The dental hygienist plays a crucial role in the treatment of gingivitis and in the prevention of its recurrence. Diseases of the gingival tissues range from common forms, such as dental plaque biofilm–induced gingivitis, to rare but potentially life-threatening forms, such as squamous cell carcinoma or acute leukemia. The dental hygienist may be the first member of the health care team to identify these lesions and bring them to the attention of the patient and other dental health professionals.
A description of the gingival tissues in health is presented in Chapter 2. To review, in health, the gingival epithelium is usually described as pink or coral pink, with significant variation based on the presence of melanin in the tissue, which is a genetic characteristic. The attached gingiva is tightly bound to the underlying connective tissue and is not movable. The surface epithelium of the attached gingiva is often stippled, shows no signs of inflammatory color changes, and the papillae fill the interdental spaces completely. The marginal gingiva reaches the tooth surface in a knife edge pattern, and there are measurable sulcus depths of less than 3 mm. The gingival epithelium consists of a keratinized oral epithelium, a keratinized or parakeratinized sulcular epithelium, and a junctional epithelium that forms the attachment to the root surface. Beneath the gingival epithelium, there is dense connective tissue coronal to the alveolar bone. This tissue is laced with bundles of collagen fibers. The normal appearance of healthy gingiva is shown in Figure 6-1.
Gingivitis is inflammation of the gingival tissues. It occurs in a periodontium with no attachment loss or in a periodontium with attachment loss that is not progressing. Gingivitis manifests as color change (redness), edema (swelling of the tissues), exudate (drainage of gingival fluid from the sulcus), and a tendency to bleed readily (hemorrhage in response to gentle periodontal probing or tooth brushing).1 In addition, there may be changes in gingival contour, loss of tissue adaptation to the teeth, and an increased flow of gingival crevicular fluid.2 Gingivitis is perhaps the most common human disease and among the easiest to treat and control. However, gingivitis is painless and often unrecognized. Many patients are unaware that they have it, even though their gums bleed, and, because it is so common, dentists and dental hygienists frequently do not emphasize its importance. Perhaps the best approach that dental hygienists and dentists can take is to inform their patients that they have a disease—gingivitis—and that it is easily treated and cured. When the balance between disease and health is understood, patients often cooperate with dental hygiene care and improve their daily oral hygiene practice to cure the disease.
Pathogenesis refers to the events in the development and progression of a disease. The pathogenesis of gingivitis is best explained by describing the histologic events as they relate to clinical signs. Extensive research on the pathogenesis of gingivitis, obtained by observing people and animals when bacterial plaque was allowed to accumulate, has explained most of the events in the development of gingival inflammation. With this knowledge, scientists have classified the development of gingival inflammation into three separate stages:
Research has also defined a fourth stage, characterized by the extension of inflammation into the alveolar bone, which is the stage of periodontal breakdown, or advanced stage.4 The fourth stage is the point at which the gingival disease has progressed to periodontal disease.
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 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
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 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.
|STAGE||CLINICAL SIGNS||PATHOLOGIC EVENTS|
|Initial (stage I)||None (subclinical infection)|
The sequence of healing events is the reverse of those described for the pathogenesis. Healing of gingivitis begins in the connective tissues. The inflammatory cells are replaced by fibroblasts, which lay down a firm extracellular matrix of collagen. With maturity, these fibers become functionally oriented and produce a dense subgingival connective tissue. This connective tissue does not permit penetration of the periodontal probe tip, thus reducing the clinical periodontal probing depth. The gingival color returns to pink as the proliferation of inflammatory cells resolves, and stippling reappears when serum no longer leaks into the tissues to cause edema.
In some cases, stable gingivitis transforms into progressive disease. This change results in advanced lesions with bone destruction, progressing from gingivitis to periodontitis.5 Periodontitis is discussed in Chapter 7.
Gingivitis has been classified into a number of categories on the basis of the clinical manifestations of the disease, etiology, association with systemic diseases, association with medications, or other causes. The gingiva mirrors the effects of many factors beyond disease-associated causes, including allergies and injuries. The classification of gingival diseases and conditions is complex and is presented in Box 6-1.5,6 The major elements of gingival diseases and conditions are described and illustrated in the remainder of this chapter.
Recession of the gingiva refers to the location of the margin of the tissue, not its condition. Recession can occur in gingivitis, or it can be associated with clinically healthy tissue. Gingival recession, which is common, increases with age. It can be localized to one tooth or extend to any number of teeth. It has been reported to be present in 8% of children and 100% of adults by the age of 50 years. Etiologic factors associated with recession are as follows7:
Recession is of clinical significance in dental hygiene care because root surfaces exposed through recession can decay and cemental surfaces can wear away, leaving the root surface sensitive. Also, these surfaces can be more difficult for the patient to clean.
Gingivitis occurs very commonly in all levels of society, rich or poor, industrial or agricultural. The most obvious symptom is bleeding gums. So many people live with this condition that they are often not aware that it is a disease. Many patients will tell the dental hygienist that they believe that everyone’s gums bleed, or they always expect their gums to bleed when they brush their teeth. Despite this common assumption, it is true that the gingiva becomes inflamed as a result of the presence of dental plaque. The following section describes gingivitis and factors that contribute to the disease.
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.
Plaque-associated gingivitis may be further classified by its location and the degree of involvement in the dentition. It may be localized to a few teeth or generalized throughout the mouth. It may be limited to the interdental papilla, spread along the entire gingival margin, or involve all of the attached gingival tissues. By definition, gingivitis does not involve the periodontal attachment tissues and there is no loss of connective tissue attachment to the tooth and no loss of supporting bone.