Stage I Gingivitis (Initial or Subclinical Stage)

Stage I gingivitis, the initial stage, occurs in the first few days of contact between microbial plaque and the gingival tissues. This stage is an acute inflammatory response that is characterized by dilation of the blood vessels and increased blood flow. The polymorphonuclear leukocytes (PMNs, or neutrophils) attach to the vessel walls and begin to migrate into the surrounding connective tissues. PMNs (white blood cells with multilobulated nuclei) are the principal defense in acute inflammation. They phagocytize (engulf) bacteria, their products, and other products of destroyed tissue. Small amounts of plasma also leak into the surrounding tissues, causing edema in the tissues. PMNs amass in the connective tissue and migrate through the sulcular epithelium into the plaque, forming exudate. Exudate from early gingival inflammation, composed mostly of serum, is referred to as gingival fluid flow. The gingival fluid is clear, not yellow (like pus), because few cells are present. A significant number of lymphocytes appear in the gingival connective tissues. These are almost all T lymphocytes, the type that do not cause tissue damage but maintain a homeostatic (stabilizing) response to bacterial infection.⁵ In addition, there are epithelial cell changes and collagen degradation caused by activation of the host immune system. These first tissue reactions to plaque infection are not visible in the gingival tissues because they do not cause obvious clinical changes. This initial inflammatory response with no outwardly observable clinical signs is a subclinical infection.⁴

Stage II Gingivitis (Early Stage)

Stage II gingivitis is referred to as early gingivitis. Lesions begin to form 4 to 7 days after plaque has accumulated in the gingival sulcus. The T lymphocytes increase in number and are localized in the connective tissue under the epithelium of the gingival sulcus. The inflammatory exudate increases; it may appear white or yellow. Clinically, the tissues appear slightly red and swollen. The increase in gingival fluid flow (exudate) reaches its peak 6 to 12 days after clinical redness is observed. The perivascular collagen fibers in the connective tissues are destroyed by the inflammation and replaced by blood plasma and inflammatory cell infiltrate. Collagen fibers that attach the underlying connective tissue to the gingival epithelium are also destroyed and gingival stippling, if present, begins to disappear, causing the gingiva to appear shiny. The junctional epithelium begins to lengthen against the root surface and it is disrupted by the migrating PMNs and lymphocytes. The gingival tissues tend to bleed when gently probed and often do so when a patient brushes and flosses. Cellular changes occur in the connective tissue fibroblasts, leading to their destruction, probably related to interaction with the lymphoid tissues. The early stage of gingivitis may continue for 21 days or longer. It is the earliest clinical evidence of gingivitis.⁴

Stage III Gingivitis (Established Stage)

After 15 to 21 days, the gingival inflammation reaches the established stage, called stage III gingivitis.⁴ In established gingivitis, there is a distinct change in the type of white blood cells seen in histologic specimens. Plasma cells, usually associated with an intense antigen-antibody response, are present. T and B lymphocytes are found in equal amounts, indicating that tissue destruction by the inflammatory reaction is taking place. B lymphocytes are related to cell surface immunity and release lymphokines that accelerate the tissue destruction in inflammation. More connective tissue collagen is destroyed and the junctional epithelium begins to thicken and extend apically on the root surface and deep into the underlying connective tissues. This activity represents a conversion of the junctional epithelium into one correctly described as pocket epithelium. The clinical probing depth increases for two reasons: the periodontal probe penetrates more deeply through the junctional epithelium into the connective tissue by about 1 mm because of the loss of collagen, and edema in the tissues moves the gingival margin coronally, increasing the probe readings.

The blood vessels proliferate into capillary loops that reach nearly to the basement membrane of the epithelium, permitting more seepage of serum into the tissues and through the sulcular epithelium. That change, along with the increased presence and activity of inflammatory cells, causes visible pus formation. Capillary proliferation also causes the gingiva to appear red. In extreme cases of congested blood cells in the gingiva, the tissue appears blue, or cyanotic, because of the presence of many oxygen-depleted red blood cells. In combination, these changes result in red, swollen, and shiny gingivae that may also exhibit noticeable pus formation and gingival exudate.

The established gingivitis lesion may persist unchanged for months or years. The condition is reversible when plaque is regularly removed, permitting the tissues to return to normal. When healing occurs, there is no residual tissue destruction.²

Stage IV Gingivitis (Advanced Stage)

Stage IV gingivitis is the advanced stage of gingivitis. The inflammatory processes have extended beyond the gingiva and into the other periodontal tissues.⁴ The extension of disease into the bone, referred to as periodontitis, is described in Chapter 7. The pathogenesis of the stages of gingivitis is summarized in Table 6-1.

Gingivitis Associated with Dental Plaque Biofilm Only.

The most common form of gingivitis found in the general population is gingivitis associated with dental plaque only, also called plaque-associated gingivitis, or gingivitis. This disease is directly related to the presence of bacterial plaque on the tooth surface.¹

Clinically, gingivitis causes a reddened gingival margin (with pocket formation as a result of gingival swelling and edema), hypertrophy, and deepened penetration of the periodontal probe on clinical evaluation. The surface of the gingiva may appear glazed or smooth, and stippling (when present in health) usually disappears. Microscopically, there is an increase in capillaries along the gingival margin and the epithelium lining the gingival sulcus is ulcerated. This ulceration results in a tendency to bleed when a periodontal probe is placed in the gingival crevice. Bleeding in response to gentle probing is the major clinical indicator of gingivitis. Another common feature of chronic gingivitis is a clear gingival fluid flow, or exudate, which appears to increase with the severity of the gingivitis. Figure 6-2 shows the typical appearance of dental plaque–induced gingivitis.

Gingivitis appears to be directly related to the amount of plaque biofilm on the tooth surface and the amount of time that the plaque is allowed to remain undisturbed. The bacterial plaque biofilm is considered nonspecific because it is not associated with any specific type of microorganisms. The mature plaque biofilm found in long-standing gingivitis has a large percentage of gram-negative bacteria. This change from gram-positive plaque associated with health, or healthy plaque, to predominantly gram-negative plaque, or pathogenic plaque, is characteristic of gingivitis.