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Professor/Honorary Consultant in Periodontology; Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King's College London
Throughout our lives, we continuously encounter micro-organisms that range from those essential for health, to those causing diseases. The oral cavity is permanently colonized by micro-organisms and our immune system has a challenging role in maintaining oral homeostasis by balancing its responses to this unique microbiota, while preserving the structural integrity of oral tissues. This article discusses relationships between oral microbial community structure and activity, specifically addressing the role of low-abundance microbial species and their interplay with the host immune system, in view of the pathogenesis of dental plaque-induced periodontal conditions.
CPD/Clinical Relevance: The knowledge of periodontal disease pathogenesis is critical for understanding periodontal risk assessment and designing effective, patient-centred treatment options.
Article
Unlike dental caries, which historically developed as a result of emerging civilizations, periodontal diseases are as old as humanity. They also affect wild and domesticated animals and continue to be one of the most prevalent diseases affecting humankind. Ancient Egyptians and the Chinese characterized periodontal diseases as inflammatory conditions, and Hippocrates discussed the aetiology, pathogenesis and treatment options for different forms of gum problems.1 Nowadays, severe periodontitis is the sixth-most prevalent condition worldwide, with an overall prevalence of 10.8% and around 743 million people affected.2 This figure corresponds surprisingly well with the seminal work of Loe et al. in Sri Lankan tea workers, who despite the fact of having high levels of plaque, calculus and gingival inflammation, showed rapid progression of periodontal disease in 8% of cases, while 11% of the examined population were largely free of alveolar bone loss.3 Modern, culture-independent methods have recently been used to characterize the subgingival microbiota of this ‘classical’ cohort of Sri Lankan tea workers, naïve to oral hygiene practices.4 Although significant differences in the overall subgingival microbial compositions were identified between shallow and deep periodontal sites, there was no obvious microbial clustering of the subjects according to their respective clinical progression groups, confirming the important role of the individual host response in the progression of the disease. Interestingly, improvements in plaque control and consequent reduction in mild disease in other cohort studies, did not necessarily result in similar reductions in the prevalence of severe periodontitis.5
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