Descriptive epidemiology deals with the occurrence, the severity and the distribution of diseases, as well as physical and/or mental incapacity, or mortality, in any selected population.
Analytical epidemiology seeks furthermore to discern the cause(s) of a disease. During the comprehensive examination of patients with periodontitis, in addition to the primary etiologic agent—plaque biofilm—other important factors such as heredity, socioeconomic status, behavior patterns, systemic diseases, risk factors as well as ethnic origin should also be ascertained as closely as possible. From this data, one can derive the likely consequences of prophylaxis and treatment, also from a public health standpoint (Albandar & Rams 2002).
In the field of periodontology, epidemiologists deal primarily with the dissemination of and the etiologic factors for gingivitis and periodontitis.
Not all results of the classic epidemiologic studies of the previous decades enjoy unquestioned acceptance today, however. The early studies did not consider all etiologic factors (see above), nor the varying forms of the disease, symptoms of activity and localization of the disease process. Furthermore, many studies did not draw conclusions concerning the treatment needs of the populations under study (AAP 1996).
Epidemiology of Gingivitis
Numerous epidemiologic studies have been performed worldwide, especially in children and adolescents. Their results reveal enormous differences. The morbidity rates (percent affected in the studied population) range from about 50 to almost 100% (Stamm 1986, Schürch et al. 1991, Oliver et al. 1998).
Further, the reported degrees of severity of gingivitis vary greatly among the studies. These differences can be explained primarily by the use of non-standardized examination methods (various indices) and the constantly changing classifications of the diseases themselves. Other etiologic considerations that could explain the large differences include the quite varied status of prevention (plaque control) in the population groups studied, as well as geographic, social and ethnologic factors.
The incidence and severity of gingivitis may even vary in the same patient group with short-term repeated examinations (Suomi et al. 1971, Page 1986). In addition, the degree of severity of gingivitis over the course of one’s life can vary enormously: It achieves its maximum in adolescents reaching puberty, then recedes somewhat, exhibiting a slight tendency to increase in adults as age increases (Stamm 1986, Fig. 178 right).
The existence of gingivitis cannot be taken as evidence that periodontitis will eventually develop (Listgarten et al. 1985, Schürch et al. 1991). The public health significance of gingivitis epidemiology may therefore be called into question.
In studies in which both gingivitis and plaque were considered, a clear positive correlation between oral hygiene and severity of gingivitis emerged (Silness & Löe 1964, Koivuniemi et al. 1980, Hefti et al. 1981).
Epidemiology of Periodontitis
Many new epidemiologic studies of periodontitis have been published from many countries (Ahrens & Bublitz 1987, Fig. 142; Miller at al. 1987; Miyazaki et al. 1991a, b, Fig. 143; Brown & Löe 1993, Fig. 141; Papapanou 1994, 1996; AAP 1996; Oliver et al. 1998). As was the case with gingivitis studies, the results must be carefully interpreted. It is very difficult to compare the results of various studies when different parameters and different measurement techniques were employed without calibration. Up until now, epidemiologic studies, especially of elderly patients, have not even considered the causes of tooth loss all the way to edentulousness (caused by periodontitis?).
Furthermore very little attention has been given to fact that the measured parameters are applicable only to individual sites around individual teeth, and cannot be taken as a generalization, for example as an indication of the loss of tooth-supporting tissues in the entire dentition.
Most epidemiologic studies are really only “momentary” studies of the extent of disease (mean values).
Only Löe et al. (1986) studied the course of attachment loss over many years longitudinally, in a group of Norwegian students and academics on the one hand and tea plantation workers in Sri Lanka on the other hand. They also compared the ethnic and socioeconomic differences between these two very different population groups. The results demonstrated that in the Norwegian group the mean attachment loss in the entire dentition was 0.1 mm per year, while this figure was 0.2–0.3 mm in those subjects examined in Sri Lanka! The molars were most often affected in both groups.
Forms of Periodontitis
Epidemiologic studies rarely differentiate between the rare, early forms of the disease which can progress very rapidly even in young adults (aggressive periodontitis), and the more widespread, usually slowly-progressing chronic periodontitis. True aggressive forms are probably quite rare (2–5% of all cases) in Europe and the USA.
More precise figures are available concerning aggressive, localized periodontitis (formerly: LJP, p. 118): In Europe, about 0.1% of young people are affected, while in Asia and Africa high morbidity rates up to 5% have been reported (Saxen 1980; Saxby 1984, 1987; Kronauer et al. 1986).
Attachment Loss—Studies in the USA
Miller et al. (1987) and Brown & Löe (1993) examined over 15,000 employed persons in the USA, ranging in age from 18 to 80 years. In addition to other parameters, most important in the studies was the measurement of attachment loss. Approximately 76% of all subjects exhibited attachment loss 2 mm or more, but only 7.6% had attachment loss of more than 6 mm. Both studies showed that loss of tooth-supporting tissues increased with age, but contended that periodontitis (and recession) cannot be termed a “disease of the elderly.”
In recent years, the CPITN was used most frequently the world over for epidemiologic studies. During the examination of 11,305 subjects in Hamburg (Fig. 142), the use of this index revealed that only 2.8% were totally periodontally healthy (Code 0) and required no treatment. Nine percent exhibited bleeding on probing (Code 1) and 44% had pocket probing depths up to 5.5 mm (Code 3). These patients required supra- and more importantly subgingival scaling, which could be performed by qualified auxiliary personnel (dental hygienist). Only in 16% of the subjects were probing depths of 6 mm and greater detected (Code 4). These patients required additional complex therapy beyond simple scaling (root planing, surgical procedures) by the dentist. Severe periodontitis (Code 4) increased with age; mild periodontitis was correspondingly less often recorded in elderly patients.
In a literature review of numerous investigations from Europe, the USA and Latin America, Miyazaki et al. (1991 a, b) encountered inconsistent results. Despite significant differences among the various countries, severe forms of periodontitis (CPITN Code 4) were observed at a level of only 10–15%.
One overall conclusion can be drawn: In Europe, the USA and Latin America, gingivitis and mild periodontitis are quite common. Profound manifestations of attachment loss are only observed in ca. 10–15% of these populations.
It is important to note, however, that scored codes or millimeter measurements do not mean that periodontitis is generalized throughout the mouth: A patient is classified as “affected” even if only a single tooth surface of the entire dentition has a single pocket depth measurement of 6 mm, corresponding to Code 4! This fact relegates the published “10–15%” affected rate to a somewhat lower level.
Periodontitis is likely more widely distributed in Asia and Africa compared to the populations described here.