Glucosamine Sulphate Versus Ginger as an Adjunctive Local Delivery Agents in Non-Surgical Periodontal Therapy (A Randomized Controlled Clinical Trial With Biochemical Analysis)

Periodontitis was described as a chronic multifactorial inflammatory disease associated with formation of plaque biofilms and characterized by progressive destruction of the tooth-supporting apparatus. Its primary manifestation includes the loss of periodontal tissue support, featured through clinical attachment loss (CAL) and radiographically alveolar bone loss with the presence of periodontal pockets which are a significant mark of the disease, hence, can progressively lead to tooth loss and gingival bleeding.

The new classification of periodontal and peri-implant diseases and conditions in 2017 classified these diseases into four main categories: First category concerned with periodontal health & gingival diseases either dental biofilm induced gingivitis or non-dental biofilm induced gingivitis. Second category concerned with periodontitis which can be classified into necrotizing periodontitis, periodontitis as a manifestation of systemic disease and periodontitis which include the forms of the disease previously recognized as "chronic" or "aggressive". Third category concerned with other conditions can affect the periodontium as systemic diseases, traumatic occlusion, mucogingival deformities, tooth related factors, periodontal abscesses and endodontic-periodontal diseases. Fourth category concerned with peri-implant diseases and conditions as peri-implant health, peri-implant mucositis, peri-implantitis and peri-implant soft & hard tissue deficiencies.

But now, Periodontitis can be described into four stages depending on the clinical attachment loss (CAL) starting from Stage 1: Initial periodontitis (CAL 1-2 mm), Stage 2: Moderate periodontitis (CAL 3-4 mm), Stage 3: Severe periodontitis with potential for additional tooth loss and Stage 4: Severe periodontitis with potential for loss of dentition (CAL ≥5 mm). Grading focuses on assessment of the risk factors as smoking, systemic factors as diabetes, and outcomes of non-surgical periodontal therapy. Grade A: Slow rate of progression (no CAL loss over 5 years), Grade B: Moderate rate of progression (CAL loss <2 mm over 5 years) and Grade C: Rapid rate of progression (≥2 mm over 5 years).

The pathogenesis of periodontal diseases is mediated by the inflammatory response to bacteria in the dental biofilm. The immune response to infection is regulated by cytokine and chemokine signals. Cytokines and chemokines (chemotactic cytokines) are the messages between cells. Cytokines are low-molecular-weight proteins involved in the initiation and advanced stages of inflammation, in which they can regulate the amplitude and the duration of the response. The genetic regulation leading to the secretion of proinflammatory cytokines from various cells is generally depending on the activation of nuclear factor kappa-B transcription. Cytokines are produced by resident cells, such as epithelial cells and fibroblasts, and by phagocytes (neutrophils and macrophages) in the acute and early chronic phases of inflammation, and by immune cells (lymphocytes) in early and advanced lesions. After recognition of the presented microbes to the appropriate cells, cytokines of the innate response, including tumor necrosis factor alpha, interleukin-1beta and interleukin-6, are the first to face in the pathogenesis pathways of the periodontal disease. It is suggested that individuals who produce high levels of these mediators in response to such thing will go through more and severe tissue loss.

In General, periodontitis is a chronic inflammation in which elimination of the virulent factors can be necessary in treatment of periodontitis by initial intervention by scaling and root surface debridement So, we should know about the importance of human gingival fibroblasts (HGFs). First, HGFs represent most prominent cells in periodontal tissue. Lipopolysaccharides (LPS)-treated HGFs produce inflammatory cytokines such as IL-6 and IL-8 and inflammatory chemical mediators such as Prostaglandin (PGE2), and second; HGFs continue to produce PGE2 IL-6, and IL-8 in the presence of LPS, unlike macrophages. So, it is known that large number of chemical mediators and cytokines was obtained from HGFs can be within the periodontal tissues. That kind of oral infection can be restricted by using antimicrobial mouth wash such as chlorhexidine. usual handling of these chemicals may induce unwanted adverse effects such as tooth staining, taste alteration and development of hypersensitivity reactions.