Presented on NIN Hyd Training for Trainers of Govt. Officials (Fluorosis )

1. C.Kamaraj
Kamineni hospitals
Skeletal flourosis

2.  The disease fluorosis is caused by an element
known as fluorine, the 13th most abundant
element available in the earth crust.

3. Chemical Properties of Fluorine
 Element of Halogen group with molecular weight
19 and atomic number 9.
 Fluorine is the most electro negative of all
elements
 This fluorine exists as a diatomic molecule with
remarkably low dissociation energy (38 K
cal/mole).
 As a result it is highly reactive and has strong
affinity to combine with other elements to produce
compounds known as Fluoride.

4. Elements that Compose the Human Body
Periodic Table of Elements
Iodine
Chlorine

5. What is Fluorosis
 Fluorosis is a disease caused by
deposition of fluorides in the hard and
soft tissues of the body. It is not merely
caused by excess intake of fluoride but
there are many other attributes and
variables which determine the onset of
fluorosis in human population. It is
usually characterised by discoloration of
teeth and crippling disorders.

6.  Worldwide in distribution
 Endemic in 22 countries
 Asia and in Asia,India and China are
worst affected
 Mexico in North and Argentina in Latin
America
 East and North Africa are also endemic

7. EXTENT OF PROBLEM
International Status
 The following countries have been identified for
the problem of fluorosis:
 Pakistan, Bangladesh,
Argentina, United States of America,
Morocco, Middle East countries,
Japan, South African Countries,
New Zealand, Thailand etc.

8. In India
The problem has reached alarming proportions
affecting at least 17 states of India:
 50-100% districts are affected - Andhra Pradesh,
Tamil Nadu, Uttar Pradesh, Gujarat, Rajasthan
 30-50% districts are affected - Bihar, Haryana,
Karnataka, Maharashtra, Madhya Pradesh,
Punjab,Orissa, West Bengal
 < 30 % districts are affected - J & K, Delhi, Kerala

10. SOURCES OF FLUORIDE
Sources of fluoride in environment
 Usually the surface water is not contaminated
with high fluoride, whereas ground water may be
contaminated with high fluoride because the
usual source of fluoride is fluoride rich rocks.
When water percolates through rocks it leaches
out the fluoride from these rocks.
 The rocks rich in fluoride are:
Flurospar- CaF2 (Sedimentary rocks, lime
stones, sand stones);
Cryolite- Na3AlFPO6 (Igneous, Granite);
Fluorapatite- Ca3 (PO)2 Ca (FCl)2

11. Sources of fluoride for human
exposure
Main sources of fluoride for human are
 Water: most assimilable form of fluoride and
hence the most toxic
 Food: from soil and water
 Air: occupational exposurefrom industries
 Medicament: Na flouride, niflumic acid, dental
products
 Cosmetic etc.

12. CHEMOBIOKINETICS AND
METABOLISM
 Ingested fluoride is rapidly absorbed through
gastrointestinal tract and lungs. The peaks are
reached after 30 min in blood.
 The rapid excretion takes place through renal system
over a period of 4 to 6 h.
 In children less than three years of age only about
50% of total absorbed amount is excreted
 Adults and children over 3 years - about 90% is
excreted.
 Approximately 90% of the fluoride retained in the
body is deposited in the skeleton and teeth
 The biological half-life of bound fluoride is several
years.
 Fluoride also passes through the placenta and also
appears in low concentrations in saliva, sweat, and

13. biochemical changes
 . Fluoride is rapidly absorbed into serum. carried
to the bone, replace hydroxyl in the bone
hydroxyapatite, creating fluoroapatite. Mainly in
trabecular bone increasing it’s density.
 The fluoride also stimulates the formation of new
irregular bone at the sites of tendon and ligament
insertions, resulting in gradual ossification of soft
tissues.
 Sclerotic type in high calcium intake and porotic
type in low calcium intake

14.  Primarily it is Fluoride which is present in drinking
water
 when F in water is more than 1.5 mg per litre,it is toxic
to health
 pH in terms of alkalinity of water promotes the
absorption of F
 calcium in the diet reduces the absorption of F
 Hard water rich in Calcium reduces the F toxxicity
 Fresh Fruits and Vit.C reduces the effect of F
 Trace elements like Molubdenum enhances the
effect of F
AGENT FACTORS

15.  In School going children seen as dental fluorosis.
 In third and fourth decade of life seen as Skeletal
Fluorosis.
 Males suffer more than females.
 Migration influences the occurrence depending
on which way people migrate.
 Illitrates suffer more frequently in the fluorotic
belts.
 Where aluminium ores are mined,it is seen as
occupational health hazard.
Host Factors

16.  High Annual Mean Temperature
 Low Rainfall
 Low humidity
 F rich Natural subsoil rocks
 Vegetables from high F belts
 Fluoridated tooth paste particularly when
used by children
 Tropical climate
 Developing Countries
Environmental Factors

17. FACTORS INFLUENCING THE
ONSET OF THE DISEASE
 Concentration of fluoride in drinking water, food,
cosmetics etc
 low calcium and high alkalinity of drinking water
 age of the individual
 duration of intake
 pregnancy
 lactating mother
 derangement in hormonal profile
calcitonin, parathormone, vitamin D and
cortisol

18. Other factors
 other trace elements in the water
 dietary intake of fluoride
 nutritional status
 water storage methods
 work patterns
 tea-drinking habits

19. Endemic flourosis
Endemic skeletal flourosis is a
chronic metabolic bone disease
caused by ingestion of large
amounts of fluoride through either
water or food in geographic areas
where high levels of fluoride occur
naturally.

20. Endemic flourosis
When more than one-fifth ( 20 % ) of
the persons surveyed in a known high
fluoride area shows positivity of the
clinical tests, it indicates the
endemicity

21. Tests for Skeletal Fluorosis Affection of the joints can be ascertained through
simple tests which can be carried out at the bed-head
side and in the field:
 COIN TEST: The subject is asked to lift a coin from the
floor without bending the knee. A fluorotic subject
would not be able to lift the coin without flexing the
large joints of lower extremity.
 CHIN TEST: The subject is asked to touch the anterior
wall of the chest with the chin. If there is pain or
stiffness in the neck,it indicates the presence of
fluorosis.
 STRETCH TEST: The individual is made to stretch the
arm sideways,fold at elbow and touch the back of the
head. When there is pain and stiffness, it would not be
possible to reach to the occiput indicating presence of
flourosis

22. Clinical Picture of Endemic Fluorosis
 Dental Fluorosis in Children
 Skeletal Fluorosis in Adults
 Non Skeletal Fluorosis

23. NON SKELETAL
MANIFESTATIONS
Neurological manifestation
 Nervousness & Depression
 Tingling sensation in fingers and toes
 Excessive thirst
 Polydypsia and polyurea

24. Muscular manifestations
 Muscle Weakness & stiffness
 Pain in the muscle and loss of muscle power

25. Urinary tract manifestations
 Urine may be much less in volume
 Yellow red in colour

26. Allergic manifestation
 Very painful skin rashes, which are perivascular
inflammation. Prevalent in women and children.
 Pinkish red or bluish red spot, round or oval
shape on the skin that fade and clear up within 7-
10 days.

27. Gastro - intestinal problems
 Acute abdominal pain
 Diarrohea
 Constipation
 Blood in Stool
 Bloated feeling (distention)
 Tenderness in Stomach
 Feeling of nausea
 Mouth sores

28. Red Blood cells
 Fluoride is ingested accumulates on the
erythrocyte membrane, Which looses calcium
content. This change causes formation of
echinocytes.
 The life span of these echinocytes is less than
the normal life span of RBC, and hence early
destruction of the RBCs in form of ecchynocytes
causes anemia.

29. Ligaments and Blood Vessel
Calcification
 A unique feature of the disease is soft tissues like
ligaments, blood vessels tend to harden and
calcify and the blood vessels will be blocked.

30. Fluoride and mental efficiency
 Excessive fluoride intake since early childhood
would reduce mental work capacity (MWC) and
hair zinc content
 Excessive fluoride intake decreased 5-hydroxy
indole acetic acid and increased norepinephrine
in rat brain

31. Clinical symptoms
 The initial symptoms usually were headache and
vague pains, arthralgia, backache, rigidity weakness.
 These were followed by multiple joint pains, mostly in
the feet, knees, and back.
 Spinal stiffness and kyphosis developed in a few
patients.
 Constipation
 Limitation of joint movement. Inability to close the fist
 Difficulty in walking
 Flexion of spine
 Neurological complications
 Bones subjected to stress are more likely to be
involved

32. Symptom
Lowerbackpain (72)
Leg pain (72)
Arm pain (42)
Hand tingling (37)
Loss of appetite (21)
Neck pain (30)
Joint dysfunction (51)
Joint deformity (29)

33. CLINICAL PRESENTATION
 · Heel pain
 · Painful and restricted joint movements
 · Deformities in Limbs
 · Hunch back
 IN EXTREME CASES
 · Paralysis,
 · Mucular wasting,
 · Premature ageing

34. SKELETAL FLUOROSIS

36. Radiographic appearance
 Spine
 Chest
 Pelvis
 Forearm
 Knees
 elbow

37. RADIOLOGICAL PRESENTATIONS
 · Osteosclerosis
 · Periosteal bone formation
 · Calcification of interosseous membrane,
ligaments, capsules, muscular attachments,
tendons.
 · Exostoses
 · Osteophytosis
 · Associated metabolic bone disease

38. Radiographic features
 Osteosclerosis (43%) –adequate ca intake- 15 to 20 yrs
exposure
 Osteopenia (40%)—inadequate ca intake-sec
hyperparathyroidism
 oseeoporotic (28%) in young adults
 osteomalacic (23%) in children
 Intermittant g rowth lines (70%)
 Diaphysealwidening (28%)
 Soft tissue calcification/ossifications (89%)
 ligaments
 tendons
 interossoeus membrane

39. Radiographic appearance
Mild osteosclerosis-sand or
granular type
Severe osteosclerosis-
coarse type

40. Prominent trabecular
thickening is seen
In radius, ulna, and
carpus.

41. dense
white
ivory like
bone
Calcificat
ion and
ossificati
on in
ligament
s

42.  Diffuse osteopenia
 Thinned trabeculae
and cortex
 Growth lines

43.  Osteopenia
 Sparse thick
trabeculae along lines
of stress
 Thinned out cortex
 Growth lines
 Calcification and
ossification at muscle
and tendon
attachment

44. osteomalacic
pattern
decreased bone
density, blurring of
trabeculae, thinning of
cortices, genu
valgum , growth
lines

45. osteomalacic pattern
Diffuse increased
density
Prominent kyphosis,
biconcave
deformities, blurred
trabecuiae, and
diffuse calcification
and ossification
of spinal ligaments.

46.  soft-tissue
ossification
Calcification and
ossification
involve attachments
of Interosseous
membranes between
radius and ulna
Cortices of radius and
ulna
are thickened.

47.  Intermittent growth
lines (arrows)
involve distal parts
of femora and
proximal parts of
tibiae.

48. Bone widening due to
skeletal fluorosis.
Diameter of ulna is
increased owing to
cortical
thickening. Overall
bone density is also
increased

49. Bone widening and
cortical thinning due
to skeletal fluorosis.
Diaphyseal
Trabeculae are sparse,
thick, and
disorganized,

56. CLINICAL CASES

58. DEFORMITY
SINGLE - APICAL MULTI - APICAL

59. MECHANICAL AXIS

60. ANATOMIC AXIS

61. DEFORMITY TRACING

62. PRE-OP PLANING

63. POST - OP POST - OP

65. PRE - OP POST - OP

77. TECHNIQUES AVAILABLE FOR
FLUORIDE REMOVAL
 Nalgondatechnique (Coagulation-precipation)
 Adsorption
 Ion –exchange
 Membrane process

78. PREVENTION