Phosphorus /certified fixed orthodontic courses by Indian dental academy

INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY
Leader in continuing dental educationLeader in continuing dental education
www.indiandentalacademy.comwww.indiandentalacademy.com
www.indiandentalacademy.com

PHOSPHOROUS
• Total body content-1kg-80% Bone & Teeth
• Mainly an intracellular ion (all cells)
• SOURCES:Milk(100mg/dl),cheese,egg
yolk,meat,fish,cereals,nuts
• Daily requirement:800mg/D
• Distribution:Serum(inorg):3-4.5mg/100ml
• Bone & teeth:22,000mg/100mg

• Blood phoshorous:whole blood-
40mg/dl(rbcs & wbcs contain lot of
phosphate,so hemolysis shld be prevented
during Phosphate estimation of blood)
• Act as a BUFFER
• Forms:inorg,org,phospholipids.
• Excretion:through urine:500mg/D
• Reabsorption inb by parathyroid hormone
• Serum phosphate decreased in
hyperparathyroidism & rickets.

• Functions:
• Bone & Teeth formation
• Formation of phospholipids,nucliec acids,
phosphoproteins,phosphate esters.
• Formation of organic phosphates
• Formation of ATP
• Synthesis of NADP,NAD,ADP,AMP
• Activation of enzymes by phosphorylation
• Buffer

• Disease state:
• Rickets:serum phosphate low
• Diabetes mellitus
• Renal Disease-retention-acidosis
• Increased levelsIncreased levels:
• hypoparathyroidism,renal rickets(familial
hypophosphatemia,vitamin D resistant rickets)
• DecreaseDecrease:
• hyperparathyroidism,celiac d,vitamin D def.

COPPERCOPPER
• Total body content:100-150mg
• Muscles,liver,bone
marrow,kidney,brain,heart,hair
• Daily req:2.5mg/d:2.5mg/d
• Sources:liver,kidney,meat:liver,kidney,meat,shell
fish,nuts,legumes,green leafy vegtables
• Blood copper:90mcg/100ml
• Rbcs-erythrocuprein
• Serum-ceruloplasmin[firmly bound]&loosely
bound to albumin.www.indiandentalacademy.com

• Absorption:duodenum
• Phytate,Ca,Fe,Zn,Mo decrease the absorption
• Functions:
• Haemoglobin synthesis
• Melanin formation
• Phosholipid & collagen synthesis
• Bone formation
• Myelin sheath integrity

•EnzymesEnzymes-ceruloplasmin,cytochrome
oxidase,cytochrome c,tyrosinase,ALA
synthetase,superoxide dismutase
•Copper containing proteinsCopper containing proteins-
hepatocuprein,cuprothionine,cerebrocuprein,hemo
cuprein
•CeruloplasminCeruloplasmin:serum ferroxidase:during Fe
transport promotes oxidation of ferrous ion to ferric
form which is incorporated into transferrin
•Superoxide dismutaseSuperoxide dismutase:enzyme which scavenges
toxic free radical superoxide ion formed during
aerobic metabolism

• Deficiency:
• Essential for hemoglobin formation-anemiaanemia
• Cytochrome oxidase contains copper so def-
oxygen starvation-neonatal ataxiaoxygen starvation-neonatal ataxia
• Connective tissue metabolism-lysyl oxidase-crosslysyl oxidase-cross
linkage of elastin & collagenlinkage of elastin & collagen-so deficiency-
weakening of vessel walls-aneurysm,rupture.also
minkes kinky hair syndromeminkes kinky hair syndrome.
• Present in Tyrosinase-melanin formationTyrosinase-melanin formation-
hypopigmentation,grey hair,flag type of hair
growth.
• Marked skl changes-osteoporosisosteoporosis & spontaneousspontaneous
fracturesfractures

•Toxicity:
•Diarrhoea
•blue-green discolouration of saliva
•hemolysis
•hemoglobinuria
•proteinuria
•renal failure

Wilson’s disease/hepatolenticular degeneration:
• Rare hereditaryhereditary disease-chromosome 13 defect
• Absorption of copperAbsorption of copper from intestine very
highhigh,ceruloplasmin formation very less,majority of
the serum copper remains loosely bound to serum
protein,albumin,so is transported to tissues like
brain & liverbrain & liver
• Clinical features:
• Progressive hepatic cirrhosishepatic cirrhosis-Portal HT,HF

•Dysfunction of lenticular region in brain-necrosis &
sclerosis of the corpus-basal ganglion syndromesbasal ganglion syndromes
•Damage to renal tubulesrenal tubules
•Copper deposits in descement’s membrane of the
eye-golden brown or yellow or green ring around the
cornea-KAYSER FLEISCHER RING
•PIGMENTATION OF NAILS, SKIN
•TREATEMENT:TREATEMENT:
•PENNICILLAMINE

MENKE’S DISEASE:
• X-LINKED RECESSICVE DISORDER of
intestinal copper absorption.
• Absorption &transport of copper at the serosal
aspect is defective.
• C/f:
• Mental retardation,temperature
instability,abnormal bone formation,susceptibility
to infection.

IRON – IN THE HUMAN
BODY
• Essential trace element.
• Total body iron content in a normal adult of 70 kg is just 3
to 5 gms.
• 75% of this is in blood, the rest is in liver, bone marrow
and muscles.
• Iron is present in almost all cells.

Iron containing proteins
Name No. of iron atoms Site
Heme containing proteins
Hemoglobin 4 RBC
Myoglobin 1 Muscle
Cytochrome oxidase 2 Mitochondria
Cytochrome b 1 Mitochondria
Cytochrome c1 1 Mitochondria
Cytochrome c 1 Mitochondria
Cytochrome b5 1 ER
Cytochrome p-450 1 ER, Mitochondria
Catalase 4 RBC
Lactoperoxidase 1 Milk
Tryptophan pyrrolase 4 Cytosol

Iron – Sulphur Complexes
Adrenodoxin 2 Adr. Mitochondria
Complex III Fe-S 2 Mitochondria
Succinate DH 4 Mitochondria
Xanthine oxidase 8 Liver
Non – Heme Containing Proteins
Aconitase 2 TCA cycle
Phe-hydoxylase 2 Liver
Transferrin 2 Plasma
Lactoferrin 2 Milk
Ferritin 4,000 Tissues
Hemosiderin many Liverwww.indiandentalacademy.com

Requirement of Iron
• Daily allowance for iron, for an adult Indian is 20 mg, out
of which about 1 – 2 mg is absorbed.
• In western countries, requirement is 15 mg/day because
the diet does not contain inhibitory substances.
• Children between 13 – 15 years need 20 – 30 mg/day.
• Pregnant women need 40 mg/day.
• Transfer of iron and calcium from mother to fetus occurs
mainly in the last trimester of pregnancy.

Sources of Iron
• Leafy vegetables (20 mg/100g)
• Pulses (10 mg/100g)
• Cereals (5 mg/100g)
• Liver (5 mg/100g)
• Meat (2 mg/100g)
• Jaggery, heart, kidney, spleen, egg-yolk, fish, nuts, figs,
dates, beans, molasses, apples, bananas etc.
• Milk is a very poor source of iron (0.1 mg/100 ml)
• Human milk contains 0.3 to 0.6 µg iron/ml.
• In a typical Indian diet, the major quantity of iron is
received from cereals because of the bulk quantity taken,
although they contain iron only in moderate amounts.
• Cooking in iron utensils.

Physiological Functions
• Iron functions mainly in the transport of oxygen to the
tissues (hemoglobin).
• It is also involved in the processes of cellular respiration.
• It is an essential component of hemoglobin, myoglobin,
cytochromes and the respiratory enzyme systems.
• The non-heme iron is completely protein-bound which
exists in the form of storage and transport.
• The non-heme iron is also utilized in the structure of the
xanthine dehydrogenase and the succinate
dehydrogenase and also in the iron and sulphur proteins
of the respiratory chain.

Regulation of Absorption of Iron
• Duodenum and jejunum are the sites of
absorption.
• Iron metabolism is unique because homeostasis is
maintained by regulation at the level of
absorption and NOT by excretion.
– When iron stores in the body are depleted, absorption is
enhanced. When adequate quantity of iron is stored,
absorption is decreased. This is referred to as ‘mucosal
block’ of regulation of absorption of iron.

Intestinal lumen
Intestinal cell
Blood stream

• Iron in the intestinal lumen enters the mucosal cell in the
ferrous state.
• This is bound to transferrin molecule present in brush
border surface of intestinal cell.
• One transferrin molecule can bind with two atoms of iron.
• This is then complexed with a specific receptor.
• This iron-transferrin-receptor is internalised.
• Iron is taken in by the cells, and receptor molecules are
externalised; this cycle is completed within 30 seconds.
• This receptor mediated uptake is more in iron-deficient
state. When iron is in excess, receptors are not produced.
• This is the basis of ‘mucosal block’.www.indiandentalacademy.com

Iron Transport in Blood
• Transport form of iron is transferrin.
• It is a glycoprotein synthesized by liver cells.
• Normal plasma level of transferrin is 250 mg/100 ml.
• In iron deficiency, this level is increased.
• Total iron binding capacity (TIBC) in plasma is 400 µg/100
ml; this is provided by the transferrin.
• Normally one-third of this capacity is saturated with iron.
This protein bound iron (serum iron) is about 120 µg/100 ml.
• In iron deficiency anemia, TIBC is increased (transferrin
level increased); but serum iron level is reduced.

Storage of Iron
• Iron is stored in liver, spleen and bone marrow.
• The storage form of iron is ferritin.
• It is seen in intestinal mucosal cells, liver, spleen
and bone marrow.
• The apo-ferritin can take upto 4,000 iron atoms
per molecule to become ferritin.
• In iron deficiency anemia, ferritin content is
reduced. When iron is given in anemia, the apo-
ferritin production is induced within a few hours.

Iron is Conserved
RBC lysis
Hb Hb – Haptoglobin complex taken
up by liver Kupffer’s cells Iron re-utilized
Globin removed
Heme Heme-Hemopexin complex
taken by hepatocytes
Porphyrin removed Bilirubin
Iron Iron-Transferrin Storage
Iron re-utilized
Iron re-utilizedwww.indiandentalacademy.com

Excretion of Iron
• Iron is a one-way element. That is, very little of it is
excreted.
• The regulation of homeostasis is done at the absorption
level.
• Any type of bleeding will cause loss of iron from the body.
• Menstrual flow is the major cause for loss of iron in
women. Women upto menopause will lose iron at a rate of
about 1 mg/day.
• The loss in male is less than 0.5 mg/day.

• Anemia results when this delicate balance is upset in one
of the three main ways.
1. Increased output
Chronic blood loss
In females – uterine bleeding
In both sexes – bleeding from alimentary tract.
1. Decreased input
Poor diet
Malabsorption
1. Increased body requirement
During rapid growth in child
In pregnancy

Iron Deficiency Anemia
• It is the most common nutritional deficiencynutritional deficiency diseases.
• About 30% of world population are anemic. All over India,
this is about 70%.70%.
• Prevalence rate of anemia is lowest (33%) in Andhra
Pradesh and highest (90%) in Rajasthan.
• 85% of pregnant women suffer from anemia.
• 15% of all maternal deathsmaternal deaths are attributed to anemia.
• Maternal anemia contributes to increase in perinatalperinatal
mortality.mortality.
• The usual Indian diet contains inhibitors of absorptionIndian diet contains inhibitors of absorption.
Hence Indians are more prone to develop iron deficiency
anemia.

Causes
• Hookworm infection
• Nutritional deficiency of iron
• Repeated pregnancy
• Chronic blood loss, e.g. bleeding hemorrhoids,
peptic ulcer, uterine hemorrhage.
• Nephrosis
• Lack of absorption, e.g. subtotal gastrectomy and
achlorhydria.
• In lead toxicity

• Red cell count 3 -4 million/cu.mm.
• Red cells become microcytic, hypochromic.
• Anisocytosis and poikilocytosis of RBCs.
Fairly uniform red cells – size
and shape (mean diameter 7.2 µ)
Definite central pallor – ring staining
Variation in size – anisocytosis
Variation in shape - poikilocytosis
Laboratory findings

Clinical Features
• Anemia results when Hb level is less than 12 g/dlless than 12 g/dl.
• When the level is lower than 10 g/dl body cells lackbody cells lack
oxygenoxygen and the patient becomes uninterested in
surroundings (apathy(apathy).
• Since iron is an important constituent of cytochromes,
their deficiency leads to derangement in internal
respiration and all metabolic processes become sluggishmetabolic processes become sluggish.

• Similar atrophy of the
epithelium in the oral
cavity and oesophagus
causes dysphagiadysphagia called
Plummer-WilsonPlummer-Wilson
syndromesyndrome which is a
known pre-cancerouspre-cancerous
condition.condition.
• Cracks or fissures at the
corner of the mouth, and a
smooth, red painfulsmooth, red painful
tonguetongue with atrophy of
filiform papillae and later
fungiform papillae.

• Koilonychia (spoon
shaped fingernails).
• Very chronic iron
deficiency anemia will
lead to impaired attentionimpaired attention,
irritability, lower memoryirritability, lower memory
and poor scholastic
performance.

Treatment
• Oral iron supplementationOral iron supplementation is the treatment of choice.
• The National Nutritional Anemia Prophylaxis Programme
was initiated in India in 1970.
– 100 mg of iron + 500 µg of folic acid for pregnant women.
– 20 mg of iron + 100 µg of folic acid to children.

FLUORIDES

0.05 – 1.89 mg/m³
Industrial exhaust
Volcanic activity
Suspended soil particles
0.06% - 0.09%
Flourspar CaF2
Flourapaptite Ca10Po4O6F2
Cryolite Na3AlF6
Volcanic rocks
Salt deposits of marine origin
Lakes, wells, river water
0.5 – 1.4 mg/kg
Sea water 0.8 – 1.4 mg/kg

Sources of fluoride
• Total daily intake is in the range of 1.7 – 3.3 mg1.7 – 3.3 mg
for adults.
• Intake of 0.05 – 0.07 mg/kg body weight0.05 – 0.07 mg/kg body weight is
considered optimum.
• 1.5 mg comes from water.
• 0.2 – 1.8 mg comes from dry food.
• Rich sources are: fish, banana, potatoes, jowar, teatea
leaves.leaves.
• Fluoride concentration in human milk ranges from
6 – 12 mg/ml.
• Whether fluoride crosses placental barrier is
debatable.

Gastrointestinal system
Rapid and almost complete absorptionRapid and almost complete absorption.
Passive absorption.
Soluble fluorides (sodium salts) completely absorbed.
100% on empty stomach
75% with a glass of milk
60% with calcium rich breakfast
Fluoride is absorbed as HFFluoride is absorbed as HF
Absorption increased in alkaline mediumAbsorption increased in alkaline medium
Remaining absorption occurs in small intestine
3 mg F as NaF

Plasma
Maximum concentration occurs in 30 – 60 minutesMaximum concentration occurs in 30 – 60 minutes.
Levels start decreasing after 2 hours.
Normal levels achieved in 24 hours which is 4microgram100ml4microgram100ml
Half life is 2 – 9 hours depending upon subject.
F occurs in both ionic and bound formsF occurs in both ionic and bound forms.
Ionic portion levels vary according to F content of water.

99% of F in human body is found in calcified tissues.
Metabolically active bone parts take up more fluoride.
After the period of growth ends the F concentration continues
to rise more slowly than before and tend to reach a
constant level.
Bones

Enamel
Highest on enamel surface compared to interior.
Dentin
Highest concentration at pulpal surface.

Excretion
Chief organ of excretion is the kidney.
High urinary flow and an alkaline urine helps in clearance.
Small amounts are also excreted via faeces and sweat.

FUNCTIONS
• Teeth development
• With vitaminD in tretment of osteoporosis
• Sodium f;ouride is a powerful inb of glycolytic
enzyme enolase
• Resistance to dental caries
• Citric acid cycle-inb of aconitase
activity,responsible for conversion of citrate to
cis-aconitase www.indiandentalacademy.com

Acute toxicity
GIT: nausea,vomiting,abdominal cramps.
Neurological:paresthesia,CNS depression.
CVS:Hypotension,shock,arrythmia.
Certainly lethal dose:32-64mg/kg
Safely tolerated dose:8-16mg/kg
Minimum lethal dose has not been established.

0.7-1.2ppm Lifelong
Prevents dental
caries
1.5-3ppm
5-10 years or
more
Milder forms of
dental fluorosis
3-8ppm
15-20years or
more
Severe form of
dental fluorosis
and milder form
of skeletal
fluorosis
>8ppm
5-10years or more Severe dental and
skeletal fluorosis.
Fluoride levels Time Effects
Chronic toxicity

Dean's Classification Criteria for Dental Fluorosis:
"Very Mild" - "Small opaque, paper white areas scattered irregularly over the tooth
but not involving as much as 25 percent of the tooth surface." (Dean 1942)
"Mild" - "The white opaque areas in the enamel of the teeth are more extensive but
do not involve as much as 50 percent of the tooth." (Dean 1942)
Very Mild/Mild Fluorosis Mild Fluorosis
Chronic toxicity:dental fluorosis

"Moderate" - "All enamel surfaces of the teeth are affected, and the surfaces
subject to attrition show wear. Brown stain is frequently a disfiguring feature.”
(Dean 1942)
“Severe" - "All enamel surfaces are affected and hypoplasia is so marked that the
general form of the tooth may be affected. The major diagnostic sign of this
classification is discrete or confluent pitting. Brown stains are widespread and
teeth often present a corroded-like appearance.” (Dean 1942)
Severe FluorosisModerate Fluorosis

Chronic toxicity:skeletal fluorosis
Osteosclerosis and osteoporosis occurs.
Thickening of cortical bone and
calcification of ligaments and tendons.
Severe pain and stiffness in joints and
spine.Deformities of upper and lower
limbs.
Crippling fluorosis is the most severe
form in which spine becomes rigid and
joints stiffen.

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