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Year : 2007  |  Volume : 18  |  Issue : 2  |  Page : 67-71
Assessment of periodontal status in dental fluorosis subjects using community periodontal index of treatment needs


Department of Periodontics, College of Dental Sciences, Davangere - 577 004, Karnataka, India

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Date of Submission05-May-2006
Date of Decision30-Sep-2006
Date of Acceptance03-Oct-2006
 

   Abstract 

Background: Periodontitis is multifactorial in nature. The various determinants of periodontal disease are age, sex, race, socioeconomic status, and risk factors including tobacco usage and oral hygiene status. However, there is inconsistent epidemiological data on the periodontal status of subjects living in high-fluoride areas. The aim of the study was to investigate the effect of dental fluorosis on the periodontal status using community periodontal index of treatment needs (CPITN), as a clinical study. The purpose of this study is to determine the periodontal status using CPITN index in a population aged between 15 and 74 years residing in the high-fluoride areas of Davangere district. The possible reasons for the susceptibility of this population to periodontal disease are discussed. Materials and Methods: 1029 subjects, aged between 15 and 74 years suffering from dental fluorosis were assessed for their periodontal status. Clinical parameters recorded were OHI-S to assess the oral hygiene status, Jackson's fluorosis index to assess the degree of fluorosis and CPITN index to assess the periodontal status where treatment need was excluded. Results: Gingivitis and periodontitis were more common in females (65.9% and 32.8%, respectively) than in males (75.1% and 24.2%, respectively). Periodontitis was significantly more common in females. As the age advanced from 15 to 55 years and above, gingivitis reduced from 81.0 to 42.9% and periodontitis increased steadily from 18.0 to 57.1%, which was significant. Periodontitis was high in subjects with poor oral hygiene (81.3%), compared to those with good oral hygiene (14.5%), which was significant. As the degree of fluorosis increased, severity of gingivitis reduced and periodontitis increased, i.e., with A degree fluorosis, gingivitis was 89.4% and periodontitis 8.5%, but with F degree fluorosis the former was 64% and the latter 35.8%, which was statistically significant. Conclusion: The results suggest that there is a strong association of occurrence of periodontal disease in high-fluoride areas. The role of plaque is well understood in contrast to the effect of fluorides on periodontal tissues. It goes a long way to reason out fluoride as an important etiological agent in periodontal disease.

Keywords: Community periodontal index of treatment needs, dental fluorosis, oral epidemiology, periodontal disease

How to cite this article:
Vandana K L, Sesha Reddy M. Assessment of periodontal status in dental fluorosis subjects using community periodontal index of treatment needs. Indian J Dent Res 2007;18:67-71

How to cite this URL:
Vandana K L, Sesha Reddy M. Assessment of periodontal status in dental fluorosis subjects using community periodontal index of treatment needs. Indian J Dent Res [serial online] 2007 [cited 2019 Nov 17];18:67-71. Available from: http://www.ijdr.in/text.asp?2007/18/2/67/32423

   Introduction Top


Epidemiological studies concerning the prevalence of periodontal disease in relation to dental fluorosis have given contradictory results. In general, a higher level of gingival inflammation has been observed in fluorosis than in non-fluorosis areas.[1],[2],[3] However, several studies have found no difference in periodontal conditions between fluoride and non-fluoride areas;[4],[5] better gingival conditions in fluoride compared to non-fluoride areas have even been reported by others.[6],[7],[8] Though the effect of fluoride on reduction of dental caries is well established, its effect on periodontal tissues is obscure.

The fluoride concentration of drinking water is considerably high of places in Davangere district, Karnataka, India, where the present study was conducted. The fluoride level ranges from 1.5 to 3.0 ppm in the drinking water; there is virtually no dental care and the socioeconomic status is low. The unique population provides us the opportunity of studying the effect of life-long exposure of fluoride in drinking water on the periodontal status of those subjects with dental fluorosis and provide evidence for long- term exposure to high-fluoride drinking water.

The factors that motivated us to undertake this study are routine clinical observation that female subjects with dental fluorosis reported to the clinic were suffering from periodontitis and the paucity of recent periodontal literature correlating periodontal health with dental fluorosis.

The purpose of the study is to evaluate periodontal status in dental fluorosis subjects and discuss the possible reasons for the susceptibility of these subjects to periodontal disease.


   Materials and Methods Top


The patients for this study were selected from the Department of Periodontics, College of Dental Sciences, Davangere District, Karnataka State. The sample consisted of 1029 subjects aged between 15 and 74 years.

Inclusion criteria included subjects suffering from dental fluorosis who reported to the clinic with bleeding gums and/or painful gums and stained teeth. Exclusion criteria included subjects with known systemic diseases and subjects with other intrinsic dental stains. These subjects were permanent residents of high- fluoride water areas.

Recording of clinical parameters included Oral Hygiene Index -Simplified (8), Jackson's Fluorosis Index (9), Community Periodontal Index Treatment Needs (CPITN) (10). The code of CPITN was interpreted for the purpose of periodontal status evaluation code 0 as healthy periodontal status, code 1 as gingivitis, and code 3 and 4 as periodontitis. The treatment need was not considered. All examinations were carried out by one examiner with the aid of both a plain mouth mirror and a WHO 621 periodontal probe (5). Fluoride concentration in water was in the range of 1.5-3 ppm, assessed by Chemical Department, Bapuji Institute of Engineering and Technology.

Statistical analysis

Data analysis was performed using chi-square test. A P value < 0.05 was considered statistically significant.


   Results Top


Distribution of the sample based on sex and periodontal status, age and periodontal status, OHI-S, and degree of dental fluorosis and periodontal status are tabulated [Table - 1],[Table - 2],[Table - 3],[Table - 4].


   Discussion Top


The studies on periodontal status of high-fluoride areas date back to 1936, the latest year being 1993, without any consistent and confirmative data. Surprisingly studies have not paid attention to the periodontal status in high-fluoride areas from a research perspective.

The present study, based on the CPITN, demonstrated a typical CPITN profile in fluorosis subjects; gingivitis was found among all ages; a low-to-moderate prevalence of shallow pockets among all ages and a low-to-moderate prevalence of deep pockets increasing with age. The relatively higher prevalence of low-to-moderate pocketing was associated with an average of more than half a sextant per subject and similarly the high prevalence of gingivitis with an average of more than half a sextant per subject was observed.

The CPITN gives normative rather than scientific information. It gives no information about the natural history of periodontal disease and is not a specific detector of the destructive agents in periodontal disease.[5] Assessment of treatment needs was excluded as it has become complicated due to recent advances in our understanding of the etiology, pathogenesis and treatment of the disease.[5]

Age is considered as one of the risk factors for periodontal diseases, i.e., the prevalence of periodontal disease varies with the advance of age. In the present study only a few subjects (1.2%) had healthy periodontal status in the age group of 15-24 years. Gingivitis was seen in all the age groups, which was highly significant similar to the observation by Murray who reported an increased prevalence of gingivitis in high-fluoride areas between the age group of 15 and 65 years.[9]

Periodontitis is a multifactorial disease that is related to age. Although periodontitis was present in all the age groups, the steady increase in periodontitis as the age advanced to 55 years was significantly similar to the result of the study conducted by Haikel et al. ,[5]

Murray conducted a study to compare gingivitis and gingival recession (loss of attachment) in residents of Hartlepool (1.2ppm-2.0ppm) and York (0.15-0.2), aged between 15 and 65 years, and found gingivitis and gingival recession to be more prevalent in high-fluoride areas than low-fluoride areas.[9] Reddy et al. conducted a study to know the prevalence and severity of periodontitis in 71 adults residing in a high-fluoride area (2-3 ppm) and concluded that there is little evidence of periodontal destruction (mean probing depth - 2.5 mm).[10] Grembowski et al. estimated fluoridation effects on periodontal disease among Washington state employees and their spouses of 20 to 34 years of age, and concluded that fluoridation has small beneficial effects on periodontal health among adults aged between 20 and 34 years relative to adults with no exposure.[11] However, in the present study the significant increase in the presence of periodontitis was observed in subjects beyond the age of 35 years.

In the present study, both males and females suffered from gingivitis and periodontitis. Females predominantly suffered from periodontitis, the reason for which needs to be evaluated. However, this is in contrast to the general trend of males getting more affected by periodontitis than females.[12]

The OHI status was moderate in a majority of subjects in spite of the non-availability of regular dental care. In the present study, gingivitis was observed in all levels of oral hygiene, and periodontitis was of a significantly increasing order regarding good-to-poor oral hygiene status. Murray found gingivitis to be more prevalent in high-fluoride areas despite good oral hygiene.[9] The gingival recession (loss of attachment) was also measured in their study and in all age groups the low fluoride residents had less recession than did members of the high-fluoride group. This is another study that indicated residents of high-fluoride areas might be at disadvantage in terms of their periodontal status.

A first attempt is made to study and correlate periodontal status with the dental fluorosis. The effect of fluorosis on periodontal structures is not studied in human beings, which may be responsible for destruction of periodontal tissues as reported in few of the medical literature.

In the present study, as the severity of fluorosis increased from degree A to F, gingivitis was observed in all the degrees and periodontitis increased from 8.5 to 35.8%. The role of dental plaque is well established; it does not explain the difference in susceptibility of a given population or individual's periodontitis. It is evident that many factors influence the etiology and pathogenesis of periodontal diseases and one such factor could be fluoride.[11]

The possible reasons for the susceptibility of this population to periodontitis are based on the following medical literature:

Firstly, an animal study conducted by Krook in cattle with dental fluorosis have showed that hypercementosis resulted from failure of resorption of cementum as an expression of fluoride intoxication.[13] Fluoride had a toxic effect on the resorbing cementocytes that eventually died and cementum necrosis progressed to cyst formation. Toxic action of fluoride on alveolar bone of permanent teeth eventually leads to osteonecrosis and recession of the alveolar crest. The gingiva obviously recedes with the receding bone.

In periodontics, data from animal studies are used extensively in studying pathogenesis due to certain similarities between the human species. The toxic effect of fluoride on cementum and bone is not dispensable for the fluorosed human teeth leading to destruction of periodontal structures through noninflammatory process which may compound the regular plaque induced inflammatory destruction in the high-fluoride areas. The use of word 'noninflammatory' process allows the author to explain the destruction effect of fluorides better.

Secondly, Vazirani reported that on gross examination of teeth with mottled enamel, the most striking point was observed in the root portion of every tooth.[14] The root surfaces were irregular, rough and revealed heavy deposits of calcified marks in the form of excessive amounts of fluoride or osteocementum at the apical region of the teeth. These teeth roentgenographically presented the following features osteosclerosis, cementosis and periapical root resorption.

Thirdly, Reddy et al. reported calcification of muscular attachments, ligaments and ossification on histopathologically which interferes with the functional movement of skeletal system.[15] The data are supported by the preliminary SEM study of human fluorosed and non fluorosed teeth by the first author of this paper who reported partial/initial mineralization of connecting tissue fibers and presence of significant amount of globular mineralized deposits exclusively in the healthy fluorosed teeth. Would these SEM changes indicate calcification of periodontal ligament fibers requires to be elucidated histopathologically.[16]

The direct evidence of toxic effect of fluoride in medical literature theoretically convinces the possibility of toxic effect of fluoride such as cemental necrosis, osteosclerosis and calcification of ligament in human periodontal region as a consequence of life time exposure to high-fluoride water levels. Based on this hypothesis presently the prevalence of periodontitis significantly observed in this study is well reported. However the toxic effects of fluorides on human periodontal tissues remain to be researched to confirm the data.

The antibacterial effect of fluoride by Rolla et al. , Yoon and Berry, the inhibition of glycolytic enzyme enolase by Kanapa and Hamiltion are the likely mechanisms where in inflammatory aspect of periodontal disease is dealt with. It is desirable that prevalence of periodontal disease observed in the present study necessitates researching the toxic biologic effects of fluoride along with biological analysis of dental plaque in order to confirm the effect of fluoride on periodontal conditions. The comparative assessment of periodontal status from non-fluoride areas was not attempted, as it would simply report the effect of plaque alone similar to earlier studies.


   Conclusion Top


No effort has been made in the literature to quote reasons for association of periodontal disease in high-fluoride areas apart from blaming oral hygiene and plaque levels. The risk factors such as age, sex and oral hygiene status for periodontal disease may not differ from high to low fluoride areas. The regular pathway of gingivitis progressing to periodontitis through an inflammatory process is well established. In addition to inflammatory process which remains common to high and low fluoride areas, the fluorosis induced changes in hard and soft tissues of periodontium requires being paid attention to suspect fluoride as an etiological (environmental) agent for periodontal disease.

A great deal of time has been spent in studying population comparing periodontal conditions between high and low fluoride areas without actually focusing on the destructive effects of fluoride on human periodontium. If we turned our attention to populations susceptible to disease it might be a fruitful area of research in understanding the etiological and pathogenesis of periodontitis, Fluorosis is a boon or a bane to periodontal structures?

Future direction

The study of periodontal status of subjects of natural high water fluoride regions from different parts of India is essential.


   Acknowledgment Top


I sincerely thank Mr. Sangam, biostatistician for his valuable help.

 
   References Top

1.Dean HT, Elvove E. Some epidemiological aspects of chronic endemic dental fluorosis. Am J Public Health 1936;26:567-75.  Back to cited text no. 1    
2.Day M. Chronic endemic fluorosis in Northern India. Br Dent J 1940;68:409-424.  Back to cited text no. 2    
3.Massler M, Schour I. Relation of malnutrition, endemic dental fluorosis and oral hygiene to the prevalence and severity of gingivitis. J Periodontol 1951;22:205-11.  Back to cited text no. 3    
4.Zimmermann ER, Leone NC, Arnold FA. Oral aspects of excessive fluoride in a water supply. J Am Dent Assoc 1955;50:272-7.  Back to cited text no. 4    
5.Haikel Y, Tiirlot JC, Cahen PM, Frank R. Periodontal treatment needs in populations of high-and low-fluoride areas of Morocco. J Clin Periodontol 1989;16:596-600.  Back to cited text no. 5    
6.Russell AL. Fluoride in domestic water and periodontal disease. Am J Public Health 1957;47:688-94.   Back to cited text no. 6  [PUBMED]  
7.Englander HR, Kesel RG, Gupta OP. The effects of natural fluoride on the periodontal health of adults. Am J Public Health 1963;53:1233-42.   Back to cited text no. 7    
8.Green JC, Vermillion JR. The simplified oral hygiene index. J Am Dent Assoc 1964;68:7-13.  Back to cited text no. 8    
9.Murray JJ. Gingivitis and gingival recession in adults from high-fluoride and low fluoride areas. Arch Oral Biol 1972;17:1269-77.  Back to cited text no. 9  [PUBMED]  
10.Reddey J, Parker JP, Africa CW, Stephen LX. Prevalence and severity of periodontitis in a high fluoride area in South Africa. Community Dent Oral Epidemol 1985;13:108-12.  Back to cited text no. 10    
11.Grembowski D, Fiset L, Spadafora A, Milgrom P. Fluoridation Effects on periodontal disease among adults. J Periodont Res 1993;28:166-72.  Back to cited text no. 11  [PUBMED]  
12.Weidmann SM, Wealtherell JA. Flouride and Human Health. WHO: Geneva; 1970.  Back to cited text no. 12    
13.Krook L, Maylin GA, Lillie JH, Wallace RS. Dental flurosis in cattle. Cornell Vet 1983;73:340-62.  Back to cited text no. 13  [PUBMED]  
14.Vazirani SJ, Sing A. Endemic dental fluorosis, radiological features of dental fluorosis. J Indian Dent Assoc 1968;40:299-303.  Back to cited text no. 14    
15.Reddy BD, Mallikarjuna CR, Sarada D. Endemic fluorosis. J Indian Med Assoc 1969; 53:275-81.   Back to cited text no. 15    
16.0 Vandana KL, George P. Comparative evaluation of periodontal changes in fluorosed and nonfluorosed healthy and periodontally diseased teeth by SEM, MDS Thesis. Accepted for publication in "Fluoride", Quarterly Journal of the International Society for Fluoride Research. Rajiv Gandhi University of Health Sciences: Davangere, Karnataka; 2000. p. 68.  Back to cited text no. 16    

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Correspondence Address:
K L Vandana
Department of Periodontics, College of Dental Sciences, Davangere - 577 004, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9290.32423

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    Tables

  [Table - 1], [Table - 2], [Table - 3], [Table - 4]

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