Dantal College Devang (Vol-5) - Ahmedabad Dental … Journal - Vol.2,Issue No. 2...Malodor and periodontitis: casual or causal? DEPARTMENT OF PERIODONTICS AND ORAL IMPLANTOLOGY, AHMEDABAD

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The journal is indexed with ‘Indian Science Abstract’ (ISA)(Published by National Science Library), www.ebscohost.com, www.indianjournals.com

The journal is printed on ACID FREE paper.

JADCH is available (full text) online:Website- www.adc.org.in/html/viewJournal.php

This journal is an official publication of Ahmedabad Dental Collegeand Hospital, published bi-annually in the month of March andSeptember.

ISSN 0976-2256E-ISSN:2249-6653

A

Pediatric dentistry provides primary care and comprehensive dental speciality treatments for infants, children, adolescents and individuals with special health care needs.

The successful practice of pediatric dentistry is nit merely the completion of any operative procedure but also ensuring a positive dental outcome for the future oral health behaviour of the individual and their family. To this end, an understanding of child development- physical, cognitive and psychosocial - is paramount. Traditionally, dental caries has been regarded as a static phenomenon, eventulation in loss of tooth structure while the basis for treatment and management of this ubiquitious disease has essentially been mechanical. However, with current developments in new dental materials, techniques and preventive strategies, a more precise understanding and appreciation of the nature of the caries process is obtained. The newer concept of using micro-invasive resin infiltrants in enamel and early dentine lesion is promoted. There have been advances in four key areas related to pediatric dentistry ;(1) caries detection tools, (2) early interventions to arrest disease progression, (3) caries risk assesement tools, (4) trends in pediatric procedures and dental materials. It is the only specialization in dentistry that is age defined and not specific to any treatment modality. Hence, with the adoption of newer material and techniques working on a child becomes one of the most satisfying experience in all dental practice.

Editor - in - ChiefDr. Darshana Shah

Co - EditorDr. Rupal Vaidya

Editorial Board:Dr. Mihir ShahDr. Vijay BhaskarDr. Monali ChalishazarDr. A. R. ChaudharyDr. Neha VyasDr. Sonali MahadeviaDr. Shraddha ChokshiDr. Bhavin DudhiaDr. M GaneshDr. Mahadev DesaiDr. Darshit DalalDr. Harsh Shah

JADCH

EDITORIAL

FROM THE EDITOR'S DESK .....................................................................................................................................................01

DARSHANA SHAH

REVIEW ARTICLES

1) MALODOR AND PERIODONTITIS: CASUAL OR CAUSAL? ........................................................................................02

SHILPI SHAH*, TEJAL SHETH**, MIHIR SHAH***, SANDIP LADANI****, PRAGNESH SOLANKI*****

ORIGINAL ARTICLES

2) DENTAL FLUOROSIS – A RETROSPECTIVE STUDY IN GANDHINAGAR DISTRICT.................................................10

PURV PATEL*, BHAVIN DUDHIA**, A. R. CHAUDHARY***, PARUL BHATIA****, YESHA JANI*****,

PURVA BUTALA******

3) KNOWLEDGE, ATTITUDE AND PRACTICE REGARDING ORAL CANCER AND SCREENING PROCEDURES

AMONG PRIMARY HEALTH CARE AND COMMUNITY HEALTHCARE WORKERS OF WAGHODIA, GUJARAT.......20

BAFNA HARSHAL P *, AJITHKRISHNAN CG**, KALANTHARAKATH THANVEER***, RICKY PAL SING*,

HEMAL PATEL****

4) EVALUATION OF SHEAR BOND STRENGTH USING THREE DIFFERENT TYPES OF ADHESIVE PRIMERS

UNDER NON-CONTAMINATED AND CONTAMINATED CONDITIONS – AN IN VITRO STUDY..................................26

NIRAV M. PATEL*, C.R. NAIK**, RAVI GUPTA***

5) AN IN-VIVO EVALUATION OF THE EFFECT OF CHEWING CORIANDER SEEDS ON SALIVARY PH. .....................31

RICKY PAL S *, AJITHKRISHNAN CG **, THANVEER K***, HARSHAL B*, HEMAL P****

CASE REPORT

6) GIANT CELL FIBROMA...................................................................................................................................................35

MANISH LIMBACHIYA*, BRIJESH PATEL*, MINAL BAKSHI*, RINA DAVE*

7) DIRECTING THE FORCE VECTOR DIRECTLY: USE OF MICRO-IMPLANTS FOR CORRECTION OF

GUMMY SMILES.............................................................................................................................................................38

HARESH AHIR*, SONALI MAHADEVIA**, KRISHNAMURTHY***, TOSHIF KUMAR****, RINKALKUMAR SHAH*****

8) ROOT PIECES ON DENTAL RADIOGRAPHS: INCIDENTAL FINDINGS WITH DIFFERENTIAL DIAGNOSIS.............43

DINESH TRIVEDI*, BHAVIN DUDHIA**, RUTU JANI***, YESHA JANI****, SANYAL SHAH*****

9) PLEOMORPHIC ADENOMA ...........................................................................................................................................48

NEHA VYAS*, SACHIN DALAL**, SAURABH JAIN***, MEGHA VYAS****

ContentsContents

JADCH

Subscription:Rate per issue: Rs. 400/-, for one year: Rs. 750/-, for three years: Rs. 2,000/-Contact: Ahmedabad Dental College & Hospital Vivekanand Society, Bhadaj-Ranchhod Pura Road, Santej, Post: Rancharda, Ta: Kalol, Dist: Gandhinagar, Gujarat, India.

B

Dear friends,

The current method of dental and medical training is dependent on professors, Obsolete Text books and opinion of the seniors who are often dogmatic and unresponsiveto new ideas.

such a method is insufficient to carry on lifelong clinical practice in a very comptent manner.

the younger doctors are computer savvy, inquisitive and want to know more. We in india are known for hardwork, logical reasoning and cultural strengths.

We have to incorporate this evidence based education into our mainstream dental education if we are going to maintain and provide the personnel for the whole global village.

the critical feature of "Evidence-Based Dentistry is that dentists, when faced with any problem in the clinical context of a patient, should be able to: perform a literature search; identify the evidence available pertaining tio the clinical condition; critically evaluate it and determine the "Best evidence" to diagnose /treat/manage the patient.

The crux of the matter in this cycle is the ability of the dentist to search and retrieve the literature in the shortest possible time in an efficient manner and apply it in practice

in the "global scenario", the term EBD became more widely used in the early 1990s, and was later formally defined by Sackett in 1996.

The first National Workshop on Evidence-Base Dentistry in India was held at College of Dental Sciences, Davangere between the 8th and 11th March 2001.

With over 85 delegates registered from all over India, it was perhaps the largest ever dedicated workshop on evidence-based dentistry in the world.

This is the beacon of what th e future holds for Evidence based dentistry in India.

1The Journal of Ahmedabad Dental College and Hospital; 5 (1), March 2014 - August 2014

Dr. Darshana ShahEditor JADCHEditorial Office:Prof. & Head Dept. of ProsthodonticsAhmedabad Dental College & Hospital,Dist.: Gandhinagar, Gujarat.Email: [email protected]

Malodor and periodontitis: casual or causal?

DEPARTMENT OF PERIODONTICS AND ORAL IMPLANTOLOGY, AHMEDABAD DENTAL COLLEGE AND HOSPITAL, GANDHINAGAR, GUJARAT, INDIA.

The Journal of Ahmedabad Dental College and Hospital; 5 (1), March 2014 - August 2014 2

Review Article

* Reader, ** Senior Lecturer, ***Professor and Head, ****Senior Lecturer, *****Tutor

INTRODUCTION:

Halitosis is a medical term first coined by Listerine

Company in 1921, used to describe “unpleasant,

offensive, stale or foul smelling breath emitted from

the mouth regardless of whether the odorous

substances in the breath originate from oral or extra-

oral sources.”

This condition is commonly responsible for social

embarrassment, emotional and psychological

distress leading to a lack of self-esteem, self-image

and self-confidence. Furthermore it may signal the

presence of disease.

Oral halitosis or oral malodor is the term, especially

used to describe bad breath with an origin within the

oral cavity. In fact most adult subjects have socially

unacceptable bad breath when waking up in the

morning. This problem is transitory and attributed

to physiologic causes such as reduced salivary flow

during sleep. Although these transitory problems

are easily controlled, persistent bad breath may be

indicative of either oral disease (i.e. Periodontal

disease, the presence of bacterial reservoir in

SHILPI SHAH*, TEJAL SHETH**, MIHIR SHAH***, SANDIP LADANI****, PRAGNESH SOLANKI*****

ABSTRACT

Halitosis can be a crippling social problem.However, in the last 5 to 6 years, it has come to the forefront of public and dental professional awareness.The mouth is home to hundreds of bacterial species that produce several fetid substances as a result of protein degradation. Volatile sulfur compound (VSC)-producing bacteriacolonizing the lingual dorsum, gingival pockets, and tonsillar crypts have recently been implicated in the generation of halitosis. Understanding causes, assessment, and treatment of oral malodor can help dental professionals find ways to decrease its prevalence and increase their patients' well-being.This article reviews the etiology and various connections among periodontal pathogenic microorganisms, periodontal disease and oral malodor from a periodontal perspective.

Keywords: halitosis, volatile sulphur compounds, gingivitis, periodontitis, role of microflora in malodor, co-relation between halitosis and periodontitis

Received: 02-12-2013; Review Completed: 15-02-2014; Accepted: 26-02-2014

mouth) or indicative of systemic disease (i.e. Hiatus

hernia, hepatic cirrhosis, renal failure, diabetes

mellitus etc.).

ETIOLOGY

The etiology of oral malodor is multifactorial. In the

presence of adequate substrate with appropriate

conditions, a sequence of events leads to the release

into the oral cavity of pungent gases that pollute

exhaled air and are perceived as bad breath.

Research has identified several microorganisms

that produce these offensive odors and provided a

fair explanation of the conditions necessary for their

production. In addition to the presence of certain

types of bacteria, the type and amount of substrate,

and oxygen and pHlevels influence the occurrence

and severity of oral malodor.

Certain chemical end-products of bacterial

putrefaction known as volatile sulfur compounds

(VSCs) are foul smelling and have been found to be 1-4

the primary culprit of engendering oral malodor.

Nonsulfur-containing compounds such as

cadaverine, putrescine, indole and skatole5,6 have

ADDRESS FOR AUTHOR CORROSPONDENCE : DR. SHILPI SHAH, Tel: +91 9374407773

also been implicated in the foul smell of oral

malodor, but their contribution is thought to be

limited.7 VSCs such as hydrogen sulfide, methyl

mercaptan and dimethyl disulfide make up more

than 90 percent of the putrid odors from the mouth.8

Two of these VSCs, hydrogen sulfide and methyl

mercaptan, account for approximately 90 percent of

the total VSCs identified with putrid odors from the 9mouth.

Source of VSC production in periodontitis

patientsAnaerobic bacteria, oxygen depletion, alkaline pH

and sulfur-containing substrates are some of the

requirements for oral malodor to occur .The

bacteria that produce these VSCs can be found by

evaluating biofilm and scraped specimens from the

lingual dorsum, gingival pockets, and tonsillar

crypts.7 (fig. 1)VSCs are produced by gram-

negative anaerobic bacteria that live on the lingual

dorsum.8 These bacteria can thrive on the tongue

because food debris accumulates rapidly on the

tongue's large surface area and papillae.Periodontal

pathogens have been positively correlated with oral

malodor.1-4,10 Several periodontal pathogens

i n c l u d i n g T r e p o n e m a d e n t i c o l a ,

Porphymonasgingivalis and Bacteroidesforsythus

have been identified, with BANA hydrolysis, on the

posterior tongue, contributing to oral malodor.11

Additional periodontal pathogens, including

F u s o b a c t e r i u m n u c l e a t u m a n d

Bacteroidesmelanogenicus have been identified as

VSC formers.8 These microorganisms produce

copious amounts of hydrogen sulfide, methyl

mercaptan and dimethyl disulfide.However, other

compounds in mouth air may also be offensive such

as diamines (e.g. Putrescine, cadaverine), indole,

skatole and butyric or propionic acid. Most of these

compounds results from proteolytic degradation by

oral microorganisms of peptides present in saliva,

shed epithelium, food debris, gingival crevicular

fluid, interdental plaque, post-nasal drip and blood.Breath malodor, a significant social and/or

psychological handicap, may be caused by several

intra- and extraoral factors.

Intraoral causes:1. Tongue coating ( primary source of malodor)2. Dentition

a. Carious lesionb. Food impactionc. Extraction wounds filled with blood clots

3. Periodontal infections like Pockets, ANUG,

Purulent discharge from gums4. Xerostomia

Extra oral Causes:Halitosis of the upper respiratory tract: Chronic

sinusitis, Nasal obstruction, nasopharyngeal

abscess, Carcinoma of larynxHalitosis of the lower respiratory tract:

Bronchitis, Bronchiectasis, Pneumonia, Carcinoma

of the lungsCauses of blood borne halitosis:Systemic diseases: Hepatic failure/ Liver cirrhosis,

U r e a m i a / K i d n e y f a i l u r e , D i a b e t i c

ketoacidosis/Diabetes mellitusM e t a b o l i c d i s o r d e r s : I s o l a t e d

PersistantHypermethioninemia, Fish odor

syndrome, Medication: Disulfiram, Dimethyl sulphoxide,

Cysteamine, Food: garlic, onion, alcohol, tobacco

ASSOCIATION BETWEEN HALITOSIS AND

PERIODONTAL DISEASE

Periodontal disease result from the combination of

many factors present in vivo. These processes

include chronic activation of immune system,

alteration in connective tissue metabolism

production of proteinases and cytokines, direct

destruction of host tissue by bacterial enzymes, and

virulence factors and a multitude of other

mechanisms. One of these volatile sulfur

compounds (VSCs) not only be associated with oral

3

SHILPI SHAH Malodor and periodontitis: casual or causal? et. al. :

The Journal of Ahmedabad Dental College and Hospital; 5 (1), March 2014 - August 2014

malodor but probably contribute to the etiology of

both gingivitis and periodontitis. Different lines of

evidence have demonstrated this association

between halitosis and periodontal disease.

An increase in production of VSCs from

periodontal pockets provides a plausible

explanation for the intensification of oral malodor

observed in pa t ients wi th per iodonta l

disease.Several studies suggest that periodontitis

increases the severity of oral malodor.7One

possible explanation is the increased amount of

substrate available to be metabolized. In patients

with periodontitis, more sulfur-containing protein

substrate is available through increased exfoliation

of epithelial cells and crevicular effusion of

leukocytes.Yaegaki and Sanada found that bleeding

on probing and periodontal pocket depth positively

correlated with the production of VSCs.4

In contrast to the view that periodontal disease

contributes to oral malodor, Bosy and colleagues

found that oral hygiene levels and not periodontal

pockets were more indicat ive of ora l

malodor,11which supports the concept that oral

malodor may be an independent entity.

Certainly, some gram-negative anaerobic bacteria,

which are not known to be periodontal pathogens

( F u s o b a c t e r i u m p o l y m o r p h u m ,

Veillonellaalcalescens, Bacteroidesfundiliformis

and Klebsiellapneumoniae) have been identified

with oral malodor.12,13 The bacteria contributing

to oral malodor in healthy individuals are most

commonly located on the posterior dorsal tongue

surface as opposed to in periodontal locations.6

As currently understood, periodontal disease

progression consists of a shift in the bacterial plaque

from a gram-positive aerobic flora to a gram-

negative anaerobic and motile flora. Some studies

suggest that the production of VSCs by these

microorganisms may contribute to the progression

of periodontal disease via breakdown of the oral

mucosa leading to bacterial invasion.

This finding suggests that the VSCs of oral malodor

could contribute in the pathogenesis of

periodontitis.

T R A N S I T I O N F R O M H E A LT H T O

GINGIVITIS:-

Gingivitis is characterized by an immune response

to antigens in bacterial plaque as well as by

alteration in connective tissue(Fig 2).One of the

earliest events associated with disease is enhanced

permeability of the lining epithelium with the

gingival sulcus. VSCs are potentially capable of

altering permeability of the gingival tissues,

including inflammatory response and modulating

functions of gingival fibroblast. Rizzo (1970)

indicated that a facilitating agent is required to

allow lipolysaccharides (LPS) to penetrate healthy

gingival epithelium and subsequently initiate an

inflammatory response.14 Studies demonstrated

that thiol participate in early stages of the

inflammatory response and may be important

initiator of gingivitis. Gingivitis results from the

induction of an immune response and may be

accompanied by alteration in fibroblast function.

Methyl mercaptan (CH SH) has been shown to 3

induce secretion of interleukin-1β (IL-1β) from

mononuclear cells. Methyl mercaptan has also been

shown to act synergistically with both LPS and IL-

1β to increase secretion of prostaglandin E and 2

collagenase, important mediators of inflammation 15and tissue destruction.

VSCs have direct effect on the formation of

extracellular matrix by human gingival fibroblast.

In addition they lower total protein production by

4



these cells.

The effect of methyl mercaptan (CH SH) on 3

collagen metabolism is a reflection of both

decreased synthesis and increased degradation of

protein. This increased degradation is likely to be

associated with inhibition of procollagen peptidase

enzymes which are essential for procollagen

processing and for cross linking to form mature

collagen fibrils.

TRANSITION FROM GINGIVITIS TO

PERIODONTITIS:In the change from gingivitis to periodontitis, there

is a continuation of all the events in the oral

malodor and gingivitis section as well as a new

group of events that occur in the development of

periodontitis (Fig.2). Periodontitis results from

destruction of both the soft and hard tissue

structures which support teeth. The transition from

gingivitis to periodontitis is mainly an anatomical

difference in which the disease progresses into the

underlying bone.Since the periodontal ligament

cells are associated with the formation and

maintenance of the mineralized supporting

structures, effects of thiols on these ligament cells

are particularly relevant. Increase in probing

pocket depth and bleeding on probing with increase

in methyl mercaptan in these pocket are also

relevant. The effects resulting from exposure to

CH3SH become increasingly important in

periodontitis.1

Yaegaki&Sanada showed a correlation between

increases in CH SH/H S concentration ratio and 3 2

10increases in periodontal pocket depth.

Studies have shown that PDL cells exposed to

methyl mercaptan (CH3SH) alter their intracellular

pHand become more acidic. In addition, they

exhibit decreased motility, lowered protein

synthesis, and alteration in collagen metabolism.

These changes are predominantly determined to the

ability of these cells to maintain or regenerate

mineralized tissues. In addition there is substantial

reduction in amount of type III collagens.16 This

observation is significant since periodontally

involved tissue are known to exhibit substantial

losses of type III collagens which decrease from 20-

30% to 4% of total collagen.17 Fibronectin in PDL

cell are also affected by VSCs.

Severity of Periodontitis

In periodontitis, different studies have shown a

correlation between VSC concentration in mouth 3,6,10air and increased pocket depth. However De

Boever (1996) found that tongue odor was

negatively correlated with probing depth

suggesting an inverse relationship between malodor

and periodontal parameters.2 Similarly Bosy et al.

(1994) did not find a relationship between

periodontal disease and the prevalence or severity 11

of halitosis.

Correlation between the presence of a

p a t h o g e n i c m i c r o f l o r a i n t h e

subgingivalmicrobiota & Halitosis

In 1994,Bosy et al.founda moderately strong

correlation between the BANA (Benzoyl- DL-

arginine-2-Napthylamide) scores with floss odor

based on trypsin like activity detected by the BANA

test . They also found that 87.5% of tooth sites were

BANA positive as compared with 74.5% of tooth 11

sites positive in healthy individuals.

A significant correlation has been found between

the presence of motile organisms and P.

intermediaon the tongue dorsum in individual with

periodontitis as opposed to periodontally-healthy

subjects. This indicates that the tongue may act as a

reservoir for some periodontopathogens that

contribute to oral malodor.



Tonzetichfound the pathogenic, proteolytic strains

of Bacteroidesmelanogenicus produced more VSCs

t h a n n o n - p r o t e o l y t i c

s t r a i n s . 1 8 T r e p o n o m a d e n t i c o l a ,

P o r p h y r o m o n a s g i n g i v a l i s ,

Porphyromonasendodontalis, Prevotellaintermedia

and Bacteroidesloescheii produced significantly

higher amount of sulfides than other bacteria.19

Other bacterial species recovered from periodontal

pocke t s such a s En t e robac t e r i a eceae ,

Bacteroidesforsythus, Centipedaperiodontii,

E i k e n e l l a c o r r o d e n s ,

Fusobacteriumperiodonticumetc. also had high

capability to generate VSCs in vitro19, 20.

FUTURE PERSPECTIVE:VSC in periodontal pockets might be used as a

predictor of periodontal disease. Many authors have

proposed to utilize hydrogen sulfide, one of

causative periodontal pathogens' products as an

indicator for disease severity. The value of this

hypothesis remains to be elucidated. It is also

interesting to determine the degree of contribution

by pocket VSC to whole mouth odor. For this study,

we have to measure VSC level in periodontal

pockets quantitatively. Then multifactor analysis

including pocket VSC level and odor level of the

tongue and the other parts of oral cavity will provide

us useful information in management of patients

with oral malodor.

CONCLUSION:An estimated 80 percent to 90 percent of all bad

breath odors originate from the mouth and are

caused by bacteria. The accumulation of plaque and

debris and the stagnation of saliva occur most

commonly in areas where tooth and tissue

crevices,posterior dorsum tongue, interdental

spaces and subgingival areas lend themselves to

stagnant microenvironments.

Although oral malodor is probably not caused by

periodontal disease; there is ample evidence to

suggest that periodontal disease increases the

severity of oral malodor. Periodontitis worsens the

severity of oral malodor by providing additional

sites of VSC production (interdental and

subgingival), an increased availability of sulfur-

containing substrate (exfoliated epithelial cells and

leukocytes) and an increased rate of methionine

metabolism (precursor to methyl mercaptan).

Periodontitis contributes to an increased tongue

coating with higher VSC production. There is

evidence to suggest that VSCs, i.e., oral malodor,

may contribute to the progression and pathogenesis

of periodontal disease via increased mucosal

permeability.

This article outlines the efficacy of volatile sulphur

compounds in causing malodor and showing the

casual and causal association among periodontal

pathogenic microorganisms, periodontal disease

and oral malodor which has been strongly

implicated but not proved.

ACKNOWLEDGEMENT: NILCONFLICT OF INTEREST: NIL

6



Fig 1. Production of volatile sulfur compounds (VSCs)

7



REFERENCES

1. Coil JM and Tonzetich J, Characterization of

volatile sulphur compounds production at

individual gingival crevicular sites in humans. J

Clin Dent 3(4):97-103, 1992.

2. De Boever EH, De Uzeda M and Loesche WJ,

Relationship between volatile sulfur compounds,

BANA-hydrolyzing bacteria and gingival health in

patients with and without complaints of oral

malodor. J Clin Dent 4(4):114-9, 1994.

3. Miyazaki H, Sakao S et al, Correlation between

8



volatile sulphur compounds and certain oral health

measurements in the general population.

JPeriodontol 66(8):679-84, 1995.

4. Yaegaki K and Sanada K, Volatile sulfur

compounds in mouth air from clinically healthy

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5. Goldberg S, Kozlovsky A et al, Cadaverine a

putative component of oral malodor. J Dent Res

73(6):1168-72, 1994.

6. Rosenberg M, Clinical assessment of bad

breath: current concepts. J Am Dent Assoc,

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7. Tonzetich J. Production and origin of oral

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8. McNamara TF, Alexander JF and Lee M, The

role of microorganisms in the production of oral

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10. Yaegaki K and Sanada K, Biochemical and

clinical factors influencing oral malodor in

periodontal patients. J Periodontol 63(9):783-9,

1992.

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oral malodor to periodontitis: evidence of

independence in discrete subpopulations. J

Periodontol 65(1):37-46, 1994

12. McNamara TF, Alexander JF and Lee M, The

role of microorganisms in the production of oral

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8, 1972.

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Instrumental evaluation of odor produced by

specific oral microorganisms. J SocCosmetChem

30:241-7, 1979.

14. Rizzo A. Histologic and immunologic

evaluation of antigen penetration into oral tissues

after topical application. J Periodontol 1970;

41:210-212.

15. Ratkay LG, Waterfeild JD, Tonzetich J.

Stimulation of enzyme and cytokine production

by methyl mercaptan in human gingival fibroblast

and monocyte cell culture. Arch Oral Biol

1995;40:337-344.

16. Lancero H, Niu JJ, Johnson PW. Exposure of

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reduces intracellular pH and inhibits cell migration.

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17. Narayanan AS, Page RC. Biochemical

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18. Tonzetich J and McBride BC, Characterization

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19. Persson S, Edlund MB, Claesson R, Carlsson J.

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MicrobiolImmunol 1990; 5: 195-201.

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H, Rosenberg M. Isolation of Enterobacteriaecea

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9



DENTAL FLUOROSIS – A RETROSPECTIVE STUDY IN GANDHINAGAR DISTRICT

PURV PATEL*, BHAVIN DUDHIA**, A. R. CHAUDHARY***, PARUL BHATIA****, YESHA JANI*****, PURVA BUTALA******

ADDRESS FOR AUTHOR CORROSPONDENCE : DR. , PHONE: 94272 19470PURV PATEL

10

Original Article

AHMEDABAD DENTAL COLLEGE & HOSPITAL, BHADAJ-RANCHHODPURA ROAD, TA:- KALOL DIST:-GANDHINAGAR.

*SENIOR LECTURER, ** PROFESSOR & HEAD, ***PROFESSOR, ****PROFESSSOR, *****SENIOR LECTURER, ******SENIOR LECTURER

ORAL MEDICINE, DIAGNOSIS & RADIOLOGY DEPARTMENT, AHMEDABAD DENTAL COLLEGE & HOSPITAL, GUJARAT.

ABSTRACT

IntroductionDental Fluorosis is an irreversible but preventable disease commonly caused by excessive intake of fluoride during critical period of teeth development. Dental fluorosis is endemic in many areas of Indian subcontinent including many districts in the North Central part of Gujarat state.

Aims & ObjectivesThe study was undertaken to correlate the severity of dental fluorosis with variables like age, gender, drinking water fluoride levels and dental caries.

Materials & MethodsA total of 53 patients (30 males and 23 females) affected with dental fluorosis were selected for the study. The subjects were assessed for their age range, severity of the dental fluorosis (based on Dean's Fluorosis Index) and their drinking water fluoride levels (determined by Ion Selective Electrode method). The subjects were also assessed for their dental caries prevalence using the DMFT index.

ResultsMajority of the subjects belonged to third and fourth decades of life followed by the second decade. The highest number of subjects manifested moderate degree of dental fluorosis followed by severe degree and mild degrees respectively. There was a positive correlation of the severity of dental fluorosis with the level of fluoride in the drinking water as well as the DMFT index of the subjects.

ConclusionA dentist often plays a prime role in detection of dental fluorosis, and hence in identification of the areas with higher water fluoride levels. This necessitates the dentists to be familiar with the clinical presentation of dental fluorosis as well as with areas affected by endemic dental fluorosis.Received: 08-10-2013; Review Completed: 12-12-2013; Accepted: 15-01-2014

INTRODUCTION

Fluorosis is described as a state of toxicity of

the trace element called fluorine within an [1]

organism. In 1901, Dr. Frederick McKay of

Colorado (USA) accidentally discovered that many

patients had apparently permanent stain on their

teeth which was often referred to as COLORADO [2]STAIN. “Shoe Leather Survey” of Trendley Dean

(1931) lead to the establishment that concentration

of fluoride in drinking water was directly correlated

with the severity of fluorosed and mottled enamel. [2,3]

However, the United States Food and Drug

Administration (1973) has listed Fluoride as an

essential nutrient for human health. The report of

WHO expert committee includes Fluoride in its list

of 14 trace elements which are physiologically

essential for normal growth and development of [2,4]

human beings.

Dental Fluorosis develops due to chronic

and excessive use of fluoride compounds, most

common causative factor being use of drinking

water with higher levels of fluoride, especially

during first 6 years of age when teeth are [3,5-12]

developing. Dental Fluorosis is more


PURV PATEL Dental Fluorosis – A Retrospective Study in Gandhinagar District et. al. :

commonly observed in patients obtaining drinking

water from tube wells, bore wells or hand pumps. [13,14]

Diet, seafood and tea intake does not influence [3]

prevalence of dental fluorosis.

There is no reported significant difference

in prevalence and severity of dental fluorosis [3,14]

related to age and gender. However, certain

studies report it to be least common within first

decade due to higher number of primary teeth and

only a few erupted permanent teeth. It is reportedly

more common in 12 – 14 years of age as maximum [1,5,12,15] permanent teeth have erupted by this age.

Some studies report greater prevalence of fluorosis [5,9,12]

among males than females. One possible

explanation might be that men drink more water

than women to compensate for fluid loss during [16]

field work. This could also be due to greater [5] number of male population in a particular area.

Fluorosis is reported to be more severe in maxillary [14]

teeth than in homologous mandibular teeth. This

was probably related to unrecognized trauma in the

maxillary teeth or other local, unspecified types of [17]

insult during tooth development. Dental

Fluorosis is observed in both primary and

permanent dentition. Primary tooth fluorosis is less

common and usually less severe than in permanent

teeth, as explained by the fact that very high fluoride

levels (> 10 ppm) are required in drinking water for

it to cross placental barrier and affect primary

dentition as most primary teeth develop during [4,8,10,18]

intrauterine life.

Dental fluorosis results in a variety of [19]

pathological changes in the structure of the teeth.

It is characterized by occasional opaque, lusterless

white spots in the enamel which constitute

questionable degree of fluorosis (based on Dean's

Fluorosis index). When the white flecks cover less

than 25% of tooth surfaces, it is said to be very mild

degree fluorosis. When the white flecks cover more

than 25% but less than 50% of tooth surfaces, it is

said to have mild degree fluorosis. Cloudy striations

or 'snow capping' white flecks covering more than

50% of tooth surfaces or presence of brown or

yellow stains constitute moderate degree fluorosis.

Porous and weak, pitted or hypoplastic tooth with

loss of its general form constitutes severe degree [4,6,11,15,19,20] fluorosis. The fluorotic changes showed

high degree of bilateral symmetry in the buccal [14]

surfaces of homologous pairs of teeth.

Contradictory reports are available in the

literature regarding the correlation of the severity of

Dental Fluorosis and the DMFT Index. Some

authors have reported that as the severity of dental

fluorosis increased, the DMFT increased upto the

level of mild fluorosis and then decreased as the

severity increased from moderate to severe [5] fluorosis. Others have reported that when

fluorosis level increases upto moderate, the DMFT

value correspondingly decreases. But as the

fluorosis level increases beyond moderate, the

DMFT rate increases in cases of severe fluorosis

due to pitting of enamel surface which promotes the [9]

accumulation of microbial plaque.

The optimal concentration of fluoride for

drinking water is that level which offers minimal

risk of dental fluorosis while providing significant [21]

protection against caries. The Environmental

Protection Agency has recommended optimum [13,15,22]water fluoride level from 0.7 to 1.0 ppm. The

World Health Organization has set a maximum

concentration of 1.5 ppm fluoride in drinking water [21] to avoid dental fluorosis. In the Indian context,

even in regions with water fluoride concentration as

low as 0.5 ppm in drinking water, mild forms of [21,22] dental fluorosis have been reported. Dental

Fluorosis is endemic in 15 states of India, including


[3-6,14,23] Gujarat. Fluorosis is endemic in almost all the

[14] districts of Gujarat. Fluorosis mostly affects

people in rural India who have no access to safe

drinking water and drink water drawn from wells or [1, 4] hand pumps.

There is a positive association between the

mean annual temperature of a place and total [9,14]

fluoride intake of people residing at that place.

There are reports of fluorosis even at places with

low water fluoride levels. This could be explained

by A. K. Susheela's explanation, that in an endemic

fluorosis area, a great amount of fluoride is

incorporated into food materials and ingested into

the body. Also, with high temperature of the place [14] necessitates greater intake of water. The

occurrence of fluorosis can vary widely among

different locations having almost the same Fluoride

concentrations in drinking water and can be affected

by a number of other factors such as nutritional

status, climate, individual susceptibility and

biological response, duration of fluoride exposure,

dissolved salts in drinking water, and most [5,11,12]importantly the frequency of fluoride intake.

A stepwise increase in severity of fluorosis

has been reported with rise in level of fluoride in [3,19] water consumed. The proposed possible

mechanisms for such severe manifestations in high

water fluoride content areas include: (1) High

atmospheric temperatures during summer months

(2) Hard physical labour activity (3) Poor nutrition,

deficient in calories and also vitamin C (4)

Continued exposure to fluoride (5) Impaired renal

function (6) Abnormal concentration of certain [4,14]trace elements.

Some standard methods for assay of

fluoride in the scientific literature include Ion

Se l ec t ive e l ec t rode , Co lo r ime t ry, Ion [24] Chromatography and Electrometry. Out of these,

Ion Selective Electrode is found to be accurate upto [13] about 98%. Dental Fluorosis is irreversible, but

preventable by appropriate and timely intervention. [4,25]

There are several basic types of water

purification systems, e.g., reverse osmosis,

distillation, filtration, oxidation, disinfection,

cation exchange softening, anion exchange, [13] activated carbon, etc. Reverse osmosis water

purification systems remove 90 to 95% of the [13,20]

fluoride content in water.

A variety of treatment modalities are

available for Dental Fluorosis, with cost being a

major limitation. In – Office bleaching is the most

commonly used method for the removal of stains.

Moreover, depending upon the clinical condition, a

synergistic approach of combining bleaching with

other modalities such as micro abrasion and

fabrication of veneers can help in gaining an [26]

excellent clinical outcome. A minimal invasive

technique combining the triad of micro reduction,

micro abrasion and conventional vital bleaching

allows good esthetics and a possible cost reduction [16]for treating mild to moderate fluorosis.

The purpose of this study is to evaluate the

correlation between high ground water fluoride

content & severity as well as extent of Dental

Fluorosis in rural areas in and around Gandhinagar

district of Gujarat state.




AIMS AND OBJECTIVESØ To estimate the occurrence of Dental Fluorosis

in patients coming to the Out Patient Department (OPD) of Ahmedabad Dental College and Hospital

Ø To evaluate the association of Dental Fluorosis with Age and Sex

Ø To estimate water fluoride level and correlate it with the degree of Dental Fluorosis

Ø To evaluate different degrees of Dental Fluorosis in terms of type and severity

Ø To estimate the incidence and severity of dental caries in patients having Dental Fluorosis

MATERIALS AND METHODS

Ø The study was conducted on 53 patients from amongst all the patients coming to the Out Patient Department (OPD) of the Oral Medicine and Radiology Department of Ahmedabad Dental College and Hospital during the period of June 2009 to September 2010

Ø Inclusion Criteria• Patients having chalky white spots or brown

staining or structural abnormalities of teeth• Patients who have lived in the same place

where they were born and have procured drinking water from the same source throughout their life

Ø Exclusion Criteria• Patients with history of being treated by

long term antibiotic medication in early childhood or whose mother has been treated by such medication during pregnancy

• Patients who had migrated to some other place after birth or who were not permanent residents of any one place since birth

• Patients who have obtained drinking water from more than one source since birth

• Patients having some severe systemic disease or condition

Ø The severity of Dental Fluorosis was estimated based on Dean's Fluorosis Index.

Ø Patients selected for the study were evaluated and examined thoroughly and the findings were recorded in a Proforma prepared specially for

the study

Ø The drinking water samples were procured from patients and sent to laboratory for estimation of fluoride content in ppm (parts per million) based on Ion Selective Electrode Method.

COLLECTION OF WATER SAMPLE

Ø The ground water pumped from the borewell into overhead water tanks comprised the source of water for samples collected in the study

Ø The water samples were collected from overhead water tanks after obtaining permission from the respective Gram Panchayats of villages under study.

Ø The water sample collected from a single place was equally divided into two unused plastic containers and precoded by the investigator and then submitted to the laboratory technician on the same day. Thus, the laboratory technician was kept unaware of the place to which the water sample belonged, to eliminate any potential bias.

Ø The same procedure was repeated for all places under study.

Ø Two samples were thus submitted from each place to the technician in order to test the same sample twice and hence eliminate major errors. The mean of two samples was taken as final reading. If the difference between the two readings was greater than 0.5 ppm, the sample was discarded; a new sample was obtained from the same place and submitted for water fluoride estimation.

Ø From the ppm content of water samples procured, a chart of fluoride content of different areas of Gandhinagar district was prepared.

RESULTS

A total of 53 patients with Fluorosis were selected for the study from the patients coming to the Out Patient Department (OPD) at Oral Medicine, Diagnosis & Radiology Department


14

of Ahmedabad Dental College & Hospital.

The Pie chart shows the distribution of 53 patients into mild, moderate and severe degrees of Fluorosis based on Dean's Fluorosis Index. There were no patients falling into 'Questionable' and 'Very Mild' categories of Fluorosis. There were 4(7.55%), 31(58.49%) & 18(33.96%) patients in 'Mild', 'Moderate' and 'Severe' categories respectively. (Fig. 1 – 3)

Figure 1: Patient with mild degree of DentalFluorosis

Figure 2: Patient with moderate degree of Dental Fluorosis

Figure 3: Patient with severe degree of Dental Fluorosis

PIE CHART



Table I demonstrates age distribution of 53 patients under the study. The patients belonged to age range from 11 to 65 years. Out of 53 patients, 14(26.41%) were in second decade; while 17(32.07%) were in third decade and the same number of patients were in the fourth decade of life

Table II shows the sex distribution of patients under study. Out of 53 patients, 30(56.60%) were males while 23(43.40%) were females.

Table III shows distribution of patients selected for the study with their birth places and the community water fluoride levels (ppm) of those places as estimated by means of Ion Selective Electrode method.The patients selected for the study were divided into two groups. Group I included 10 patients who came from places having community water fluoride level 1.5 ppm or below. Group II included 43 patients who came from places having community water fluoride level above 1.5 ppm. There were more patients having moderate and severe degree fluorosis in Group II as compared to Group I.

Table I

-

Distribution of patients with various degrees of Fluorosis according to Age

Distribution of age

Mild

Moderate Severe Total

0 to 9

0

0

0 010 to 19

1 (25%)

7 (22.58%) 6 (33.33%) 14 (26.41%)20 to 29

1 (25%)

9 (29.03%) 7 (38.89%) 17 (32.07%)30 to 39 2 (50%) 12 (38.71%) 3 (16.67%) 17 (32.07%)40 to 49 0 1 (3.22%) 0 1 (1.89%)50 to 59 0 2 (6.45%) 0 2 (3.77%)60 to 69 0 0 2 (11.11%) 2 (3.77%)

70 and above 0 0 0 0Total 4 31 18 53

Table II - Distribution of patients with various degrees of Fluorosis according to Sex

Distribution of Sex

Mild Moderate Severe Total

Male 2 (50%) 19 (61.29%) 9 (50%) 30 (56.60%)Female 2 (50%) 12 (38.71%) 9 (50%) 23 (43.40%)Total 4 31 18 53

15



Table III – Distribution of patients with various degree of Fluorosis

according to Community Water Fluoride Level

Group Place Water F level (ppm)

Mild Moderate Severe Total

Patients

Group

I (≤ 1.5

ppm)

Vadsar

1.3

0

2

0

2

Nasmed

1.4

0

2

1

3

Chandlodiya

1.5

1

2 0

3

Bhamriya 1.5 1 0 1 2

2 (20%)

6 (60%)

2 (20%) 10

Group

II ( >

1.5

ppm)

Ghatlodiya

1.6

0

1

1

2

Thol

1.8

1

1

0

2

Nava Vadaj

1.9

0

2

0

2

Odhav

2

0

3

2

5

Santej

2

0

2

3

5

Julasan

2.7

0

2

2

4

Pansar

2.8

0

5

1

6

Bapunagar

2.8

1

2

6

9

Rakanpur 3 0 2 1 3

Mehsana 3 0 2 0 2

Kadi 3 0 3 0 3

2 (4.65%) 25 (58.14%) 16 (37.21%) 43

Total 4 31 18 53


Table IV demonstrates the distribution of patients selected for the study based on their chief complains.

Table IV - Distribution of patients with various degrees of Fluorosis based on Chief Complain

Chief Complain

Mild

Moderate

Severe

Total

Stains

2 (50%)

13 (41.93%)

13 (72.22%) 28 (52.83%)

Pain

1 (25%)

10 (32.26%)

3 (16.67%)

14 (26.41%)

Decay

1 (25%)

3 (9.68%)

0

4 (7.55%)

Extraction 0 3 (9.68%) 1 (5.55%) 4 (7.55%)

Gum Problems 0 1 (3.22%) 0 1 (1.89%)

Prosthetic Problems

0 1 (3.22%) 1 (5.55%) 2 (3.77%)

Total 4 31 18 53


Table VI shows caries experience of patients based on DMF Index (Decayed, Missing, and Filled) in each of the mild, moderate and severe fluorosis categories. Out of 53 patients selected for the study, there were 7(13.20%) patients with DMF score 0, 10(18.87%) patients had DMF score 1 or 2, 16(30.19%) patients had DMF score 3 to 5, while 20(37.74%) patients had DMF score from 6 to 12 or beyond. Among the 31 patients with moderate degree Fluorosis, 11(35.48%) patients had DMF score of 3 to 5 and other 11(35.48%) patients had DMF score equal or above 6. Among the 18 patients with severe degree Fluorosis, 4(22.22%) had DMF Score 3 to 5, 9 (50%) patients had DMF score equal to or above 6.

Table V - Arch wise distribution of fluorosed TeethTeeth affected Maxillary teeth Mandibular teeth Total

Incisors 47 (20.70%) 24 (10.57%) 71 (31.28%)Canine 29 (12.77%) 23 (10.13%) 52 (22.91%)

Premolars 28 (12.33%) 27 (11.89%) 55 (24.23%)Molars 25 (11.01%) 24 (10.57%) 49 (21.58%)Total 129 (56.83%) 98 (43.17%) 227


DISCUSSION

Dental Fluorosis develops due to chronic and excessive use of fluoride compounds by the patients, most common causative factor being use of drinking water with higher levels of fluoride,

[3,5-12]especially during first 6 years of age.

According to the present study, Dental Fluorosis is most common in second and third decades of life. This is in accordance with literature which reports it to be least common within 5 – 7 years of age due to higher number of primary teeth and only few erupted permanent teeth. It is reportedly more common around 12 – 14 years of age as all permanent teeth (except third molars) have

[1,5,12,15]erupted by this age. However, some authors report no significant difference in prevalence and severity of dental fluorosis between various ages. [3,14]

There is no reported significant difference in prevalence and severity of dental fluorosis

[3,14]between males and females. However, some studies report greater prevalence of Fluorosis

[5,9,12]among males than females. This is in accordance with the present study. One possible explanation might be that men drink more water than women to compensate for fluid loss during

[12,14]field work.

All the patients in the present study were residing (since birth) at places having community water fluoride levels well above the optimum level (0.7 – 1.2 ppm) as suggested by World Health

Organization and Environmental Protection Agency as well as above that of Indian standards (0.5 ppm).The places under present study belong to Ahmedabad, Gandhinagar & Mehsana districts of Gujarat state, which is an Endemic Fluorosis state, as reported in National

[3-6,14]Oral Health Survey. This is in accordance with reports in literature that fluorosis is caused by consumption of water with fluoride level

[1,13,15,21,22]above optimum. Most of patients under study consumed drinking water provided by community supplies since birth, which contained optimal water fluoride above normal. Dental fluorosis is reported to be more commonly observed in patients obtaining drinking water from tube wells, bore wells or hand pumps rather than tap water, draw wells or rivers, because the surface water is known to

[13,14]contain less fluoride than ground water. There is a tendency of increase in severity of Dental Fluorosis in patients with increase in

[3,19]Community Water Fluoride level. This is in accordance with the present study.

Among the patients under the moderate and severe categories, most reported with chief complain of brown stains and mottled teeth since childhood or adolescence. This is in accordance with high fluoride content of drinking water consumed by them during critical period for development of dentition, as

[3,5-12]revealed by this study. The other major chief complaint was that of pain associated with a carious tooth, which is common in fluorosed

[5,19]teeth. Very few patients with mild degree of


Fluorosis presented for the study, which reflects the fact that Fluorosis of a moderate degree is much more noticeable due to presence of brown stains than mild degree of Fluorosis which often goes unnoticed.

Dental Fluorosis is found to be more severe in maxillary teeth than in homologous mandibular teeth, with maxillary incisors as most commonly involved teeth group, in the present study. This is in accordance with the reports in

[14]literature. This was probably related to unrecognized trauma in the maxillary teeth or other local, unspecified types of insult during

[17]tooth development.

There is an increase in prevalence of dental caries with increase in severity of Dental Fluorosis in the present study. This is in accordance with studies reporting elevated caries levels associated with the brittleness of

[3]moderately and severely mottled teeth. However, some authors have reported that when Fluorosis severity increased from normal to moderate, the DMFT value correspondingly decreased, while as the fluorosis level increased beyond moderate, the DMFT rate increased. The DMFT increased in cases of severe Fluorosis due to pitting of enamel surface which promoted the accumulation of microbial plaque. [9] While, some authors have reported that as the severity of Dental Fluorosis increased the DMFT increased upto the level of mild Fluorosis and then decreased as the severity

[5]increased from moderate to severe Fluorosis.

In the present study, there are more patients with greater DMFT scores among the patients with moderate and severe degree of Fluorosis as compared to those with mild degree of Fluorosis.

SUMMARY AND CONCLUSION

• Majority of patients came from Ahmedabad, Gandhinagar & Mehsana districts of Gujarat state, which are areas of Endemic Fluorosis according to National Oral Health Survey

• Majority of patients affected with Dental Fluorosis belonged to second, third and fourth decades of life.

• There was a slight male predominance among the affected patients.

• Amongst the patients with Dental Fluorosis, a step wise increase in severity of fluorosis was noted with increase in drinking water fluoride content (estimated by Ion Selective Electrode Method).

• Majority of patients fell into moderate to severe degree Fluorosis categories of Dean's Fluorosis Index

• There was an increase in Caries prevalence with corresponding increase in severity of Dental Fluorosis.

• Among the treatment modalities evaluated, Bleaching was found to give esthetically acceptable results in patients with brown stains while veneers were satisfactory as treatment modality for hypoplastic enamel with surface irregularities in patients with severe degree of Fluorosis.

REFERENCES

1. Alien. Fluorosis – Causes, Symptoms, and Treatment. Content Corner.com 2008.

2. Amrit T, Ved J. Fluorides and Dental Caries – A Compendium. Publication of the Journal of Indian Dental Association 1986.

3. Jagan Kumar B, Clement R, Aswath N. Prevalence of dental fluorosis and associated risk factors in 11 – 15 year old school children of Kanyakumari District, Tamilnadu, India: A Cross Sectional survey. Indian J Dent Res 2008; 19(4): 297 – 303.

4. Vineet D, Maheep B. Physiology and toxicity of fluoride. Indian J Dent Res 2009; 20(3): 350 – 5.

5. Tuli A, Rehani U, Aggrawal A. Caries experience evidenced in children having dental fluorosis. Int J Clinical Ped Dent 2009; 2(2): 25 – 31.

6. Bronckers A, Lyaruu D, DenBesten P. The Impact of Fluoride on Ameloblasts and the mechanisms of Enamel Fluorosis. J Dent Res 2009; 88(10): 877 – 93.

7. Fatemeh V, Anne M, Paula J. Sources of dietary fluoride Intake in 6-7 year old english children



receiving optimally, sub-optimally, and non-fluoridated water. Journal Public Health Dent 2006; 66(4): 227 – 34.

8. Teresa A, Steven M, John J, Barbara B, Julie M, Phyllis J. Associations between intakes of fluoride from beverages during infancy and dental fluorosis of primary teeth. Journal of the American College of Nutrition 2004; 23(2): 108 – 16.

9. Ramezani G, Valaei N, Eikani H. Prevalence of DMFT and Fluorosis in the students of Dayer City (Iran). J Indian Soc Pedod Prevent Dent 2004; 22(2): 49 – 53.

10. Jian R, Asgeir R, Anne S, RuiZhe H, ZhiLun W, Kjell B. Dental fluorosis in children in areas with fluoride polluted air, high fluoride water, and low fluoride water as well as low fluoride air: A study of deciduous and permanent teeth in the Shaanxi p rov ince , China . Acta Odontologica Scandinavica 2007; 65: 65 – 71.

11. Ana A, Carlo E, Juan F, Gerardo M, Mirna M, Sayde O. Dental fluorosis in cohorts born before, during, and after the national salt fluoridation program in a community in Mexico. Acta Odontologica Scandinavica 2006; 64: 209 – 13.

12. Choubisa S. Endemic fluorosis in Southern Rajasthan, India. Fluoride 2001; 34(1): 61 – 70.

13. Prabhakar A, Raju O, Kurthukoti A, Vishwas T. The effect of water purification systems on fluoride content of drinking water. J Indian Soc Pedod Prevent Dent 2008; 26(1): 6 – 11.

14. Sudhir K, Prashant G, Subba Reddy V, Mohandas U, Chandu G. Prevalence and severity of dental fluorosis among 13 to 15 year old school children of an area known for endemic fluorosis: Nalgonda district of Andhra Pradesh. J Indian Soc Pedod Prevent Dent 2009; 27(4): 190 – 6.

15. Lia Silva C, Efigenia F, Leila N, Lucia M, Edson P. Beliefs and attitudes about endemic dental fluorosis among adolescents in rural Brazil. Rev Saude Publica 2010; 44(2): 261 – 6.

16. Harikumar V, Arun A. Management of mild to moderate fluorosis with a combined chemomechanical approach. Annals and Essences of Dentistry 2010; 2(3): 73 – 6.

17. Vera S, Dorte H, Carolina T, Thais M, Sven P. Prevalence and distribution of demarcated opacities and their sequelae in permanent 1st molars and incisors in 7 to 13 year old Brazilian children. Acta Odontologica Scandinavica 2009; 67: 170 – 5.

18. Dhar V, Jain A, Van Dyke T, Kohli A. Prevalence of gingival diseases, malocclusion and fluorosis in school going children of rural areas in Udaipur district. J Indian Soc Pedod Prevent Dent 2007; 25(2): 103 – 5.

19. Susheela A, Bhatnagar M, Gnanasundaram N, Saraswathy T. Structural aberrations in fluorosed human teeth: Biochemical and scanning electron microscopic studies. Current Science 1999; 77: 1677 – 81.

20. Pediatric Dentistry – Special Supplemental Issue. Access, January 2000.

21. Parkar S, Ajithkrishnan C. Estimation of fluoride concentration in Community water supply & packaged drinking water sold in Vadodara City – A Comparative Study. J Indian Assoc Public Health Dent 2010(15): 105 – 9.

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KNOWLEDGE, ATTITUDE AND PRACTICE REGARDING ORAL CANCER AND SCREENING PROCEDURES AMONG PRIMARY HEALTH CARE AND COMMUNITY HEALTHCARE WORKERS OF WAGHODIA, GUJARATBAFNA HARSHAL P *, AJITHKRISHNAN CG**, KALANTHARAKATH THANVEER***, RICKY PAL SING*, HEMAL PATEL****

ABSTRACT

Background: India has the highest rate of oral cancer in world and there is a 60% rise in past three decades. Mortality rate for oral cancer is higher in population with poor access to oral health care. With 72% of Indians residing in rural areas they have a better access to community health care providers (CCPs) and primary health care providers (PCPs) who, could play a major role in oral cancer prevention and reduce death rate.

Objectives: The study aimed at evaluating knowledge, attitude and practice regarding oral cancer and screening practices among CCP's and PCP's by using pretested questionnaire.

Material and Methods: A cross sectional questionnaire study was conducted among all CCP's and PCP's of Waghodia, Vadodara. A self designed, modified close ended and pre-piloted questionnaire was used for recording data. Mean and percentage were used for statistical analysis.

Results: 78.24% believed that prevention and early detection was important, while 53% had actually referred cases in past one year. All believed tobacco to be a risk factor for oral cancer but only 49% answered for other factors. 91.37% were ready to be a part of continuing education (CE).

Conclusion: The participants had deficient knowledge about the risk factors for oral cancer and were ready to participate in CE.

Key-words: Oral Cancer, Health Care Workers, Gujarat

Received: 12-11-2013; Review Completed: 22-01-2014; Accepted: 13-02-2014

ADDRESS FOR AUTHOR CORROSPONDENCE : DR. , PHONE: 8469048732BAFNA HARSHAL P

20

Original Article

*P.G. STUDENT, **PROF. & HEAD, ***PROFFESOR, ****SR.LEC, DEPT.

DEPT. OF PUBLIC HEALTH DENTISTRY, K.M. SHAH DENTAL COLLEGE

INTRODUCTION:

The World Health Organization reports a

worldwide death toll from tobacco use to be four

million per year. The death toll is expected to rise to [1]

ten million per year by 2020's or early 2030's.

Tobacco is thought to be one of the most important

etiological factors in development of oral cancer.

India has the highest rate of oral cancer in the world

with a 60% increase in past three decades and no

improvement in the mortality rate has been seen [2]

during this period.

Oral cancer is a disease with known high risk factors

and an asymptomatic phase with identifiable

clinical features. The mortality rate for oral cancer

is higher in population who traditionally experience [3]poor access to the oral health care system. Also

unfortunately, for a large segment of high-risk

individuals, access to dental care is limited where

dental surgeons can help to identify these

individuals and provide necessary treatment. About

those residing in rural areas, they have a better

access to non dental CCPs and PCPs. Therefore,

CCPs and PCPs could play a major role in

prevention of oral cancer and reducing death toll

owing to oral cancer. One way to achieve these

goals is to develop a network of dental and other

healthcare providers to promote the early screening


of oral soft tissue lesions that may be pre-cancerous [4]or cancerous.

India has a population of 1.21billion and with 72% [5] [6]

of the Indian population residing in rural areas, ,

the government has implemented various rural

health strategies and national programmes through

Primary and community health care centres,

National Cancer Control Programme (NCCP) being

one of them. Lack of such a network with regards to

oral health care practices in India and unavailability

of oral health professionals to provide on site basic

oral health services discourages further the [7]

integration of oral health services in these centres.

Thus it becomes necessary for these health care

workers to play a role in oral cancer prevention and

therefore the present study was proposed to assess

the knowledge of oral cancer, attitude towards it

prevention and screening practice of oral cancer

among CCPs and PCPs Waghodia Taluka,

Vadodara, Gujarat.

MATERIAL AND METHODS:

Ethical approval was obtained from the Institutional

Ehics committee. Permissions were obtained from

the Chief District Health Officer (CDHO) of

Vadodara district and the Block Health Officer of

Waghodia Taluka to conduct the survey at the

primary and community health care centres of

Waghodia taluka. The purpose and procedure of the

study was informed to each participant and

participant information sheet was provided to them.

Also informed consent was obtained from each

participant who was willing to participate in the

study.

A pilot study was conducted in the beginning for

testing of validity and reliability of the developed

questionnaire among four Experts and four

respondents. The medical officers were considered

as experts while the other staff members were

BAFNA HARSHAL KAP regarding Oral Cancer among PCP's and CCP's et. al. :

21

considered as respondents and four from each were

chosen randomly by lottery method as participants

for pilot study. The validity of questionnaire using

Concurrent Validity method was 90.3. The

reliability results obtained by test – retest was

89.92% which showed a high agreement.The sampling frame included all Medical officers,

staff nurses, health workers, health educator, and

health assistants working at these centre's during the

study period i.e. from June 2012 to August 2012

which constituted a total of 85 subjects. The

individuals who were not willing to participate in

the study or were absent at the centre during three

consecutive visits were excluded from the study.

For each health care centre the questionnaire was

administered on first day of visit and recollected on

the second day by the principal investigator himself.

The participants who were absent on the first day of

visit were contacted over the phone and a later date

was fixed with them for the questionnaire fill up. All

the absent individuals responded in the first call.

Data was collected with the help of a self designed,

modified close ended & pre-tested questionnaire

used in English and Gujarati language. The Gujarati

version was validated by back translation method.

The questionnaire consisted of six, four and five

questions pertaining to knowledge of Oral cancer,

screening practice of Oral cancer and attitude

towards Oral cancer prevention respectively.

The data was analyzed using Descriptive statistical

analysis i.e. percentage in Microsoft Excel 2007

spreadsheet.


RESULTS:

As seen in Table 1 participants had a good level of

knowledge regarding oral cancer prevalence, its

ability to metastasize and its life threatening

potential.

Table 1: Table showing knowledge of participants

regarding oral cancer

Table 2 shows that participants had good level of

knowledge about different methods for detection of

oral cancer but only less than half had actually

referred patients for suspicious oral cancer cases in

past 12 months. A larger no agreed that health care

providers needed more education about oral cancer

screening.

Table 2: Table representing knowledge of oral

cancer screening among the participants

The participants had a positive attitude towards

prevention of oral cancer development, while a

larger number believed that its early detection could

help in successful treatment of the patient (Table 3).

As seen in Fig.1 and Fig.3 participants had good

knowledge about different types of oral cancer and

the signs and symptoms of oral cancer but a fewer

participants (Fig.2) were aware of different

causative agents responsible for oral cancer

development.

Figure 1: Distribution of subjects according to their

knowledge regarding different types of oral cancer

Figure 2: Distribution of subjects according to

knowledge regarding different causes of oral cancer

Sr.no Question Yes No Total

1.

Occurrence of oral cancer is common in India

90.59%

(N=77)

9.41%

(N=8)

100%

(N=85)

2.

Oral cancer can metastasize

87.05%

(N=74)

12.95%

(N=11)

100%

(N=85)

3 Oral cancer is life threatening disease.

85.88%

(N=73)

14.22 %

(N=12)

100%

(N=85)


1. Awareness regarding different methods for detection of oral cancer

65.88%

(N=56)

34.22% (N=29)

100% (N=85)

2. Referral of patients to dental specialist for suspicious oral cancer cases in last 12 months

41.17% (N=35)

58.83% (N=50)

100% (N=85)

3. Ability to detect oral cancer 78.82% (N=67)

21.18% (N=18)

100% (N=85)

4. Health care providers needed more education about oral cancer screening.

78.82% (N=67)

21.18%(N=18)

100% (N=85)


1. Early detection can lead to successful treatment of oral cancers

98.82%

(N=84)

1.18%

(N=1)

100%

(N=85)

2.

Oral cancer develops by chance and nobody can do anything to prevent it.

41.17%

(N=35)

58.83%

(N=50)

100%

(N=85)



Figure 3: Distribution of subjects according to

knowledge regarding sign and symptoms of oral

cancer

Figure 4: Attitude of participants towards

prevention of oral cancer

The subjects (Fig.4) were willing to participate in

educational courses related to screening of oral

cancer, and become a part of organized networks

promoting oral cancer screening. Also they believed

that strict laws should be introduced against the sale

of to bacco.

DISCUSSION:

Oral cancer is on the increase with incidence rates [7]having doubled over the last ten to 15 years. The

death toll is expected to rise to ten million per year [1]

by 2020's or early 2030's. Prevention of oral

cancer, and reducing cancer-related burden and

deaths could be achieved by an integrated program

that involves health care providers, health care

organizations, the government at various levels, and

the public.

The present study was conducted to assess the

knowledge of oral cancer, attitude towards it

prevention and screening practice of oral cancer

among CCPs and PCPs of Waghodia, Gujarat. This

study, concerning oral cancer, was the first of its

kind among the health care workers of Waghodia

who comprised of a total of 85 in number.

Out of 85 workers, 77 (90.59 %) answered that oral

cancer was commonly occurring among the Indian

population which is consistent with oral cancer

prevalence data provided by IDA (Indian Dental [2]

Association), suggestive of good awareness

among the PCP's and CCP's.

A high percentage of workers i.e. 73 (85.88 %),

agreed to the statement that “oral cancer is a life

threatening disease” and a similar number of 74

(87.05%) agreed that oral cancer could spread to

other parts of the body. A total of 84(98.82 %)

workers believed that early detection of oral cancer

could help in successful treatment of such cases,

this could be the reason that all the 85 subjects were

willing to participate in educational courses related

to screening of oral cancer and similar number of

individuals 81(95.29%) were ready to participate in

established or organized networks to promote

screening of oral cancer. These findings are in

agreement with those of Kumar M and Macpherson [3], [7]

LMD et al.

Of the 85 workers 78 (91.77 %) answered correctly

that oral cancer included cancer of lips, cancer of

tongue and cancer of other parts of mouth and

oropharynx. While a similar no. of subjects 63

(74.11%), answered correctly that oral cancer



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