Comparison of Salivary Neuropilin-1 (NRP-1), Cotinine and C-Reactive Protein (CRP) Levels With Periodontal Clinical Parameters in Smokers and Non-Smokers With Different Periodontal Diseases

The aim of this clinical study is to compare the levels of salivary Neuropilin-1 (NRP-1), cotinine, and C-reactive protein (CRP) among smokers and non-smokers who are systemically and periodontally healthy, as well as those with gingivitis and periodontitis, and to correlate these biomarkers with periodontal clinical parameters. The ultimate goal is to determine the potential impact of smoking on periodontal health and disease through these biomarkers.

"Periodontal diseases" encompass a range of chronic inflammatory conditions affecting the gingiva, alveolar bone, and periodontal ligaments. The process begins with gingivitis, characterized by sulcular pathogenic bacterial accumulation in the gingiva, and can progress to periodontitis, involving impaired host immune response and destruction of connective tissue attachment. Inflammation in affected tissues, degradation of connective tissue, and biochemical signaling in alveolar bone remodeling contribute to the observed clinical morbidity.

Plaque-induced gingivitis is a reversible inflammatory condition resulting from microbial biofilm accumulation on teeth and inadequate removal. It is characterized by gingival redness, swelling, and a tendency to bleed easily. With proper oral hygiene measures, it can resolve spontaneously within approximately one week. In susceptible individuals, gingivitis may progress to periodontitis. Periodontitis is characterized by connective tissue attachment loss and alveolar bone destruction following an inflammatory host response to periodontal pathogens. These destructions lead to the formation of pathological pockets, increased mobility, chewing dysfunction, patient discomfort, and ultimately tooth loss.

The role of specific bacterial species clusters in periodontal disease has been studied using various methods, from classical cultural techniques to molecular, genomic, and proteomic approaches. Certain bacterial species, such as Porphyromonas gingivalis, Tannerella forsythensis, and Treponema denticola, are commonly associated with periodontal disease. As periodontal disease progresses, the number of gram-negative and anaerobic bacteria in dental plaque increases. However, the presence of microbial biofilm alone may not be sufficient for disease development. The disease arises when the balance between microbial biofilm and host response is disrupted, leading to dysbiosis or an excessive immune response to microbial presence.

During periodontal infection, the release of bacterial leukotoxins, collagenases, fibrinolysins, and other proteases contributes to tissue destruction. Epithelial cells serve as a physical barrier against pathogens and initiate innate and adaptive immune responses. Dendritic Langerhans cells in the epithelium capture microbial antigens and transport them to lymphoid tissue for presentation to lymphocytes. This is followed by infiltration of neutrophils, granulocytes, and lymphocytes into the periodontal lesion. Neutrophils attempt to phagocytose and eliminate bacteria but may be insufficient against the size and chronic persistence of microbial biofilm. This intense chronic inflammatory response leads to alveolar bone resorption by osteoclasts and degradation of connective tissue fibers by matrix metalloproteinases, resulting in granulation tissue formation.