الفهرس 
Introduction .Only 14 pages are availabe for public view
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Abstract
One of the most significant risk factors in the development and progression of periodontal disease is smoking (Suratri and Notohartojo, 2016). Moreover, it has been demonstrated by clinical evidence that cigarette smoking may negatively influence the healing outcome following both surgical and non-surgical periodontal therapy. Smokers were proved to have a marked less favourable response compared to non-smokers after scaling and root planning (Abu-Ta’a, 2014), modified Widman flap surgery, adjunctive antimicrobial therapy, and during periodontal maintenance following active therapy (Gunsolley, 2006). Following regenerative therapy, compromised healing in intrabony and in gingival-recession defects in smokers has also been reported (Tonetti, Pini-Prato and Cortellini, 2005).
Significant less improvement in clinical parameters among smokers than non-smokers has been shown in a lot of studies. A 6 year longitudinal study proved that smokers presented around 50% less improvement in probing depth and clinical attachment levels than non-smokers (Ah MK et al., 2000). In addition to, cigarette smoke may directly impact the self-healing capacity of the alveolar process even in the absence of a plaque biofilm (Benatti et al.,2005).
Cigarette smoking has been proven to be able to compromise PDL celladhesion to root planed surfaces, which might affect the susceptibility to periodontal regeneration following new attachment therapy (Gamal & Bayomy, 2002).
A decreased response to treatment was reported in smokers compared with non smokers as measured by decreased probing depths and increased clinical attachment levels (Ah MK et al., 2000). The effect of cigarette consumption level and previous smoking history on the response to active periodontal treatment was evaluated. The results indicated that smokers who smoked more than 20 cigarettes/day responded less favorably to therapy than smokers who smoked less than 19 cigarettes/day, and past smokers (Kaldahl et al., 1996)
It was also proved that smoking exerts a destructive effect on the result of guided tissue regeneration treatment of intrabony defects with bioresorbable membranes. The exact mechanism by which smoking hinders the outcome of GTR treatment is not yet understood, but it has been proven in in vitro studies that nicotine and smoking by-products negatively affect the proliferation, attachment, and chemotaxis of periodontal ligament cells and strengthen the effect of periodontal pathogen toxins (Tonetti et al., 2005). Moreover, it has been observed in smokers that nicotine and reduced oxygen transport and metabolism caused by carbon monoxide induced reduced peripheral blood supply because of vasoconstriction (Ma, Zheng and Cheung, 2008).Therefore , it appears that smoking interferes within several stages of the reparatory/regenerative process in the periodontal wound and as a result compromises healing in general. This in turn may interpret the impaired flap survival, characterized by the increased frequency of membrane exposure observed in smokers versus non-smokers (Mahendra, 2014). Smoking cessation appears to be an influential factor in periodontal therapy and smokers should be encouraged to stop smoking as a part of their periodontal management (Chambrone et al., 2013).
Cessation of smoking has an additional useful effect in reducing probing depths after non-surgical treatment over a 12-month period (Preshaw et al., 2005). It has been shown that the rate of tooth loss among men who left smoking was about 50% lower than the rate of current smokers, yet it was still obviously higher than the rate among non-smokers (Krall et al., 2008). Arrested progression of periodontal bone loss and attachment loss was detected when individuals refrained from smoking (Bergstrom et al., 2000). Although the precise mechanisms that cigarette smoking can affect periodontal tissues are not completely understood, it is obvious that it is still the most significant preventable risk factor for periodontitis (Singh et al., 2014).
IL-1β is a key pro-inflammatory cytokine that is discharged after infection, injury, or antigenic challenge. It has been known by multiple studies for its role as a multi-functional signaling molecule that influence nearly all cell types, either alone or in combination with other pro-inflammatory cytokines (Dinarello, 1996) (Dinarello, 2002). In periodontal inflammation, IL-1β is primarily synthesized by macrophages and dendritic cells, but gingival fibroblasts, periodontal ligament cells and osteoblasts can also express it (Liu et al., 2010). Increased IL-1β is has been detected in periodontal tissue, gingival crevicular fluid (GCF) and saliva of patients with periodontitis and plays an integral role in the etiology of the periodontal disease (Tobón et al., 2008)(Engebretson et al.,2002)(Liu et al., 2010) .
The arachidonic acid metabolite PGE2 is an inflammatory mediator released by action of the enzyme cyclooxygenase from various cell membranes. PGE2 induces vasodilatation, increases vascular permeability, emphasize pain perception by bradykinin and histamine, changes connective tissue metabolism and enhances osteoclastic bone resorption. PGE2 was found in tissue samples from patients with gingivitis and is believed to be involved in the pathogenesis of periodontal disease. (Goodson et al., 1974) (Noguchi and Ishakawa, 2007)
Salivary IL1-β and PGE2 levels have been reported to be increased with periodontal disease severity and decreased with therapy. High sensitivity and specificity for periodontal disease have also been reported; which suggests that they could be useful surrogate indicators for the presence and severity of periodontal disease. (Sánchez et al., 2013)
Summary and Conclusion
The aim of this study was to assess the period of smoking abstinence needed before any periodontal surgery in order to reverse the negative effects of the reported increased levels of inflammatory markers (IL-1β and PGE2 in this study) associated with smoking on the healing and the periodontium.
This study was performed on three groups, each contained ten patients. The first group contained ten smokers that succeeded to quit smokers. The second group contained ten smokers that continued to smoke. The third contained ten non smokers. All patients in all groups fulfilled the clinical criteria of established chronic periodontitis. Any patient having any systemic illness that might affect the result was excluded from the study. Patients using other forms of tobacco were also excluded. Salivary samples were taken from all patients in all groups after initial periodontal therapy. Then samples were taken after one and two months from quitting smoking in the smoking quitters group. While, in the smokers that continue to smoke and non smokers ; samples were taken after one and two months from the baseline salivary sample. Salivary interleukin 1 beta and prostaglandin E2 were measured in the samples as inflammatory markers.
After analysis of salivary samples using ELISA; it was proven that levels of IL 1β and PGE2 decrease significantly in the smoking quitters and non smokers after one month then decrease again after two months significantly. Smoking quitters and non smokes reach levels close to each other after two months. However, smokers that continue to smoke have non significant decrease all through the study.
As a conclusion, the best period to quit smoking before any periodontal surgery is two months in order to have better prognosis.