Juvenile periodontitis.

Our knowledge of juvenile periodontitis is still fragmentary. In 50 years we have advanced from the concept of diffuse atrophy of the alveolar bone (Gottlieb 1923) through the theory of non-inflammatory, degenerative disease of the periodontium (Orban & Weinmann 1942) to the present conception of juvenile periodontitis (Manson & Lehner 1974, Waerhaug 1977a) as a periodontal disease appearing in young individuals with inflammation always present. Only the clinical picture of the disease is quite clear as Baer described it (1971): rapid destruction of the alveolar bone, not commensurate with the local irritants, around more than one permanent tooth in otherwise healthy adolescents. The etiology and etiopathogenesis of juvenile periodontitis have remained unknown. The bacteriological findings of Scransky et al. (1970) and Newman et al. (1974), suggesting some Gram-negative rods as an etiological factor, are still controversial. Neither is the theory of Lehner and his coworkers (1974), that juvenile periodontitis is a selective, cell-mediated immunodeficiency condition, fully accepted. Heredity is an etiologic factor for which there is more evidence. Several authors have found a familial pattern of the disease and it might be either an autosomal, recessive trait (Fourel 1972, Jorgenson et al. 1975) or an X-linked dominant disease (Melnick et al. 1976). These two statements are, however, also controversial. The prevalence rates vary from 0.1% to 17.6%. Although there could be racial variations, the estimated prevalence rates also vary within racial groups, suggesting that there must be great variations in methods and diagnostics. Juvenile periodontitis seems to exist in all racial groups throughout the world and although comparable prevalence figures are difficult to obtain, it seems that the disease is less common in Caucasoid populations and more frequent in India and Africa. The claim of female preponderence requires further investigation.