OF “P “ PRESENT IN

ORGANIC PHOSPHOROUS COMPOUNDS

LOWEST IN BONES&TEETH

DIETARYREQUIREMENTS

INFANTS-240mgADULTS-800mgAdolesents,pregnant,lactating

women-1200mgThe ratio of Ca:P OF 1:1-ADULTThe ratio of Ca:P OF 2:I-CHILDREN

SOURCES

MILKCEREALSLEAFY VEGETABLESMEATEGGS

SERUM PHOSPHATE

LEVEL OF THE WHOLE BLOOD-40mg/dlSerum-3-4mg/dlHigh content of phosphate-RBC,WBCSERUM PHOSPHATE MAY EXIST IN 3

FORMS-FREE FORM(40%) COMPLEX FORM(50%) BOUND FORM(10%)

FUNCTIONS

DEVELOPMENT OF BONES &TEETH MAINTENANCE OF Ph in blood IT FORMS AN INTERMEDIATE STAGE

INMETABOLISM OF FATS&CARBHOHYDRATES-PHOSPHORYLATION

IN BUILDING ORGANIC PGOSPHATES&CATALISTS ESSENTIAL TO STRUCTURE&FUNGTION OF CELLS

FORMATION OF –PHOSPHOPROTEINS, MILK PHOSPHATES&NUCLEOPROTEIN OF CELLS

PROVIDE ENERGY RICH BONDS IN SUCH AS ATP IMP-MUSCLE CONTRACTION

THEY FORM COENZYME AS PYRIDOXAL PHOSPHATE

ABSORPTION

TAKES PLACE IN THE SMALL INTESTINE IN THE FORM OF SOLUBLE INORGANIC PHOSPHATE

70% OF BLOOD PHOSPHOURS IS ABSORBED

AN EXCESS OF Ca,Fe,Al interfere with the absorption

Calcitriol promotes the absorption

REGULATION

BLOOD LEVELS ARE MAINTAINED BY-PTH

PHOSPHATASE ACTIVITY VIT-D

EXCRETION

ABOUT 2/3rd OF PHOSPHATE IS EXCRETED IN URINE/day

Renal threshold is-2mg/dl

DISEASE STATES

HYPOPHOSPHATEMIAHYPOPHOSPHATEMIA

HYPERPHOSPHATEMIAHYPERPHOSPHATEMIA

DEFICIENCY STATES

RICKETSOSTEOMALACIA

RICKETS

VIT-D DEFICIENT RICKETS -ANY DISORDER IN THE VIT-D-Ca-P AXIS

WHICH RESULTS IN HYPOMINERALISED BONE MATRIX

-FAILURE OF ENDOCHONDRAL OSSIFICATION

-INFANTS DEVELOP THE CHARECTERISTIC BONY DEFORMITIES

MARKED GENU VARUM SHOWING RADIO OPACITY SHOWING POOR MINERALIZATION

X-ray showing pseudofracture from an adult who has x-linked hypophosphatemic rickets

Closer view of knee showing thick growth plates that appear fuzzy&widened knee joints

C/FIRREGULAR CALCIFICATION OF

BONES&TEETH CHANGES IN THE BONES-EPIPHYSEAL

PLATE METAPHYSIS SHAFTBOWING OF HANDS &LEGSCOLLAPSATION OF CHEST WALL

O/MONTEETH DEVELIOPMENTAL ABNORMALITIES OF

DENTIN&ENAMEL DELAYED ERUPTION MISALIGNMENT OF THE TEETH IN JAWS HIGH CARIES INDEX WIDE PREDENTIN ZONE& MUCH

INTERGLOBULAR DENTIN RETARDED ERUPTION RATE

VIT D RESISTANT RICKETS

ALSO CALLED FAMILIAL HYPOPHOSPHATEMIA,REFRACTORY RICKETS,PHOSPHATE DIABETES

DEFECTS IN REABSORPTION OF WATER PHOSPHATE, Ca MAY LEAD TO RICKETS,OR MALACIA

INHERITED AS X-LINKED DOMINANT TRAIT

MALES>FEMALESNORMAL VIT-D METABOLISM

C/FSHORTENING OF STATUREBOWING OF THE LEGSDEVELOPMENT OF ANKYLOSIS OF

SPINEPRESENCE OF PSEUDOFRACTURES

O/M-MARKED EFFECTS ON TEETHLARGE PULP CHAMBERSPULP HORNS EXTENDING TO DGJMULTIPLE NON VITAL TEETH WITH

ASSOCIATED GINGIVAL FISTULASABSENCE OF LAMINA DURA

H/FENLARGED PULP HORNDENTIN EXHIBITS CLEFTINGMICROCLEFTS SEEN WITH IN THE

ENAMEL

TREATMENTCALCITRIOL, MULTIPLE DOSES OF

PHOSPHATE, ENDODONTIC THERAPY

OSTEOMALACIA

DEFICIENCY OF VIT-D IN ADULTS COMMON IN POSTMENOPAUSAL

FEMALES WITH LOW DIETARY INTAKE OF Ca

ENDEMIC IN INDIA, JAPAN,CHINAETIOLOGY:MALABSORPTION

C/F SOFTENING&DISTORTIONOF THE SKELETON –

FRACTURE PELVIC DEFORMITIESO/M PERIODONTITISR/FLONGITUDINAL HAIRLINE FRACTURES ARE SEEN

IN THE LONG BONES Eg:pelvis,spine&legs

H/FCORTICAL BONE IS THINOSTEOID BONES ARE FOUND ON THE

TRABECULAETREATMENT-DIETARY VIT-D,-HORMONAL THERAPYFLOURIDE ADMINISTRATION