CLINICAL FEATURES OF EARLY-ONSET PERIODONTITIS

CLINICAL FEATURES OF EARLY-ONSET PERIODONTITIS

ARTICLE1 1 CLINICAL FEATURES OF EARLY-ONSET PERIODONTITIS JASIM M. ALBANDAR, D.D.S., PH.D.; L. JACKSON BROWN, D.D.S., PH.D.; HARALD LOE, D.D.S. The ...

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ARTICLE1 1

CLINICAL FEATURES OF EARLY-ONSET PERIODONTITIS JASIM M. ALBANDAR, D.D.S., PH.D.; L. JACKSON BROWN, D.D.S., PH.D.; HARALD LOE, D.D.S.

The authors estimate the prevalence of early-onset periodonti-

tis, or EOP, in U.S. adolescents and describe the clinical features that occur at an early

stage in those who have EOP. In 1986 and 1987, about 10.0 percent of African-American, 5.0

percent of Hispanic and 1.3 percent of white U.S. adolescents

had EOP. Clinical features that may be useful in the early detection of EOP include overt gingival inflammation, dental calculus and a high rate of caries, restorations and tooth loss.

Qarly-onset periodontitis, or EOP, is a destructive disease that develops in children, adolescents and young adults. EOP occurs in three forms: localized, generalized and incidental.' In the United States, about 300,000 14- to 17-year-old adolescents are affected.2 One characteristic of this disease is the rapid progression of attachment loss, as shown by increased attachment loss in affected teeth and increased numbers of affected teeth over time.3 Without successful treatment, EOP may result in a pronounced loss of teeth.4 Early detection can facilitate the successful management of EOP. Although much work is currently directed at developing biochemical and microbiological assays for this disease, there are currently no reliable chairside methods for detecting EOP at an early stage. Currently, early detection depends primarily on clinical and radiographic examination methods. In this report, we assess the prevalence of EOP in U.S. adolescents and describe some clinical features that can help clinicians identify patients who are at a higher risk of developing this disease. SUBJECTS AND METHODS

Study design. We conducted a national survey during the 19861987 school year, using a multistage probability sample of U.S. schoolchildren. We studied students ages 13 to 17 years who were in grades eight through 12 in public and private schools clustered within 174 school districts. We screened a total of 14,013 students for their oral and periodontal health. Twelve dentists, who were trained by the National Institute of Dental Research, or NIDR, and contractor staff from Westat, a survey research firm, performed the clinical examinations. Clinical examinations. The examiners assessed attachment loss at the mesiobuccal and midbuccal surfaces of all permanent teeth, excluding third molars. They used the NIDR periodontal JADA, Vol. 128, October 1997 1393

-D ES RESEARCH

0 3.2 | 1 2.3;

| 11 10.2 d: 0.2

t 1t1 1

_

| 11 | _0 ;0.50 ;_ e _

_

~~'~~'ui~~~ Figure 1. Percentage of U.S. adolescents with early-onset periodontitis in 1988-1987, by age group and classification group.

probe (a 2-millimeter yellowand-black-banded probe) and rounded the measurements to the lowest whole millimeter. They also considered the presence or absence of gingival bleeding on gentle probing at the same sites and assessed subgingival calculus with the NIDR probe or the No. 17 explorer. The examiners identified subgingival calculus as calcified deposits on the root surface that extend greater than 1 mm below the gingival margin. They also examined the subjects for caries and dental restorations in their permanent dentition.5 Classification of earlyonset periodontitis. We defined subjects with periodontal attachment loss of 3 mm or greater in one or more teeth as having EOP. Then we divided these subjects into three EOP

groups-localized, generalized and incidental-based on the extent and severity of the at-

g

~ Mm; XJ¾KA

Figure 2. Percentage of sites with gingival bleeding and with subgingival calculus, by classification group.

1394 JADA, Vol. 128, October 1997

tachment loss. Subjects in the localized group had EOP that affected primarily the incisors and first molars. The subjects had attachment loss of 3 mm or greater in four or more teeth including two or fewer canines, premolars and second molars. Subjects in the generalized group had EOP that affected several teeth, including more than two canines, premolars and second molars. The generalized EOP group also included subjects who exhibited attachment loss and a generalized tooth loss. The incidental EOP group included subjects who did not meet the criteria of localized or generalized EOP and had one or more teeth with attachment loss. The subjects in this

group

typically had one to three teeth

RESEADCI with attachment loss and three or fewer missing teeth. If the subjects

had

no

teeth with at-

tachment loss of 3 mm or greater, they were included in no-periodontitis,

the

or control, description of

group. A detailed

the classification criteria is published in another

study.'

We compared the subjects in localized, generalized and

the

0.23*

incidental EOP groups with

subjects

the

in the

titis group with presence of

and the

no-periodon-

regard

to the

gingival bleeding

subgingival calculus and frequency of missing, de-

cayed

or

0.06*

filled teeth. We also

compared

the

prevalence

EOP in the 13- to

of

15-year-old

subjects with that of the

16- to

17-year-old subjects. We performed the

comparison

the classification analysis

among

groups

using

of variance for unbal-

anced data. All estimates were based on data weighted to represent the U.S. population of these ages.

Figure 3. Number of extracted teeth resulting from dental disease, by

classification group and tooth type.

RESULTS

We found that the prevalence of EOP among U.S. adolescents from 1986 to 1987 varied considerably by race and ethnicity. White adolescents had the lowest level of

EOP;

0.05 percent,

0.01 percent and 1.20 percent of the

7.5

subjects showed general-

ized, localized and incidental forms of EOP,

respectively. and Hispanic

African-American adolescents had valence of

a higher preperiodontitis. Among

African-American adolescents, 1.6 percent, 1.0

percent and 7.5

percent of the subjects showed

generalized, localized and incidental EOP, respectively. H a Among Hispanic adolescents, 0.3

percent,

0.2

percent

and

MM

4.4

percent of the subjects showed

generalized, localized and inci-

Figure 4. Number of carious

or

filled surfaces, by classification group.

JADA, Vol. 128, October 1997 1395

[SIAR CHI

Figure 5. Localized early-onset periodontitis in a 13-year-old white girl.

I

I

I Figure 6. Generalized early-onset periodontitis

dental EOP, respectively. We found that slightly more males (3.7 percent) had EOP than females (3.0 percent). The prevalence of EOP was higher in the older age group, with 2.7 percent of 13- to 15year-old subjects and 4.0 percent of 16- to 17-year-old subjects being affected by EOP (Figure 1). In addition, the increase in the prevalence of subjects with EOP between the two age groups was higher in the generalized form (2.5 times, or from 0.2 to 0.5 percent) than in the localized form (1.5 times, or from 0.2 to 0.3 percent) or the incidental form (1.4 times, or from 2.3 to 3.2 percent). This evidence suggests that EOP is age-dependent and may begin at or after ages 12 to 13 years. We found significantly higher percentages of sites showing 1396 JADA, Vol. 128, October 1997

In an

African-American boy.

gingival bleeding in the generalized (P < .0001), localized (P < .0001) and incidental (P < .0001) EOP groups as compared with the no-periodontitis group (Figure 2). Furthermore, we found that subjects with generalized or localized EOP had significantly more sites showing gingival bleeding than those subjects with incidental EOP. Similarly, subjects with EOP had significantly higher percentages of sites with subgingival calculus than subjects with no periodontitis (P < .0001). Subjects with generalized and localized EOP had the highest percentages of sites with subgingival calculus (Figure 2). We found that the number of teeth extracted as a result of dental disease was significantly higher in the generalized (P .002), localized (P < .0001) and inciden<

tal (P < .0001) groups as compared with the no-periodontitis group (Figure 3). The subjects with EOP had a mean of 0.24 extracted teeth, but the subjects with no periodontitis had a mean of 0.06 extracted teeth (P < .001). We found that the subjects with EOP had noticeable caries. We found an average of 7.7 surfaces showing untreated caries or fillings. The subjects in the no-periodontitis group had 5.8 surfaces with untreated caries or fillings (P < .0001). We found that subjects with generalized or incidental EOP had a significantly higher number of surfaces with untreated caries or fillings than the subjects in the no-periodontitis group (P < .0001). However, the difference between the localized group and the no-periodontitis group was

RESEADCHI Clearly, there are subpopulations with higher and lower occurrences of EOP than the national average. One subpopulation with a higher prevalence of EOP than the national average is San Antonio. A study reported that 26 percent of the subjects in a group of Hispanic adolescents from San Antonio had EOP.'3 In our study, we assessed attachment loss at only two sites per tooth, the mesiobuccal and midbuccal surfaces. The systematic bias of using this measurement protocol has been assessed in this population. When we compared our measurement protocol to a measurement protocol that assesses six sites per tooth, our estimates indicated that our two-site protocol underestimated the prevalence of attachment loss in this population by 26 percent.'4 Another potential source of error in assessing the prevalence of EOP in our sample is

not statistically significant

(Figure 4). DISCUSSION

This study reports the prevalence of EOP in a representative national sample of U.S. adolescents and outlines some clinical features of this disease to help dentists manage periodontal problems in adolescents and young adults. The findings show that EOP occurs with a relatively high prevalence in African-American and Hispanic adolescents and with a relatively low prevalence in white adolescents. This is consistent with the findings of other studies that found a low prevalence of EOP in white adolescents,6-9 and a high frequency of occurrence in adolescents of African descent7',0 and in South American adolescents.

11,12

Our study sample showed the occurrence of EOP in 13- to 17-year-old U.S. adolescents in the mid-1980s. Our estimates show that about 10.0 percent of African-American, 5.0 percent of Hispanic and 1.3 percent of white adolescents had EOP. These estimated averages are based on data for the whole nation.

the bias caused by selecting a threshold of attachment loss of 3 mm or greater. Although this was necessary because of the relatively high error margin inherent in the clinical measurement of attachment loss, some false-negative sites (having a true attachment loss of less than 3 mm) were probably missed. Because of our estimated underestimation, the true prevalence in this population should be inflated by a factor of 0.33 percent. Accordingly, the true prevalence of EOP in 13to 17-year-olds using a threshold of attachment loss of 3 mm or greater would be 13.3 percent of African-American adolescents, 6.65 percent of Hispanic adolescents and 1.73 percent of white adolescents. Hence, the prevalence of EOP is expected to be generally higher than the figures we report in this study. Our study showed that adolescents with EOP have a high

A.

Figure 7. A case of localized earlyonset periodontitis, or EOP, in a 14-year-old white girl (A), progressing to generalized EOP and affecting most of her teeth eight years later (B).

B.

~~I I

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RE[S[ARCH prevalence of gingival bleeding and subgingival calculus, and that the strength of the association between these two parameters and EOP appears to be attenuated by ethnicity. The occurrence of gingival bleeding and subgingival calculus is highest among Hispanic adolescents, somewhat lower in African-American adolescents and lowest in white adolescents.15 This is consistent with other reports of heavy accumulations of dental plaque and calculus, plus a high prevalence of gingival inflammation, in Hispanic adolescents.'3 It has been suggested that adolescents with juvenile periodontitis have little gingival inflammation and dental calculus.'6 This, however, was not supported by our findings, which showed that in subjects with localized or generalized EOP, 21.1 percent to 24.5 percent of the sites exhibited gingival bleeding and 36.2 percent to 39.8 percent of the sites exhibited subgingival calculus. In comparison, in subjects with no periodontitis 5.5 percent of the sites had gingival bleeding and 3.9 percent of the sites had subgingival calculus. Similar findings have been reported in another study that compared these parameters between a group of subjects with juvenile periodontitis and a control group of subjects without juvenile periodontitis.17 Subjects with EOP had more dental caries and tooth loss as compared with subjects with no periodontitis. Subjects with localized EOP had more tooth loss and less untreated caries than subjects with other forms of EOP. This finding is probably the result of the clinical criteria used to classify EOP. Our pres1398 JADA, Vol. 128, October 1997

ent findings (Figure 2) and our previously reported results3 indicate that localized and generalized EOP are similar and that they are distinctively different from incidental EOP. We found that the subjects' sex did not have a significant effect on the occurrence of EOP. However, males had a slightly higher rate of occurrence than females. Representative cases. For illustrative purposes, we are presenting radiographs of three representative cases of adolescents with EOP. The first set of radiographs was taken of a 13-year-old white girl with localized EOP (Figure 5). The second set of radio-

I

Early-onset penodonthis is a destructive disease that, if left untreated, may progress rapidly, causing pronounced tooth

loss.

graphs was taken of an African-American boy with generalized EOP affecting most of his teeth (Figure 6). The third set of radiographs (Figures 7A and 7B) was taken of a white girl who experienced a rapid progression of EOP. At 14 years of age, she was diagnosed with localized EOP affecting the incisors, first molars and one second molar (Figure 7A). When we examined her eight years later, radiographs showed extensive loss of alveolar bone affecting most of her teeth (Figure 7B). This rapid progression of attachment loss and a high incidence of tooth loss over time

have been described in other studies.34"8 This case stresses the importance of early identification and treatment of affected subjects. CONCLUSION

EOP is a destructive disease that affects about 10 percent of African-American, 5 percent of Hispanic and 1.3 percent of white U.S. adolescents between 13 and 17 years of age. If left untreated, EOP may progress rapidly, causing pronounced tooth loss. There are currently no reliable chairside laboratory assays that can be used to detect EOP at its early stage. Therefore, dental professionals should rely on clinical and radiographic criteria of the disease for early identification of patients at risk. These criteria usually include loss of periodontal attachment and alveolar bone support of teeth, which is commonly disclosed through the use of the periodontal probe and dental radiographs. Other clinical features that may alert dentists include African-American or Hispanic adolescents with generalized overt gingival inflammation, dental calculus and a high level of caries, restorations and tooth loss. Dentists should watch patients with most or all of these features for early signs of periodontal attachment loss. . Dr. Brown is senior director, Health Policy Resource Center, American Dental Association, Chicago. Dr. L6e is a professor, School of Dental Medicine, University of Connecticut Health Center, Farmington. The authors thank Dr. John A. Burmeister, Virginia Commonwealth University Clinical Research Center for Periodontal Diseases, Richmond, Va., for providing the radiographs in Figures 5 and 6.

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Dr. Albandar Is a professor of perio-

dontology, Dental Faculty, University of Bergen, Norway, and Is a visMng sclentist, Natlonal Institute of Dental Research, National Institutes of Health, Natcher Building, Room 4AS-19B, 45 Center Drive, Bethesda, Md. 2089248401. Address reprint requests to Dr. Albandar.

J Periodontol 1996;67:960-7. 5. National Institute of Dental Research. Oral health surveys of the National Institute of Dental Research: diagnostic criteria and procedures. Bethesda, Md.: DHHS, National Institutes of Health, 1991; publication no. 912870. 6. Saxen L. Prevalence ofjuvenile periodontitis in Finland. J Clin Periodontol

1980;7:177-86.

7. Saxby MS. Prevalence ofjuvenile periodontitis in a British school population. Community Dent Oral Epidemiol

1984;12:185-7.

8. Kronauer E, Borsa G, Lang NP. Prevalence of incipient juvenile periodontitis at age 16 years in Switzerland. J Clin Periodontol 1986;13:103-8. 9. Aass AM, Albandar JM, Aasenden R, Tollefsen T, Gjermo P. Variation in prevalence of radiographic alveolar bone loss in subgroups of 14-year-old schoolchildren in Oslo. J Clin Periodontol 1988;15:130-3. 10. MacGregor ID. Radiographic survey of periodontal disease in 264 adolescent schoolboys in Lagos, Nigeria. Community Dent Oral

Epidemiol 1980;8:56-60. 11. Albandar JM, Buischi YA, Barbosa MF.

Destructive forms of periodontal disease in

adolescents: a 3-year longitudinal study. J Periodontol 1991;62:370-6. 12. Lopez NJ, Rios V, Pareja MA, Fernandez 0. Prevalence of juvenile periodontitis in Chile. J Clin Periodontol 1991;18:529-33. 13. Cappelli DP, Ebersole JL, Kornman KS. Early-onset periodontitis in HispanicAmerican adolescents associated with A. actinomycetemcomitans. Community Dent Oral

Epidemiol 1994;22:116-21. 14. Kingman A, Albandar JM. Validity of partial recording of attachment loss in earlyonset periodontitis (Abstract no. 1722). J Dent Res (Special Issue): 1997;76:229. 15. Albandar JM, Brown LJ, Brunelle JA, Loe H. Gingival state and dental calculus in early-onset periodontitis. J Periodontol 1996;67:953-9. 16. Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971;42:516-9. 17. Albandar JM. Juvenile periodontitispattern of progression and relationship to clinical periodontal parameters. Community Dent Oral Epidemiol 1993;21:185-9. 18. Gunsolley JC, Califano JV, Koertge TE, Burmeister JA, Cooper LC, Schenkein HA. Longitudinal assessment of early onset periodontitis. J Periodontol 1995;66:321-8.

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