Clinical course of chronic periodontitis. I. Role of gingivitis

The purpose of this study was to determine the influence of long-standing gingival inflammation on periodontal attachment loss. On the basis of repeated examinations, the present report describes the influence of gingival inflammation on the initiation of periodontitis from 16 to 59 years of age.

The data originated from a 26-year longitudinal study of Norwegian males, who practiced daily oral home care and received state-of-the-art dental care. The initial examination included 565 individuals. Subsequent examinations took place in 1971, 1973, 1975, 1981, 1988 and 1995. Thus, the study covers the age range of 16-59 years. All tooth sites were divided into four categories according to their history of gingival inflammation over the entire observation period: sites always scoring GI = 0, GI = 1 and GI = 2 sites (GI = gingival index). Sites disclosing various GI scores at different observation periods were not considered.

The mean cumulative attachment loss for non-inflamed (GI = 0) sites in individuals approaching 60 years of age was 1.94 mm. Sites always scoring GI = 1 yielded 2.42 mm, and sites that always scored GI = 2 exhibited 3.31 mm of periodontal attachment loss. At interproximal sites of all three groups where gingival trauma was assumed to be minimal or non-existent, only very few sites expressed attachment loss due to gingival recession (2-4%). At interproximal sites always scoring GI = 0, 20% loss of attachment was in the form of pocket formation by 59 years of age. The GI = 1 and the GI = 2 cohorts exhibited attachment loss with pocket formation in 28% and 54%, respectively.

This study has shown that, as men approach 60 years of age, gingival sites that throughout the 26 years of observation bled on probing had approximately 70% more attachment loss than sites that were consistently non-inflamed (GI = 0). Before 40 years of age, there was a slight increase in periodontal attachment loss due to pocket formation, but after this, the frequency increased significantly. Loss of attachment due to gingival recession was very small in all three groups. The fact that sites with non-inflamed gingiva also exhibited some loss of attachment and pocket formation may be explained by fluctuation in the variations of tissue status during long observation intervals combined with the presence of subclinical inflammation.