Gingival and Periodontal Diseases
Periodontal diseases range from simple and early inflammation of marginal gingiva to advanced gingivitis and subsequently periodontitis. A good classification system is crucial in identifying and differentiating the various kinds of periodontal diseases.
Different classification systems of periodontal diseases have been used for years and also replaced by newer classification systems as the knowledge of understanding microbiology, etiology, pathogenesis and host response have improved vastly over the past few decades.
The current classification has many changes seen which is drastically different from the previous classifications. The most noticeable change is that periodontitis is now classified based on the rate of progression of the disease and not on the age of onset.
The term ‘adult periodontitis’ is discarded since this form of periodontitis is seen in wide range of ages and found both in primary and permanent dentitions. Hence, the term ‘chronic periodontitis’ was chosen because it does not reflect the age of individual rather reflects the rate of progression of periodontal disease, which is slow in nature.
The term ‘early onset periodontitis’ has been discarded as this form of periodontitis is seen in various ages and in older individuals too. Thus, the term ‘aggressive periodontitis’ was chosen. Progressive periodontal disease can be either localized or generalized. The term ‘localized aggressive periodontitis’ replaces localized juvenile or localized early onset periodontitis. The term ‘generalized aggressive periodontitis’ replaces generalized juvenile or generalized early onset periodontitis. The term ‘pre-pubertal periodon-titis’ has been discarded and is currently described as localized or generalized periodontitis or periodontitis as manifestations of systemic disease.
The present classification system highlights the role of certain systemic conditions like smoking and diabetes that can modify periodontitis and that certain systemic conditions that can cause destruction of periodontium such as neutropenia and leukemias.
Increasing evidence indicates that gingivitis is not a single disease, but an assortment of diseases that are the end result of a variety of different processes. Inflammation of gingiva by bacteria is most common, but pathological changes in the gingiva can also result from systemic conditions (e.g. puberty), drugs (e.g. amlodipine) and neoplasms (e.g. leukemia). Hence, any disease that primarily affects gingival tissues should be primarily classified as a gingival disease.
The gingival diseases associated with children, adolescents and young adults have several common characteristics. Universal features include clinical signs of inflammation, signs and symptoms that are confined to the gingiva, reversibility of the disease on removal of the etiology, and the presence of microbial plaque to initiate or exacerbate the severity of the lesion.
Oral cavity can be regarded as a single microbial ecosystem or macroenvironment because the colonization of oral cavity starts at the time of birth. Within hours of birth the sterile oral cavity gets colonized by facultative and aerobic bacteria, which will be followed by anaerobic bacteria by 2nd day. By 2 years of age there will be around 400 different kinds of bacteria. After tooth eruption, a more complex oral flora is established. However, all these species are seen to be living in harmony with the host. But, however, there is an imbalance in this relationship between the host and microorganisms, disease prevails which is controlled by various other factors.
Oral environment is dominated with saliva, which is very complex in composition. Although saliva is not a good medium for supporting the growth of bacteria, it is likely that organisms shed from intraoral reservoirs find transient residence in saliva. Oral cavity provides two types of surfaces for colonization—soft and hard tissue (teeth)—main difference being soft tissue desquamation; hence the colonies are shed frequently whereas the hard surface provides a solid medium for the bacteria to adhere and develop complex layers.
Dental plaque: Dental plaque is clinically defined as a structural resilient yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restoration.
It is a complex procedure initially involving the formation of pellicle (glycoprotein, phosphoproteins) around the tooth surface. Then the early bacterial colonization takes place with facultative aerobic gram-positive organisms. Some of the early colonizers are Actinomyces and Streptococcus sanguis which adhere to the pellicle through adhesins. Later plaque maturation takes place with co-aggregation of secondary colonizers including Fusobacterium nucleatum, Prevotella intermedia, Porphyromonas gingivalis, Capnocytophaga, etc. Thus in maturation of plaque there is a transition from the early aerobic gram-positive facultative species to an anaerobic gram-negative species.
Health is not a static condition, it is a dynamic state in which the living and functioning individuals remain in balance with a constantly changing environment. These changes in environment also cause changes in tissue activity so that normal function can continue, a process known as homeo-stasis. If the environmental changes over-ride this homeo-stasis, the normal function cannot continue and this change is termed as disease.
B-cell response (antibody-mediated immune system). Plaque bacteria produce a number of factors (virulence factor), which causes disease directly, or individually by stimulating the immune and inflammatory system. It is now known that individuals prone to periodontal disease have an aberrant immune inflammatory response to plaque which is genetically determined.
Host modulation: Periodontal disease is multifactorial in nature as a result of interaction between plaque microorganism and host responses. Host modulation refers to the alteration/modification of host response to the microbial stimulus by the use of number of medications. The two major categories are NSAIDs and inhibition of MMPs.
Prostaglandin E2 (PGE2), a product of cyclooxygenase pathway has been shown to increase the amount of alveolar bone destruction by amplifying local inflammation. NSAIDs block COX pathway thus decreasing PGE2 synthesis. A number of NSAIDs have been used including ibuprofen, flurbiprofen, indomethacin, ketoprofen and naproxen.
Matrix metalloproteinases are a family of proteolytic enzymes secreted by a number of cells including leukocytes, epithelial connective tissue cells whose primary function is degradation of extra-cellular matrix components. Tetracycline and other drugs of the same group show to inhibit the MMPs production from the host, primarily the neutrophil MMPs. In doing so they increase host resistance to connective tissue destruction forms of tetracycline are submicrobial dose of tetracycline/doxycycline and chemically modified tetracycline.
It is the inflammation of gingiva which results from the bacteria located at the gingival margin. The association of plaque with gingival inflammation made it a frequently postulated cause of gingivitis. The initial histologic changes from health to plaque-induced gingivitis may not be evident clinically (Page and Shroeder, 1976; Bimstein et al, 1985) but as gingivitis progresses, clinical signs becomes more obvious.
Plaque-induced gingivitis begins at the gingival margin and can spread into the deeper gingival component. Clinical signs of gingival inflammation involve the change in color, contour, size, shape, consistency and surface texture are associated with a stable periodontium which exhibits no loss of periodontal attachment or alveolar bone. The classic clinical indicators of signs of inflammation are bleeding on probing and color change from pink/coral pink to reddish pink or erythematous gingiva. In children, gingivitis is not intense as that found in young adults with similar quantity of accumulation of dental plaque (Mattson and Goldberg, 1985).
In the initial and established stages of gingivitis, dental plaque is predominantly comprised of gram-positive aerobic microorganisms including Streptococcus mitis, S. sanguis, Actinomyces viscosus, A. naeslundii and Eubacterium spp. As age advances, development and severity of gingivitis is mainly dependent on the quality of the plaque rather than the quantity and the other contributing factors like the host immune response, environmental, genetic and the behavioral factors. The common clinical signs and symptoms of gingivitis include redness, edema, bleeding on probing, tenderness and enlargement (Loe et al, 1965; Suzuki, 1988) (Figure 1).
Radiographically no changes will be seen as the inflammation is confined only to the gingival sulcus. Histologic changes include proliferation of basal junctional epithelium leading to apical and lateral cell migration, vascular dilatation and vasculitis of blood vessels adjacent to the junctional epithelium, progressive destruction of collagen fibers, cytopathologic alteration of resident fibroblasts and progressive inflammatory cell infiltrate (Page and Shroeder, 1976).
Since the 19th century, evidence suggests that the tissues of the periodontium are modulated by androgens, estrogens and progesterone. Much of this evidence has come from observing the changes in gingival tissues during distinct endocrino-logic events (puberty, menstrual cycle, pregnancy, etc.).
The principal explanation for sex steroid hormone-induced changes in the gingiva has pointed to changes of microbiota in dental plaque, immune function, vascular properties and cellular function in the gingiva. Sex steroid hormones will affect the host by influencing cellular function (in the blood vessels, the epithelium and the connective tissue) and immune function, and together with hormone-selected bacterial populations occupying the gingival sulcus, induce specific observable changes in gingival tissues (Mariotti, 1994).