Learned and unlearned concepts in periodontal diagnostics: a 50‐year perspective

Abstract

In the past 50 years, conceptual changes in the field of periodontal diagnostics have paralleled those associated with a better scientific understanding of the full spectrum of processes that affect periodontal health and disease. Fifty years ago, concepts regarding the diagnosis of periodontal diseases followed the classical pathology paradigm. It was believed that the two basic forms of destructive periodontal disease were chronic inflammatory periodontitis and 'periodontosis'- a degenerative condition. In the subsequent 25 years it was shown that periodontosis was an infection. By 1987, major new concepts regarding the diagnosis and pathogenesis of periodontitis included: (i) all cases of untreated gingivitis do not inevitably progress to periodontitis; (ii) progression of untreated periodontitis is often episodic; (iii) some sites with untreated periodontitis do not progress; (iv) a rather small population of specific bacteria ('periodontal pathogens') appear to be the main etiologic agents of chronic inflammatory periodontitis; and (v) tissue damage in periodontitis is primarily caused by inflammatory and immunologic host responses to infecting agents. The concepts that were in place by 1987 are still largely intact in 2012. However, in the decades to come, it is likely that new information on the human microbiome will change our current concepts concerning the prevention, diagnosis and treatment of periodontal diseases.

Familial periodontal disease in the cayo santiago rhesus macaques

“…The net outcome of periodontal disease extent and severity appears dependent upon the characteristics of the oral microbial ecology. These include colonization/emergence of some opportunistic pathogens that appear to alter the local environment affecting the overall microbiome attributes and burden, and act in concert with host responses that are regulated by genetics and modified by the environment in humans [Kinane and Bartold, 2007; Hajishengallis et al, 2012; Armitage, 2013; Ebersole et al, 2013; Wade, 2013; Kornman and Polverini, 2014; Duran-Pinedo et al, 2014]. Since descendants of each of these matrilines still exist within the population and preliminary data suggests an increased risk of demonstrating periodontitis in living animals within the 065 matriline.…”

Differential Gene Expression Profiles Reflecting Macrophage Polarization in Aging and Periodontitis Gingival Tissues

“…Chronic infection of the subgingival sulcus with complex microbial biofilms containing putative periodontopathogens results in a persistent inflammatory response that results in collateral destruction of both soft tissues (gingiva, periodontal ligament, connective) and hard tissues (alveolar bone) (Armitage, 2013). Substantial evidence has documented associations of disease with specific species of bacteria in these pathogenic biofilms (Wade, 2013) and has determined an array of innate immune, inflammatory, and adaptive immune responses that are triggered by these bacteria (Hajishengallis, 2014, Souza and Lerner, 2013).…”

Epidemiología de las Enfermedades Periodontales en el Uruguay. Pasado y presente

“…They were considered degenerative since they showed excessive clinical symptoms but with a small number of local irritants (43,44) .…”

“…In turn, sites with attachment loss lower than 2mm were found mainly in younger people (<20 years and 20 -29 years) and 4% were in the group aged >60. In addition, attachment loss >6mm increased noticeably from 1.8% (<20 years) to 44.3% (>60 years) (36) .…”