Periodontitis is a chronic inflammatory condition caused by dental biofilms. Clinically this disease is characterized by periodontal pockets and loss of attachment ultimately leading to tooth loss1. 

Ghrelin is a peptide hormone, predominantly secreted in the stomach and is also known as hunger  hormone. Ghrelin demonstrates immunomodulatory properties of which the anti-inflammatory activity depends on the levels of acylation. This process occurs due to suppression of IL-8 production by TNF-α or lipopolysaccharide stimulated oral epithelial cells .1 

Ghrelin also demonstrates inflammatory properties with low grade inflammation with higher acylated ghrelin levels being observed in chronic periodontitis patients. 

Ghrelin interacts through endogenous ligand for the growth hormone secretagogue receptor (GHS-R)  to specifically inhibit the expression of proinflammatory anorectic cytokines such as IL-1β, IL-6 and  TNF-α.2 

Leptin, a product of the obese gene, is a 16-kDa non-glycosylated peptide hormone. It is synthesized  mainly in adipocytes, which regulate weight control and modulate other physiological functions,  such as regulation of neuroendocrine and reproductive systems. 

Leptin also stimulates the immune system by enhancing pro-inflammatory cytokine production and  phagocytosis by macrophages3. 

Ghrelin has shown dose dependent inhibition of leptin induced cytokine expression, while leptin  upregulated GHS-R expression on human T-lymphocytes. 

To our knowledge, no studies have correlated ghrelin, leptin and periodontal disease. Thus, our  study aims to explore the relationship between ghrelin and leptin in periodontal health and disease in  gingival crevicular fluid (GCF), whilst evaluating Body mass index (BMI) in obese patients.4