“This aim of this document is to provide health professionals, especially cardiologists and periodontists, a better
understanding of the link between atherosclerotic CVD and periodontitis and, on the basis of current information, an
approach to reducing the risk for primary and secondary atherosclerotic CVD events in patients with periodontitis.”
Porphyromonas gingivalis (Pg), a Gram-negative anaerobic black-pigmented rod bacterium, has been recognized as the most potent etiologic bacte-rium in human chronic periodontitis. It possesses a variety of putative virulence factors providing both tissue destruction and host evasion including lipopolysac-charides (LPS), fi mbriae, various proteinases, etc. These factors actively participate in periodontal tissue destruction. However, recent evidence suggests that Pg has also evolved mechanisms to inhibit or confuse host immune systems. Thus, Pg is suggested to behave not only like an “active invader”, but also like a “stealth element” in periodontal lesions. In the present study, repeated exposure of Pg components induced tolerance resulting in selective inhibition of cytokine produc-tion of both monocytes and gingival fi broblasts in a different fashion from that described for LPS in Escherichia coli. It was also revealed that Pg LPS induced a unique dendritic cell subset with a CD14+CD16+ phenotype that exhibited weak maturation. In animal studies, administration of live Pg or its LPS exerted a regula-tory effect on systemic markers such as triglycerides or adiponectin. Taken together, these fi ndings suggest that Pg may be able to adapt to the local immune defense, contributing to the connection between systemic and periodontal disease.
Bacterial sampling of prepared root canals is used to determine the presence and character of the remaining microbiota. However, it is likely that current sampling techniques only identify organisms in the main branches of the root canal system whereas it is unlikely that they can sample areas beyond the apical end-point of preparation and filling, or in lateral canals, canal extensions, apical ramifications, isthmuses and within dentinal tubules. Thus, it may be impossible by current techniques to identify residual post-treatment root canal infection. In histologic observations of root apices, bacteria have been found in inaccessible inter-canal isthmuses and accessory canals often in the form of biofilms. There is no in vivo evidence to support the assumption that these bacteria can be entombed effectively in the canal system by the root filling and thus be rendered harmless. As a consequence of this residual root infection, post-treatment apical periodontitis, which may be radiographically undetectable, may persist or develop as a defence mechanism to prevent the systemic spread of bacteria and/or their byproducts to other sites of the body. Histologic observation of root apices with surrounding bone removed from either patients or human cadavers has demonstrated that post-treatment apical periodontitis is associated with 50–90% of root filled human teeth. Thus, if the objective of root canal treatment is to eliminate apical periodontitis at a histological level, current treatment procedures are inadequate. It is essential that our knowledge of the local and systemic consequences of both residual post-treatment root infection and post-treatment apical periodontitis be improved. The continued development of treatments that can effectively eliminate root infection is therefore a priority in clinical endodontic research. Post-treatment disease following root canal treatment is most often associated with poor quality procedures that do not remove intra-canal infection; this scenario can be corrected via a nonsurgical approach. However, infection remaining in the inaccessible apical areas, extraradicular infection including apically extruded dentine debris with bacteria present in dentinal tubules, true radicular cysts, and foreign body reactions require a surgical intervention.
This position paper addresses the role of supra- and subgingival irrigation in the treatment of periodontal diseases. It was prepared by the Committee on Research, Science and Therapy of the American Academy of Periodontology. The document is divided into two portions, consisting of supragingival irrigation and subgingival irrigation. In their respective segments, these treatment techniques are assessed as monotherapies and as adjuncts to conventional treatment. The conclusions drawn in this paper represent the position of the American Academy of Periodontology regarding irrigation therapy in the treatment of periodontal diseases.
“This chapter summarizes evidence that links herpesviruses, especially HCMV and EBV, to the development of severe types of periodontitis, and outlines potential mechanisms by which herpesviruses may contribute to periodontal tissue breakdown. It is suggested that the coexistence of periodontal HCMV, EBV and possibly other viruses, periodontopathic bacteria, and local host immune responses should be viewed as a precarious balance that has the potential to lead to periodontal destruction.”
Erdheim-Chester disease is a rare systemic lipogranulomatous disorder of adults that shares some histopathologic features similar to Langerhans’ cell histiocytosis and that results in characteristic radiographic changes in the long bones. Relatively few cases have been reported in the jaws. We present a literature review of jaw cases and the first case report to describe detailed radiographic and pathologic features of jaw involvement, as well as clinical, radiographic, and histopathologic follow-up of the untreated jaw lesions.
Recently, it has been recognized that oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight. The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases. Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed: (i) metastatic spread of infection from the oral cavity as a result of transient bacteremia, (ii) metastatic injury from the effects of circulating oral microbial toxins, and (iii) metastatic inflammation caused by immunological injury induced by oral microorganisms. Periodontitis as a major oral infection may affect the host’s susceptibility to systemic disease in three ways: by shared risk factors; subgingival biofilms acting as reservoirs of gram-negative bacteria; and the periodontium acting as a reservoir of inflammatory mediators. Proposed evidence and mechanisms of the above odontogenic systemic diseases are given.
“Recently, it has been recognized that oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight. The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases. Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed: (i) metastatic spread of infection from the oral cavity as a result of transient bacteremia, (ii) metastatic injury from the effects of circulating oral microbial toxins, and (iii) metastatic inflammation caused by immunological injury induced by oral microorganisms. Periodontitis as a major oral infection may affect the host’s susceptibility to systemic disease in three ways: by shared risk factors; subgingival biofilms acting as reservoirs of gram-negative bacteria; and the periodontium acting as a reservoir of inflammatory mediators. Proposed evidence and mechanisms of the above odontogenic systemic diseases are given.”
Ischemic osteonecrosis (10) is not so much a disease in its own right as it is the natural consequence of a wide variety of systemic and local factors capable of compromising marrow blood flow (Table 1).1,9 It is the condition for which the term cavitation was coined in the orthopedic literature, and it is one of a select group of interrelated diseases able to deterio·rate and hollow out medullary spaces (Fig 1)1.10: First described in 1794 in a case of septic necrosis of the femoral head, this enigmatic disease is as old as the dinosaurs, but it has been poorly understood and has such subtle radiographic changes that until recently it was seldom diagnosed before end-stage damage. 1 ).13 Contemporary research has so enhanced our understanding of its basic pathophysiology that it now bears little resemblance to the entity once known as “aseptic osteomyelitis.”
In most countries, coronary heart disease is one of the leading causes of morbidity and death. This report reviews the current evidence indicating that oral conditions (specifically periodontitis) may be a risk factor for atherosclerosis and its clinical manifestations and provides new preliminary data. This review is done in the context of the research indicating that inflammation plays a central role in atherogenesis and that there is a substantial systemic microbial and inflammatory burden associated with periodontal disease. Our review concentrates on 5 longitudinal studies that show oral conditions being associated with the onset of coronary heart disease while controlling for a variety of established coronary heart disease risk factors. In addition to published evidence, preliminary findings from our Dental Atherosclerosis Risk in Communities study also indicate that periodontal disease is associated with carotid intimal-medial wall thickness, a measure of subclinical atherosclerosis, adjusting for factors known to be associated with both conditions.