Comparison of the clinical features of chronic and aggressive periodontitis

In the late 1800s, what is now known as chronic periodontitis was clinically characterized as a slowly progressive destruction of the periodontium due to the accumulation of lime deposits on the teeth (21), or calcic inflammation of the peridental membrane secondary to deposits of salivary and ⁄ or serumal calculus (13). The calcified deposits were considered to be mechanical irritants that led to gingival recession and a generalized or even pattern of bone loss (13, 21). Throughout most of the 20th century, this form of periodontitis has been considered an inflammatory disease associated with local irritants and the formation of dental plaque (biofilms) on tooth surfaces (4). This concept prevails today. What is now known as generalized aggressive periodontitis was not clearly described until the latter part of the 20th century. However, G.V. Black used the terms phagedenic pericementitis and chronic suppurative pericementitis to describe patients who suffered from a rapid destruction of alveolar bone (14). In the past three decades, authors have used a variety of terms for cases in which there is generalized severe periodontal destruction in young patients, including generalized juvenile (16, 94), rapidly progressive (46, 64), or simply severe periodontitis (18). In most respects, the disease clinically resembles chronic periodontitis except the affected individuals are much younger and the rate of progression is assumed to be rapid since there is extensive periodontal damage in a young person. Current views regarding the major characteristics of localized aggressive periodontitis have been considerably influenced by historical perspectives of the disease. In a series of papers from 1920 to 1928, Bernard Gottlieb of the University of Vienna School of Medicine described an unusual form of periodontal disease that primarily affected some or all of the permanent incisors and first molars of young individuals (29–33). Based on certain histological observations such as thin cementum on extracted teeth from affected sites, he believed that the disease was due to defective deposition of cementum or cementopathia (32–34). Gottlieb applied the principles of classical pathology as they were practiced in the 1920s, which stated that all human non-neoplastic diseases could be classified as either inflammatory or non-inflammatory (4). Since his adolescent patients did not exhibit the intense gingival inflammation ordinarily seen in other patients (i.e. adults) with periodontitis, he believed that the disease was a non-inflammatory or degenerative condition. It was claimed that initial stages of the disease were not associated with local irritants such as dental plaque or calculus, and therefore the disease was subsequently referred to as diffuse atrophy of the alveolar bone or periodontosis (34, 63). According to this hypothesis, the alveolar bone degenerated and the teeth drifted apart or migrated without the formation of periodontal pockets (90). Since it was thought that continuous deposition of cementum was required in order to prevent the apical migration of epithelium along the root surface, pockets formed at sites that were supposedly afflicted with cementopathia. As a secondary phenomenon, once a pocket formed, it became susceptible to colonization by oral bacteria and was ...a potential trap for accumulating deposits from saliva (63). In the final stage of the disease, bacterial toxins and other irritants eventually caused some inflammation, which contributed to additional loss of bone and connective tissue attachment to the