A New Look at the Etiology and Pathogenesis of Early‐Onset Periodontitis: Cementopathia Revisited

Abstract

For more than 20 years, investigators have unanimously agreed that human periodontitis is caused by bacterial colonization of the surfaces of the teeth and their extension apically. Recently, several investigators have demonstrated that most, if not all, individuals manifesting the early-onset, aggressive forms of periodontitis have abnormalities in their peripheral blood phagocytes which can be detected as abnormal cell motility or adherence. Because of the major role of these cells, especially the neutrophilic granulocytes, in host defense against the microbial onslaught at the gingival sulcus, these leukocyte abnormalities have been considered to be the major determinant of susceptibility to microbial infection and invasion of the periodontal tissues. In recent years the possibility that other etiologies may be involved has not been seriously considered. The purpose of the present communication is to focus attention on the idea that factors other than bacteria and host defense mechanisms may be of significance. We specifically want to call attention to a potentially important role for root cementum.

Cell Attachment Activity of Cementum Proteins and Mechanism of Endotoxin Inhibition

“…However, diseased roots support neither the attachment nor the growth of fibroblasts, and extracts of diseased cementum inhibit fibroblast growth (Fernyhough and Page, 1983;Pitaru and Melcher, 1983;Olson et al, 1985). These data, as well as other studies, indicate that cementum contributes to the repair of periodontal connective tissue and restoration of soft tissue attachment to roots affected by periodontal disease (Lindskog and Bloml6f, 1983;Page and Baab, 1985;Knox and Aukhil, 1988).…”

Analysis of the periodontal microbiota in childhood-type hypophosphatasia

“…PgE2 production might be induced in resident joint cells after deposition of pyrophosphate crystals in joint and bone tissue (Dayer et al, 1987;Girschick et al, 1999a;Schumacher, 1995). PgE2 is a potent pain mediator and can be an effective stimulator of bone demineralization resulting in skeletal and tooth hypomineralisation, cementum hypoplasia, and premature exfoliation of the primary teeth (Bergmann and Schoutens, 1995;Girschick et al, 1999a;Kawaguchi et al, 1995;Page and Baab, 1985;Raisz, 1995;Saito et al, 1991). The clinical severity of the symptoms has been classified into clinical types according to severity and age of onset.…”

“…Periodontitis can be viewed as a disturbance of the microbial ecology resulting in an increase in the number of Gram-negative and anaerobic bacteria. Case reports have described an association between HP and periodontitis (Baab et al, , 1986Page and Baab, 1985;Watanabe et al, 1993). Baab et al (1985Baab et al ( , 1986 reported the presence of putative periodontal pathogens in the subgingival microflora and elevated levels of serum antibodies to the periodontal pathogen Porphyromonas gingivalis in HP patients.…”

Occurrence and appearance of cementum hypoplasias in localized and generalized juvenile periodontitis

“…This finding was in support of Gottlieb's (18) idea that periodontitis was associated with 'cementopathia'. Page & Baab (21) have suggested that several cases in previously published reports of early exfoliation of deciduous teeth and juvenile, prepubertal, and rapidly progressive periodontitis are in fact due to hypophosphatasia and the associated abnormalities in cementum formation. Page & Baab (21) have suggested that several cases in previously published reports of early exfoliation of deciduous teeth and juvenile, prepubertal, and rapidly progressive periodontitis are in fact due to hypophosphatasia and the associated abnormalities in cementum formation.…”