Smoking Is Injurious to Pulp

Introduction

The infamous habit of smoking is a worldwide menace that has an influence on various tissues including the dental pulp, its treatments and outcomes. ¹ In direct contact with the oral tissues, tobacco smoke delivers an array of chemical pollutants such as nicotine, carbon monoxide and hydrogen cyanide. These alter the fluid dynamics of any healthy tissue, influencing the physiological processes of inflammation and/or pain mediation.

Effects on the Vascular System

Functional modifications of the vascular system like vasoconstriction and reduced tissue perfusion and morphological alterations including thickening of arteriole walls are among the principal impacts of smoking. Smoking reduces blood flow volume, brings about compromised endothelial dependent vasorelaxation, platelet aggregation and endothelial cell dysfunction. The vascular changes, increased permeability of the vascular tissue wall and increased osmotic pressure (OP)² may be misdiagnosed as pulpal lesions due to altered tissue response. Pulpal vessels show signs of vascular dysfunction restricting nutrient supply and impeding cellular repair suggesting that smoking could contribute to early tissue death within the pulp cavity.³ Free radicals and other components in cigarette smoke further decrease the blood’s oxygencarrying capacity with resultant increase in the levels of carboxyhemoglobin in the blood, causing oxidative stress. Any one of these pathophysiologic pathways could potentially affect the health of the tooth pulp as well as its surrounding tissues.⁴ The reduction in blood flow limits adequate supply of blood and oxygen to mucosal flaps elevated during surgical endodontics. Interestingly, microcirculatory changes are largely reversible, which forms the basis for smoking cessation protocols implemented around surgical procedures.

Local and Systemic Effects

Though blood flow in the dental pulp is regulated by neuronal, local and humoral mechanisms and the effect of systemic blood pressure on pulpal blood flow is more prominent than that of local mechanisms, smoking has both local and systemic effects on pulpal blood flow.⁵ Nicotine causes the release of catecholamines (adrenaline, noradrenaline and isoprenaline) via stimulation of the sympathetic ganglion, adrenal medulla and sympathetic nerve endings causing peripheral vasoconstriction and ischemia in any healthy tissue⁶ with resultant circulatory disturbances and thrombosis which may mineralize leading to pulp stone formation within the tooth. Vasoconstriction and reduction in blood flow is seen within two weeks of nicotine treatment. Under ischemic conditions, the normal clearance effect of blood flowing through a tissue decreases, possibly endangering the viability of the pulp, with early signs of inflammation. Nicotine also influences wound healing between days 6 and 10 (Mosely et al., 1978). Calcitonin gene-related peptide (CGRP), a neuropeptide from afferent nerves in human pulp tissue which affects pulpal blood flow and pulpal inflammation, was significantly higher in the pulp of smokers than non-smokers.⁷ These degenerative changes in the systemic circulation and autonomic nervous system alter homeostasis in the dental pulp affecting its normal functioning.

Effect on Pain Perception

Vasoconstriction and decreased blood flow, along with ischemic effects of nicotine, may alter tooth pain sensation and the sensibility of the pulpal myelinated fibres. In a preliminary study, Awawdeh found that neuropeptides NKA, SP and CGRP found in painful teeth were reduced in smokers.⁷ Another study showed that smokers need comparatively more amount of local anaesthesia than non-smokers.⁸ Therefore, smokers may display unusual clinical symptoms/signs compared to non-smokers due to altered pain and inflammatory conditions.

Effects on Immune System

Although the peripheral leukocyte counts are higher in smokers, tobacco appears to undermine the host immune system by interfering with the innate and acquired immune response with impaired chemotaxis and function of neutrophils, impaired phagocytosis, production of protease inhibitors and PGE², reduced cytokine levels, generation of free radicals in healthy and diseased tissues and suppression of immunoglobulins A, G, and M. Smoking is known to induce a chronic systemic inflammatory response increasing C-reactive protein levels in serum.³ Thus, once bacterial infection begins in the pulp and surrounding tissues, smokers are less likely than non-smokers to be able to limit the destruction. Cigarette smoking also alters macrophages (Schwartz & Weiss 1994) and T-cell lymphocyte functions, decreasing antibody levels and increasing the levels of pro-inflammatory mediators (IL−6, TNFα, C-reactive protein). Smokers are immunologically deficient in factors like TNF-a and hBD-2, suggesting that dental pulp of smokers possesses limited defense mechanisms, affecting their endodontic prognosis and indicating a cause for their reported inferior outcome.⁹ Reduced GCF in smokers (Kinane & Radvar 1997), further reduces the volume of antibodies and other defense molecules entering the oral cavity and disturbs the balance between the reactive oxidase species and its buffers, the antioxidants. Such imbalance will affect the lipids in membranes, intracellular proteins and most importantly damage DNA, leading inevitably to cellular death.¹

Endodontic Effects

Smoking has local and systemic effects on the microcirculation, wound healing and the immune system, along with impairment of hard and soft tissue healing, and is associated with wound infection after soft tissue incision procedures.¹⁰ These factors along with oxidative stress on inflamed periapical tissues of smokers further contribute to a greater number and/or size of periapical lesions than in non-smokers.¹¹ Even after adjusting for several covariates such as age, gender, number of teeth, endodontic status, quality of root filling, and diabetic status, tobacco smoking was strongly associated to the presence of radiographically diagnosed periapical lesions.¹²

A dose-response relationship between tobacco smoking and root canal treatment (RCT) has been found (Krall et al., 2006). A recently published systematic review states that smokers are 2.5 times more likely to have apical periodontitis, with RCT being three times more prevalent, compared to non-smokers.¹³ Several confounding factors were identified in the study such as misinformation regarding the period of time subjects had smoked, as well as the frequency of smoking and the number of cigarettes consumed. Another study has shown that the prevalence of apical periodontitis in hypertensive smokers (92%) is significantly higher than in non-smokers (44%).¹⁴ Tobacco smoking can delay the periapical healing of the root filled teeth by hindering bone and tissue repair by stimulating osteoclastic cells and reducing angiogenesis. Continued destructive processes establish persistent apical periodontitis, which may ultimately lead to tooth loss. Although the exact mechanisms are unknown, smoking interferes with the wound healing process, which may influence the prognosis and treatment outcome of vital pulp therapy. However, a study by G Kunert et al., 2015 showed no statistically significant correlation between smoking status and success of pulpotomy procedures.

Smoking compromises functioning of mesenchymal stem cells, thereby affecting regeneration in pulp as well as inhibiting differentiation of human dental pulp stem cells.¹⁵ It is known to delay fibroblast migration to the wound area leading to accumulation at the periphery of the wound which may prevent healing and increase scarring (Wong et al., 2004). In addition to their production of collagen, elastic and reticular fibres, fibroblasts orchestrate proliferation, migration and secretion of proteins such as cytokines and growth factors. Nicotine inhibits myofibroblast differentiation in human fibroblasts in vitro (Fang & Svoboda, 2005). Nicotine also suppresses the cytodifferentiation and mineralization of HDPCs.¹⁶

Cigarette smoking has local and direct pro-inflammatory effects on inflamed periapical tissues with increased levels of products of lipid peroxidation, such as 8-isoPGF (2a), and products of the LOX-pathway. Negative effects of smoking habit on apical periodontal tissue can be observed in provoking the release of bone decalcification chemical signals, hindering the intake of Ca+2 by the GIT system, leading to bone destruction in periapical region. Prior to endodontic treatment, the periodontal status of the patient is thoroughly assessed as teeth of periodontally maintained smokers have a two-fold greater chance of being lost and an even greater chance is seen in non-periodontally maintained patients who smoke (McGuire & Nunn, 1996).

Smokers are also associated with an increased prevalence of root caries and are at increased risk of marginal periodontitis. Therefore, when root filled teeth are being restored in smokers, extra care must be taken to ensure that margins are supragingival and maintenance regarding diet and oral hygiene is optimal.¹⁰

Conclusion

The association of root canal treatment risk varies with years of exposure, magnitude and frequency of tobacco smoking as well as period of abstinence suggesting that smoking may have a causal role in the development of lesions that result in root canal treatment, and, conversely, that smoking prevention, abstinence and cessation are critical strategies to reduce the risk of root canal treatment. Smokers have an increased prevalence of root caries and are also at increased risk of marginal periodontitis. Various vascular alterations in smokers predispose them to higher incidence of pulp stones.

Smokers may affect healing of soft and hard tissues and smoking cessation programme could be developed prior to endodontic treatment and may be an important prognostic factor of apical periodontitis. The present review has focussed on profound impact of smoking upon pulp tissue which has an impact on the pulp environment further modifying the functionality of the pulp.

Conflict of interest

None.