The multiple protective-barrier functions associated with normal oral mucosa directly affect risk of acute infection. Normal oral mucosa reduces levels of oral microorganisms colonizing the mucosa by shedding the surface layer; it also limits penetration of many compounds into the epithelium by maintaining a chemical barrier. Normal salivary gland function promotes mucosal health.
Oral mucositis can be complicated by infection in the immunocompromised patient. Specific organisms may play a role in upregulating proinflammatory cytokines via bacterial metabolic products such as liposaccharides. Also, oral organisms can disseminate systemically in the setting of ulcerative oral mucositis and profound, prolonged neutropenia.[2,3,4,5]
Many of the medical and scientific terms used in this summary are found in the NCI Dictionary of Genetics Terms. When a linked term is clicked, the definition will appear in a separate window.
Many of the genes described in this summary are found in the Online Mendelian Inheritance in Man (OMIM) database. When OMIM appears after a gene name or the name of a condition, click on OMIM for a link to more information.
There are several hereditary syndromes that involve endocrine or neuroendocrine glands,...
Both indigenous oral flora and hospital-acquired pathogens have been associated with bacteremias and systemic infection. As the absolute neutrophil count falls below 1,000/mm3, incidence and severity of infection rise. Patients with prolonged neutropenia are at higher risk of developing serious infectious complications.[7,8] Compromised salivary function can elevate risk of infection of oral origin.
Other oral sites, including the dentition, periapices, and periodontium, can also become acutely infected during myelosuppression secondary to high-dose chemotherapy.[9,10,11,12] A systematic review of the MEDLINE/PubMed and EMBASE databases for articles published between January 1, 1990, and December 31, 2008, reported (from three studies) that the weighted prevalence of dental infection/abscess during chemotherapy was 5.8% (standard of error, 0.009; 95% confidence interval [CI], 1.8-9.7). Dental management before cytoreductive therapy is initiated can substantially reduce the risk of these infectious complications.[14,15,16]
Changes in infection profiles in myelosuppressed cancer patients have occurred over the past three decades. This evolving epidemiology has been caused by multiple factors, including the use of prophylactic and therapeutic antimicrobial regimens and decreased depth and duration of myelosuppression via growth factor therapy. Gram-positive organisms, including viridans streptococci and Enterococci species, are associated with systemic infection of oral origin. In addition, gram-negative pathogens, including Pseudomonas aeruginosa, Neisseria species, and Escherichia coli, remain of concern.
Myeloablated cancer patients with chronic periodontal disease may develop acute periodontal infections, with associated systemic sequelae.[3,9,10,11,12] Extensive ulceration of sulcular epithelium associated with periodontal disease is not directly observable yet may represent a source of disseminated infection by a wide variety of organisms. Inflammatory signs may be masked by the underlying myelosuppression. Thus, neutropenic mouth care protocols that reduce microbial colonization of the dentition and periodontium are important during myelosuppression. Topical therapy may include the following:
Oral rinses with 0.12% chlorhexidine digluconate.
Irrigation with effervescent (peroxide) agents, which may affect anaerobic bacteria colonizing the periodontal pocket.
Gentle mechanical plaque removal, including dental brushing and flossing.