The objective of this report was to determine the radiographic patterns of alveolar bone loss in early-onset periodontitis (EOP) cases in a selected Malaysian population. The radiographs of 55 cases of EOP patients were examined and the radiographic patterns were classified as follows: Type I: bone destruction on first molars and/or incisors only; Type II: bone destruction on first molars and/or incisors and several additional teeth (less than 14 teeth); Type III: generalized bone destruction (greater than 14 teeth), but with involvement noticeably more extensive on the first molars and/or incisors; Type IV: generalized bone destruction (greater than 14 teeth), but with no more bone loss on the first molars and/or incisors than on other involved teeth. Sex, age, and missing teeth were also recorded. Out of 55 cases, 47 cases, 22 males and 25 females, were classified into the types mentioned above; the remaining 8 cases were excluded due to too many missing teeth. It was found that 7 (14.9%) were Type I; 12 (25.5%) were Type II; 7 (14.9%) were Type III; and 21 (44.7%) were Type IV. There was a predominance of first molar/incisor involvement in Types I, II, and III with the maxillary first molars most frequently involved followed by the mandibular central incisors. Type I occurred in the younger age group and Types II, III, and IV mainly in the older age group. It was concluded that EOP in this patient sample resembled that of western society.
Studies to elucidate the role of genetics as a risk factor for periodontal disease have gone through various phases. In the majority of cases, the initial 'hypothesis-dependent' candidate-gene polymorphism studies did not report valid genetic risk loci. Following a large-scale replication study, these initially positive results are believed to be caused by type 1 errors. However, susceptibility genes, such as CDKN2BAS (Cyclin Dependend KiNase 2B AntiSense RNA; alias ANRIL [ANtisense Rna In the Ink locus]), glycosyltransferase 6 domain containing 1 (GLT6D1) and cyclooxygenase 2 (COX2), have been reported as conclusive risk loci of periodontitis. The search for genetic risk factors accelerated with the advent of 'hypothesis-free' genome-wide association studies (GWAS). However, despite many different GWAS being performed for almost all human diseases, only three GWAS on periodontitis have been published - one reported genome-wide association of GLT6D1 with aggressive periodontitis (a severe phenotype of periodontitis), whereas the remaining two, which were performed on patients with chronic periodontitis, were not able to find significant associations. This review discusses the problems faced and the lessons learned from the search for genetic risk variants of periodontitis. Current and future strategies for identifying genetic variance in periodontitis, and the importance of planning a well-designed genetic study with large and sufficiently powered case-control samples of severe phenotypes, are also discussed.