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Periodontal Disease: Part I

Biological Mechanisms

Recent epidemiological research has yielded important information that has improved clinicians' understanding of periodontal disease. Analysis of these results is difficult to interpret, however, due to the variety of diseases, epidemiological measurements and methods, and sample populations under evaluation. It is the focus of this discussion to identify the consequences of periodontal disease and to simultaneously delineate the mechanism of periodontal disease.

Gingivitis is characterized by a gingival inflammation that may or may not involve bleeding, and is generally caused by the presence of bacteria in plaque. Gingivitis does not cause the loss of periodontal attachment or hard tissue and is frequently reversible by the removal of plaque and calculus. Periodontitis involves the combination of gingival inflammation and the destruction of connective tissue and bone. This inflammatory disease is also the result of a complex interaction between bacterial infection and host response, and it manifests in three basic forms: 1) juvenile periodontitis, which affects children; 2) progressive periodontitis, which is associated with specific host factors and affects adolescents; and 3) adult periodontitis, the most common form, which is directly related to local etiological factors. The most recent epidemiological data on periodontal disease in the United States indicate that 50% of all adults have gingivitis and that 67% of the population have subgingival calculus. Adult periodontitis is present in approximately 30% and 40% of the population that have periodontal pockets greater than 4 mm and attachment loss of 0.3 mm, respectively.1

Consequences of Periodontal Disease

The dental professional must perform a meticulous clinical examination in order to recognize the symptoms and effects of inflammation and to determine the differential diagnosis of normal gingiva, gingival infection, and periodontal disease (Table 1). Since periodontal disease is often insidious in its development, specific symptoms may not be evident in a particular patient. Early recognition of gingival and periodontal signs may prevent the disease from developing into a more severe condition.


Gingival Disease

The initial development of gingivitis is the result of a gingival response to an accumulation of bacterial plaque on the cervical aspect of a tooth. This plaque is largely composed of microorganisms and bacteria, and is often referred to as "microbial dental plaque." In an inflammatory response to the invasion of bacterial plaque, the migration and infiltration of leukocytes occurs in the junctional epithelium and gingival sulcus, which increases the flow of gingival fluid and causes the breakdown of collagen. Although evidence of disease may not be apparent in this phase, the persistence of microbial dental plaque and the inflammatory response to this invasion will reveal the presence of gingivitis in the future.

As the condition of the gingiva continues to deteriorate, the acute status of the tissue will be indicated by its pigmentation. The pale pink shade of healthy gingiva is changed into a bright red color as the tissue is affected by the disease. The shift in tissue color also indicates the increase of gingival fluid caused by local inflammation and the proliferation of plasma cells in the junctional and sulcular epithelium. As collagen and connective tissue fiber are destroyed in this region, gingival pockets begin to develop.

The size of the free and attached gingiva are also affected by the disease. The free gingiva and papillae become enlarged, and the attached gingiva is decreased as the gingival pockets deepen. The curved shape of the free gingival tissue around each tooth is characterized by a rounded, rolled contour, and the papillae exhibit a flattened, cratered appearance. Influenced by the inflammation, the tissue surface may appear smooth or shiny; it can also demonstrate hyperkeratosis and a fibrotic aspect. These conditions may disappear spontaneously or upon probing bleeding, and may also cause suppuration and white fluid in the pocket epithelium. Apical migration of the junctional epithelium causes visible gingival recession that exposes the root surfaces; the exact level of recession and attachment is determined by probing.


Periodontal Disease

When the disease is limited to the gingival tissue, the reversal of the infection should be considered as a primary treatment objective. Consequently, diagnosis of the periodontal infection should be clearly defined early in the treatment. Since the presentation of the disease is different in each patient, the available therapies (eg, surgical, nonsurgical, scaling, antibiotics) must be explained in detail. The patient should also receive instruction in hygiene management through daily behavior modification or infection control.

Early stages of periodontal disease are characterized by the progression of the gingival inflammation into deeper periodontal structures and alveolar bone. Bacteria enter the sulcus supragingivally, which extends the inflammation and the concurrent inflammatory response, and results in the loss of connective tissue attachment and alveolar bone. The destruction of connective tissue occurs below the junctional epithelium and migrates along the root surface. The coronal portion of junctional epithelium is flattened, and Sharpey's fibers are altered by a thin superficial layer of endotoxin from the bacterial breakdown. Without treatment, the persistence of the chronic inflammation deepens the periodontal pockets.

In advanced stages of moderate periodontitis, the destruction of the periodontal structures and bone support occurs. This often results in increased tooth mobility and furcation involvement; advanced periodontitis is characterized by significant loss of alveolar bone support and increased tooth mobility.


Tooth Loss

If left untreated, periodontal disease can result in permanent tooth loss. The patient may develop painful abscesses or have difficulty eating prior to tooth loss, and experience aesthetic, functional, and social complications thereafter. The replacement of lost teeth often requires the utilization of extensive restorative procedures, such as implant or prosthetic therapy. While these modalities can be predictably and successfully used to restore healthy patients, such options cannot be pursued if the periodontal disease has not been completely stabilized or if excessive bone loss has occurred. Clinical research also suggests that untreated or uncontrolled periodontal disease increases one's risk of heart disease and diabetes.


Pain and Halitosis

Prior to the management of periodontal disease, it is frequently necessary to treat patient discomfort. In a diseased state, patients may perceive the effects of periodontal probing to a greater extent. A clinical study by Heins et al confirmed that anterior sulci are less pain tolerant than posterior gingival sulci and that facial sulci are less tolerant than corresponding oral sulci.2

The dental literature has also indicated the existence of a direct relationship between halitosis and periodontal disease. Produced by anaerobic bacteria breakdown, volatile sulfuric compounds have been detected in gingival sulcus sites. As with the aesthetic and functional factors, these effects must be addressed by comprehensive periodontal treatment.


Mugogingival Complications

One sequelae of periodontal disease and its treatment is the loss of interdental papillae, which may compromise aesthetics - particularly in the maxillary anterior region. Nordland and Tarnow proposed a classification system in order to identify the degree of papillary height lost. This classification should assist clinicians in the development and selection of novel surgical techniques for papillary augmentation.3


Radiographic Analysis

The final aspect of the diagnostic evaluation is the radiographic analysis, which is performed to determine the level of periodontal involvement (eg, vertical and angular reduction, horizontal bone loss, furcation involvement, ligament space). A recent article demonstrated the importance of the comparison of the radiographic and clinical response to periodontal therapy following mechanical treatment and oral hygiene instruction.4

(Continued from page 1 )

Mechanism of the Periodontal Disease


The periodontium is the functional unit that surrounds and supports the dentition and is composed of the gingiva, the periodontal ligament, the cementum, and the bone. Gingiva is constituted by the free gingiva, the attached gingiva, and the interdental papilla. The periodontal ligament - fibrous connective tissue - is located in the periodontal space between the alveolar bone and the cementum, which provides attachment for the periodontal fiber groups.  The bone, which is adjacent to the ligament space, is formed by the lamina dura - the linear radiopaque bony lining of the tooth socket - and alveolar bone.



The oral cavity is a complex environment that is capable of supporting a variety of microorganisms (eg, bacteria, yeasts, protozoa, viruses, fungi) that normally have an equilibrate relationship with the host system. Salivary components, exudates, and epithelial cells are abundant sources of nutrition for oral flora, which are protected from potential pathogens by bacterial antagonists, lysosomes, peroxydase, and immunoglobulins. Buccal bacteria are eliminated from the region by the flow of saliva, gingival fluid, mastication, hygiene maintenance, and epithelial cell desquamation. In order to be sustained in the oral environment, the microbiological flora and buccal microorganisms require specific adhesive chemical mechanisms to be present.

Periodontal disease combines inflammatory pathology of an infectious origin and that localize in the periodontium. Although much research has been conducted on periodontal disease etiopathogenesis, these findings have yet to fully define the condition. Such studies, however, have produced evidence that indicates the etiology of periodontal disease is connected to bacterial and immunity factors. This pathology is an inflammatory lesion that responds to bacterial invasion. Bacteria is an etiological primary agent whose evolution is determined by immunological factors in the host. While the immunity factors are protective agents in a healthy state, these factors can cause tissue destruction when they occur in conjunction with the inflammatory process. The virulent factors of the bacteria responsible for periodontal disease can be organized into three categories:

  • Factors that provide colonization of the host periodontal site, in which pathogenic germs penetrate a susceptible site and proliferate.
  • Factors that destroy the periodontium directly by bone resorption (ie, enzymes and toxins) or indirectly with mediators from the immune and nonimmune systems. Numerous enzymes (eg, proteinases, peptidases, aminopeptidases, and collagenases) are responsible for the degradation and use of free proteins, and various strains of bacteria and their byproducts induce bone resorption and immunopathological mechanisms that result in periodontal destruction.
  • Factors of the host defense system, which responds to the invasion of the bacteria.

Bacterial infection is the primary cause of destructive periodontal disease, which forces the host tissue to release enzymes to control the spread of the bacteria. Unfortunately, these enzymes also damage the surrounding tissues that support the dentition. The bacteria also stimulate host cells to produce cytokines that stimulate cells in the periodontium to produce matrix metalloproteins (MMPs), enzymes that destroy the collagen framework of the periodontal tissue. This destruction of collagen produces the classic symptoms of periodontitis.5 While it is acknowledged that bacteria initiate periodontal disease, it is actually the host-derived MMPs that cause the majority of the tissue destruction (Figure 1).



  1. Oliver RC, Brown LJ, Löe H. Periodontal diseases in the United States population. J Periodontol 1998;69(2):269-277.
  2. Heins PJ, Karpinia KA, Maruniak JW, et al. Pain threshold values during periodontal probing: Assessment of maxillary incisors and molar sites. J Periodontol 1998;69(7):812-818.
  3. Nordland WP, Tarnow DP. A classification system for loss of papillary height. J Periodontol 1998;69(10):1124-1126.
  4. Machtei EE, Hausmann E, Schmidt M, et al. Radiographic and clinical responses to periodontal therapy. J Periodontol 1998;69(5):590-595.
  5. Golub LM, Lee HM, Greenwald RA, et al. A matrix metalloproteinase inhibitor reduces bone-type collagen degradation fragments and specific collagenases in gingival crevicular fluid during adult periodontitis. Inflamm Res 1997;46:310-319.
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