**2. Histopathology of gingivitis**

The plaque biofilm causes most of the injury to the periodontal tissue through indirect mechanisms dependent on initiation and propagation of inflammatory host tissue reactions. The development of gingivitis is mainly the infiltration of the connective tissues by numerous defense cells, particularly neutrophils, macrophages, plasma cells, and lymphocytes. The accumulation of these defense cells and the extracellular release of their destructive enzymes cause destruction of collagen and subsequent proliferation of the junctional epithelium leading to vasodilatation, increased vascular permeability, and hyperplastic gingival tissues. Clinically it appears as erythematous and edematous gingiva: the clinical appearance of gingivitis. The classic studies of Page and Schroeder [6] described the basic understanding of histologic changes that occur in the gingival tissues as the initial, early, established, and advanced gingival lesions. These are histologic descriptions only, primarily based on findings in experimental animals.

#### **2.1 The initial lesion**

The initial lesion develops within 2–4 days of the accumulation of plaque at a site free of plaque biofilm, which is evident microscopically since the gingival tissues always have characteristics of a low-grade chronic inflammatory response as a result of the continual presence of the subgingival biofilm. In other words, the initial lesion corresponds to the histologic picture that is evident in clinically healthy gingival tissues. This low-grade inflammation characterized by vasodilatation and increased vascular permeability along with upregulation of intercellular adhesion molecule-1 (ICAM-1) and E-selectin in gingival vasculature facilitates migration of neutrophils and monocytes into the connective tissue. This influx of fluid flow from the vessels increases the hydrostatic pressure in the local microcirculation resulting in increased gingival crevicular fluid (GCF) flow.

#### **2.2 The early lesion**

The early lesion corresponds to the early clinical signs of gingivitis and characterized by erythematous clinical appearance of gingiva due to proliferation of capillaries and vasodilatation [7]. The predominant infiltrating cell types are neutrophils and T lymphocytes [7]. The basal cells of these epithelial structures proliferate apically resulting in edema of gingival tissues and deepening of gingival sulcus. The subgingival biofilm proliferates apically in this ecologic environment rendering plaque control difficult in these areas. The early gingival lesion may persist indefinitely, or it may progress further.

#### **2.3 The established lesion**

The established lesion corresponds to clinical appearance referred to as "chronic gingivitis" and depends on many factors, such as composition and quantity of the plaque biofilm, host susceptibility factors, local and systemic risk factors. A study by Page and Schroeder [6] defined established lesion as mainly dominated by plasma cells with inflammatory cell infiltrate in connective tissues and destruction of collagen fibers. Neutrophils accumulated in the tissues, which are also a major source of matrix metalloproteinase-8 (MMP-8; neutrophil collagenase) and MMP-9 (gelatinase B), release their lysosomal enzymes in the inflamed gingival tissues causing destruction of collagen bundles. This is followed by deepening of sulcus and formation of ulcerated pocket epithelium along the tooth surface resulting

**13**

stress [9].

*Pathogenesis of Gingivitis*

**2.4 The advanced lesion**

**3. Host susceptibility**

and regeneration.

reinstituted.

*DOI: http://dx.doi.org/10.5772/intechopen.91614*

environmental and genetic risk factors.

between the tooth and the gingival soft tissues.

**3.1 Role of host susceptibility in gingivitis**

formation to periodontal regeneration and repair.

in bleeding on probing which is a common feature of chronic gingivitis. These inflammatory changes are still completely reversible if effective plaque control is

The advanced lesion, as described by Page and Schroeder [6], marks the transition from gingivitis to periodontitis which is determined by many factors, such as composition and quantity of the biofilm, the host inflammatory response, and

The tooth has a unique situation in the mammalian biology and presents a special challenge to the immune system [8]. The marginal gingiva includes the epithelial and connective tissue attachment apparatus that provides a biological seal

The oral cavity is a unique microenvironment where millions of bacteria live in harmony with our host defense mechanisms, with the bacterial host balance maintained by the amount of bacterial load through our regular oral hygiene practices. It is therefore important to understand the cellular and molecular elements involved in the pathways from health to disease and from disease to repair

Even though the development of gingivitis after plaque accumulation is a universal finding, the rate or speed of development and the degree of the clinical inflammatory response are variables between individuals, even under similar plaque accumulation conditions [9]. The studies recognizing the role of host contributing to the pathology of periodontal disease was a major breakthrough [10]. Various studies using the experimental gingivitis model showed 13% of all individuals representing a "resistant" group [9, 11, 12]. The factors modulating the appearance of gingival inflammation in response to plaque accumulation are mainly exacerbated gingival response to plaque, including metabolic factors such as puberty and pregnancy; genetic factors such as Down syndrome; nutritional factors such as vitamin C deficiency; the intake of drugs such as those leading to gingival enlargement; systemic diseases such as leukemia, immune deficiencies, and diabetes mellitus; and other conditions such as

Gingivitis and periodontitis are the result of a coordinated action of clearly defined cellular players (proinflammatory and anti-inflammatory), which communicate with each other [13]. An inflammatory reaction can develop in two directions, either being destructive or regenerative depending on the bacterial antigen load and properties. If destructive, the innate immune reaction is followed by an adaptive or specific immune response, associated with the loss of tissue structure to create space for the immune process, and resolution of inflammation is associated with the regeneration of these structural hard and soft tissue components. It is therefore important to understand the cellular and molecular elements involved in the pathways from health to disease and from disease to repair and regeneration. The complex biological mechanisms occur in many phases from bacterial biofilm

in bleeding on probing which is a common feature of chronic gingivitis. These inflammatory changes are still completely reversible if effective plaque control is reinstituted.

## **2.4 The advanced lesion**

*Oral Diseases*

**2.1 The initial lesion**

**2.2 The early lesion**

nitely, or it may progress further.

**2.3 The established lesion**

**2. Histopathology of gingivitis**

primarily based on findings in experimental animals.

in increased gingival crevicular fluid (GCF) flow.

The plaque biofilm causes most of the injury to the periodontal tissue through indirect mechanisms dependent on initiation and propagation of inflammatory host tissue reactions. The development of gingivitis is mainly the infiltration of the connective tissues by numerous defense cells, particularly neutrophils, macrophages, plasma cells, and lymphocytes. The accumulation of these defense cells and the extracellular release of their destructive enzymes cause destruction of collagen and subsequent proliferation of the junctional epithelium leading to vasodilatation, increased vascular permeability, and hyperplastic gingival tissues. Clinically it appears as erythematous and edematous gingiva: the clinical appearance of gingivitis. The classic studies of Page and Schroeder [6] described the basic understanding of histologic changes that occur in the gingival tissues as the initial, early, established, and advanced gingival lesions. These are histologic descriptions only,

The initial lesion develops within 2–4 days of the accumulation of plaque at a site free of plaque biofilm, which is evident microscopically since the gingival tissues always have characteristics of a low-grade chronic inflammatory response as a result of the continual presence of the subgingival biofilm. In other words, the initial lesion corresponds to the histologic picture that is evident in clinically healthy gingival tissues. This low-grade inflammation characterized by vasodilatation and increased vascular permeability along with upregulation of intercellular adhesion molecule-1 (ICAM-1) and E-selectin in gingival vasculature facilitates migration of neutrophils and monocytes into the connective tissue. This influx of fluid flow from the vessels increases the hydrostatic pressure in the local microcirculation resulting

The early lesion corresponds to the early clinical signs of gingivitis and characterized by erythematous clinical appearance of gingiva due to proliferation of capillaries and vasodilatation [7]. The predominant infiltrating cell types are neutrophils and T lymphocytes [7]. The basal cells of these epithelial structures proliferate apically resulting in edema of gingival tissues and deepening of gingival sulcus. The subgingival biofilm proliferates apically in this ecologic environment rendering plaque control difficult in these areas. The early gingival lesion may persist indefi-

The established lesion corresponds to clinical appearance referred to as "chronic gingivitis" and depends on many factors, such as composition and quantity of the plaque biofilm, host susceptibility factors, local and systemic risk factors. A study by Page and Schroeder [6] defined established lesion as mainly dominated by plasma cells with inflammatory cell infiltrate in connective tissues and destruction of collagen fibers. Neutrophils accumulated in the tissues, which are also a major source of matrix metalloproteinase-8 (MMP-8; neutrophil collagenase) and MMP-9 (gelatinase B), release their lysosomal enzymes in the inflamed gingival tissues causing destruction of collagen bundles. This is followed by deepening of sulcus and formation of ulcerated pocket epithelium along the tooth surface resulting

**12**

The advanced lesion, as described by Page and Schroeder [6], marks the transition from gingivitis to periodontitis which is determined by many factors, such as composition and quantity of the biofilm, the host inflammatory response, and environmental and genetic risk factors.
