**3. Periodontal pathogenesis**

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, and gingival bleeding [10].

**7**

**Figure 2.**

*development of gingivitis and periodontitis.*

*Pathogenesis of Periodontal Disease*

**3.1 Periodontal histopathology**

of the fibroblasts [6, 11–13].

alveolar bone [6, 11–13].

*DOI: http://dx.doi.org/10.5772/intechopen.86548*

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

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

**3.2 Immune responses in the pathogenesis of periodontal disease**

In normal health conditions, periodontal tissues are capable of coping with the presence of bacteria through several mechanisms of the host immune system (e.g., **Figure 3**) [14]. However, when the balance between the infection control mechanisms and the subgingival biofilm is lost [15], which includes *Porphyromonas* 

*Histopathological lesions of periodontal pathogenesis. Initial, early, established, and advanced lesions of the* 
