**3.1 Periodontal histopathology**

*Periodontal Disease - Diagnostic and Adjunctive Non-surgical Considerations*

**2.4 Gingiva**

of how structure determines function [4].

**3. Periodontal pathogenesis**

and gingival bleeding [10].

mastication. In addition, the periodontal ligament has the capacity to act as a sensory receptor necessary for the proper positioning of the jaws during mastication, and, very importantly, it is a cell reservoir for tissue homeostasis, regeneration, and repair [4].

Gingiva is a portion of the oral mucosa covering the tooth-carrying part of the alveolar bone and the cervical neck of the tooth. Three parts of the gingiva can be distinguished (e.g., **Figure 1d**): (1) free gingiva (FG), (2) interdental gingiva (IG), and (3) attached or inserted gingiva (AG) [6]. Histologically, the epithelial component of the gingiva shows regional morphological variations that reflect the adaptation of the tissue to the tooth and alveolar bone. These include the epithelium that covers a connective tissue, chorion, or lamina propria. A keratinized stratified squamous epithelium protects the lamina propria of the gingiva on its masticatory surfaces and a nonkeratinized epithelium protects the lamina propria on its crevicular and junctional surfaces [6, 9]. The junctional epithelium plays a crucial role since it essentially seals off periodontal tissues from the oral environment. Its integrity is thus essential for maintaining a healthy periodontium. Periodontal disease sets in when the structure of the junctional epithelium starts to fail, an excellent example

During pathological conditions, such as inflammation, the periodontal connective tissues, including the gingiva, undergo many changes. Clinically detected gingival overgrowth is one of the alterations that occurs in chronic periodontitis. It is caused by a variety of etiological factors and is exacerbated by local bacterial biofilm accumulation, because the periodontopathogen products act on the gingival tissues activating cellular events that induce the alteration of connective tissue homeostasis and the destruction of the alveolar bone [9]. Likewise, junctional epithelial cells differ considerably from those of the gingival epithelium. There are polymorphonuclear leukocytes and monocytes that pass from the subepithelial connective tissue through the junctional epithelium and into the gingival sulcus. The mononuclear cells, together with molecules they secrete and others originating from junctional epithelial cells, blood and tissue fluid, represent the first line of

Periodontitis is a chronic multifactorial disease characterized by an inflammation of the periodontal tissue mediated by the host, which is associated with dysbiotic plaque biofilms, resulting in the progressive destruction of the toothsupporting apparatus and loss of periodontal attachment [1, 10]. The bacterial biofilm formation initiates gingival inflammation; however, periodontitis initiation and progression depend on dysbiotic ecological changes in the microbiome in response to nutrients from gingival inflammatory and tissue breakdown products and anti-bacterial mechanisms that attempt to contain the microbial challenge with in the gingival sulcus area once inflammation has initiated. This leads to the activation of several key molecular pathways, which ultimately activate host-derived proteinases that enable loss of marginal periodontal ligament fibers, apical migration of the junctional epithelium, and allows apical spread of the bacterial biofilm along the root surface [1]. Therefore, the primary features of periodontitis include the loss of periodontal tissue support, manifested through clinical attachment loss and radiographically assessed alveolar bone loss, presence of periodontal pocketing,

defense in the control of the perpetual microbial challenge [4].

**6**

The development of gingivitis and periodontitis can be divided into a series of stages: initial, early, established, and advanced lesions (e.g., **Figure 2**) [11, 12]. The initial lesion begins 2–4 days after the accumulation of the microbial plaque. During the initial lesion, an acute exudative vasculitis in the plexus of the venules lateral to the junctional epithelium, migration of polymorphonuclear (PMN) cells through the junctional epithelium into the gingival sulcus, co-exudation of fluid from the sulcus, and the loss of perivascular collagen were observed. The early injury develops within 4–10 days. This lesion is characterized by a dense infiltrate of T lymphocytes and other mononuclear cells, as well as by the pathological alteration of the fibroblasts [6, 11–13].

Subsequently, the established lesion develops within 2–3 weeks. This lesion is dominated by activated B cells (plasma cells) and accompanied by further loss of the marginal gingival connective tissue matrix, but no bone loss is yet detectable. Several PMN continue to migrate through the junctional epithelium, and the gingival pocket is gradually established. Finally, in the advanced lesion, plasma cells continue to predominate as the architecture of the gingival tissue is disturbed, together with the destruction of the alveolar bone and periodontal ligament. It is characterized by a conversion of junctional epithelium to the pocket epithelium, formation of denser inflammatory infiltrate composed of plasma cells and macrophages, loss of collagen attachment to the root surface, and resorption of the alveolar bone [6, 11–13].
