Other periodontal diseases

Acute, or exaggerated, forms of gingivitis can arise due to a variety of predisposing factors or circumstances including HIV infection, diabetes, pregnancy, puberty, menstruation, stress, or the use of oral contraceptives.

Pregnancy gingivitis
The exaggerated gingivitis seen in pregnancy is linked to an increase in the proportions of the black-pigmented anaerobe, P. intermedia, during the second trimester, possibly due to the increased levels of steroid hormones in GCF.

Acute streptococcal gingivitis

This condition affects the gingivae which can result in severe illness. The gingivae become red, swollen and full of fluid (oedematous), the temperature is raised and the regional lymph nodes are also enlarged. Lancefield Group A streptococci (S. pyogenes) can be isolated from the affected gingivae. This disease is usually preceded by a sore throat and hence it is possible that there is a direct spread of S. pyogenes from throat to gingivae.

Acute herpetic gingivitis

The majority of infectious cases of gingivitis are bacterial in origin but occasionally viral gingivitis is seen, predominantly in young people. The commonest form is acute herpetic gingivitis, the causative agent of which is Herpes simplex type 1 (HSV-1). Acute herpetic gingivitis is seen usually in children and appears as ulcerated swellings of the gingivae which are acutely painful. The symptoms may persist for 7 to 21 days and herpetic lesions may concomitantly be present on lips or any area of the oral mucosa. The diagnosis is usually made on clinical criteria although cytological smears and cytopathic effects following culture have been used for confirmation; direct immunofluorescence is also used for diagnosis. Antiviral agents (e.g. acyclovir and penciclovir) can be effective treatments.

Diabetes mellitus-associated gingivitis

The relationship between diabetes and periodontal disease may be bi-directional. Both conditions stimulate the release of pro-inflammatory cytokines that have a direct effect on the periodontal tissues. In general, patients with diabetes have more severe episodes of gingivitis compared with healthy controls, especially in younger subjects whose condition is poorly controlled. Many of the host response traits that confer susceptibility in periodontal disease in otherwise healthy individuals are exaggerated in diabetics. Susceptibility traits include neutrophil dysfunction, altered cross-linking and glycosylation of collagen, defective secretion of growth factors and subsequent impaired healing. Diseased sites have higher proportions of Capnocytophaga, and other periodontal pathogens including P. gingivalis and spirochaetes. Sometimes, non-oral bacteria (e.g.

staphylococci) have been isolated. These changes in microflora may reflect a compromised host defence. Periodontal disease may increase insulin resistance in diabetic patients. Periodontal pathogens may raise pro-inflammatory mediators that result in insulin resistance and an increase in blood glucose, thereby predisposing individuals to develop type 2 diabetes. Mechanical treatment of periodontitis, when combined with antimicrobial agents, can improve glycaemic control.

HIV-associated periodontal disease

The impaired immune response in HIV patients can result in colonization of subgingival sites by opportunistic oral pathogens, such as Gemella, Dialister, Streptococcus and Candida spp.. Classical periodontal pathogens, such as P. gingivalis, T. forsythia and spirochaetes are not necessarily prevalent.