Gingival health

Gingivitis is the most commonly occurring gingival disease and manifests as reversible inflammation along the gingival margin. The severity and duration of gingivitis can be modified by factors that influence the bacterial-host cell interactions, including systemic factors (e.g., endocrine changes associated with puberty, pregnancy, diabetes) medications and malnutrition. A key feature of gingivitis is inflammation without destruction of the periodontal structures. Development of gingivitis is clearly dependent upon the presence and accumulation of bacterial plaque. [Lamon et al 2006]

Gingivitis is clinically detectable within days after plaque control efforts are discontinued. It is the more mature pathogenic plaque that is the precipitant of the initial gingival lesion. The bacteria during days 0–2 exhibit Gram-positive cocci and rods and approximately 30% Gram-negative cocci and rods. The second phase of plaque maturation takes place during days 1–4 and is characterized by the appearance and increase in fusobacteria and filaments. The third phase (4–9 days) is characterized by the appearance of spirilla and spirochetes. [Gold, 1991]

Pathological changes in gingivitis are associated with the presence of microorganisms in the gingival sulcus and along the gingival margin. These organisms are capable of synthesizing products (e.g., collagenase, hyaluronidase, protease or endotoxin) that cause damage to the gingival tissue. [Carranza,1996]. These changes can be classified into three stages after plaque removal efforts cease:

In the evaluation of the clinical features of gingivitis it is important to pay attention to subtle tissue changes as they may be of significant diagnostic importance. A systematic clinical approach requires a close assessment of gingival shape, colour, consistency, surface texture, bleeding and discomfort. Change in colour is an important clinical sign of gingivitis. The normal gingival colour is “coral pink” – for this reason when the gingival margin becomes redder and inflamed this indicates an increase in vascularization. The colour changes associated with chronic gingivitis differ from those of acute gingivitis. The more chronic the pathology the tissue takes on a red or bluish red colour while the colour of gingival tissues in acute gingivitis have a more bright red erythema. [Carranza, 1996] Chronic gingivitis is characterized by gingival redness, edema, bleeding, changes in tissue contour, loss of tissue adaptation to the teeth, and changes in flow of gingival crevicular fluid.

Subgingival plaque is formed in the protected environment found between the gingival margin and the tooth surface. Due to this location, the main nutritional component is gingival crevicular fluid (GCF), which is responsible for the predominance of asaccharolytic species. [Darveau et al., 1997] GCF has been shown to contain a number of antimicrobial components, as part of the innate immune response, which includes lysozome, complement and vascular permeability enhancers such as bradykinin, thrombin and fibrinogen. [Darveau et al., 1997]

Investigations into bacteria associated with a healthy gingival crevice found that Streptococcus spp., Actinomyces spp., Capnocytophaga spp., Eubacterium spp., Fusobacterium spp., and Veillonella spp. predominate. [Darveau et al., 1997; Listagarten, 1994] It has been reported that gingivitis can develop within 10-21 days where an oral hygiene regime has stopped. [Loe et al., 1966] This can cause a shift to pathogenic bacteria [Socransky et al., 1998], predominantly gram-negative anaerobes and spirochetes. A number of bacterially derived compounds can help elicit an innate immune response, including inflammatory mediators. [Page, 1991] This causes local inflammation and swelling of the gingiva which leads to the characteristic appearance of gingivitis. [Bernimoulin, 2003] To the patient, gingivitis is characterized by bleeding gums when brushing. [Pihlstrom et al., 2005]

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