Relationship of trace element homeostasis and immuno inflammatory response to smoking index

Abstract EN

To evaluate the magnitude of cigarette smoking relative to the inflammatory status in periodontal tissues and their relationship to antioxidant status, trace elements homeostasis and immunological response.

The study involved 45 male smokers' wit periodontitis (age range 30-45) who were equally divided into 3 groups according to their smoking pattern (mild, moderate, and heavy smokers).

An allied age-matched group of 15 healthy non-smokers was also included.

Evaluation of clinical and histological parameters as well as assessment of serum cotinine (the metabolite of nicotine) antioxidant status [vitamin E, glutathione peroxidase enzyme (GSH-Px), reduced glutathione (GSH), and lipid peroxidation product, malondialdehyde (MDA); trace elements (selenium, cadmium, zinc, and copper); ceruloplasmin (Cp), metallothionein, cytokines [interleukin-1 B (IL-1B) and interleukin-6 (IL-6)] and soluble intercellular adhesion molecule-1 (ICAM-1) were conducted in selected cases. Smokers exhibited variable inflammation in periodontal tissues relative to the smoking pattern.

They expressed high levels of metallothionein in plasma reflecting an attempt to defend against free radicals.

A reduction in antioxidant determinants, alterations in trace elements homeostasis and induction of cytokines and soluble adhesion molecule were identified in relevance to smoking intensity verified by serum cotinine levels. Advanced periodontitis in smokers was related to smoking duration.

The reduced antioxidant status potentiates the inflammatory response.

Trace elements imbalance induced by smoke inhalation coordinates with toxic impetus initiating cytokine induction of ICAM-1 which sustains the inflammatory state and retards healing and repair.