title: The paradox of painless periodontal disease.
abstract: Periodontal diseases, primarily gingivitis and periodontitis, are characterised by progressive inflammation and tissue destruction. However, they are unusual in that they are not also accompanied by the pain commonly seen in other inflammatory conditions. This suggests that interactions between periodontal bacteria and host cells create a unique environment in which the pro-algesic effects of inflammatory mediators and factors released during tissue damage are directly or indirectly inhibited. In this review, we summarise the evidence that periodontal disease is characterised by an accumulation of classically pro-algesic factors from bacteria and host cells. We then discuss several mechanisms by which inflammatory sensitisation of nociceptive fibres could be prevented through inactivation or inhibition of these factors. Further studies are necessary to fully understand the molecular processes underlying the endogenous localised hypoalgesia in human periodontal disease. This knowledge might provide a rational basis to develop future therapeutic interventions, such as host modulation therapies, against a wide variety of other human pain conditions.
authors.affiliation: Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
authors.forename: E
authors.initials: E
authors.lastname: Gaurilcikaite
authors.affiliation: Department of Oral Surgery, Dental Institute, King's College London, London, UK.
authors.forename: T
authors.initials: T
authors.lastname: Renton
authors.affiliation: Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
authors.forename: A D
authors.initials: AD
authors.lastname: Grant
mesh_terms: D005891:Gingivitis / Q000382:microbiology / Q000503:physiopathology*; D006801:Humans; D064307:Microbiota / Q000502:physiology; D010146:Pain / Q000382:microbiology / Q000503:physiopathology*; D010518:Periodontitis / Q000382:microbiology / Q000503:physiopathology*; D010519:Periodontium / Q000294:innervation / Q000382:microbiology / Q000503:physiopathology; D015398:Signal Transduction; D020886:Somatosensory Disorders / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology
keywords: bacteria; inflammation; pain; periodontitis; protease