Smoking may be associated with increased sensitivity to temporomandibular disorders (TMDs); however, the relationship is complex. The Orofacial Pain Prospective Evaluation and Risk Assessment study, funded by the National Institute of Dental and Craniofacial Research, represents a groundbreaking investigation, having enrolled and tracked over 4,000 participants over a period of five years [1]. The study identified various environmental and life events associated with an increased risk of developing TMDs and their progression to chronicity [2]. Among these factors, a lifetime history of smoking was notably linked to TMD incidence [2,3], showing a positive association with a hazard ratio of approximately three to four times higher compared to non-smokers [4]. We propose several underlying mechanisms through which smoking may influence the development and chronicity of TMDs. These factors contribute to a complex interplay, elevating the risk of TMD onset in smokers and promoting the persistence of the disorder once established.

Smoking is known to elevate systemic inflammation [5], which may affect the temporomandibular joint (TMJ) and surrounding tissues, potentially contributing to the onset and persistence of TMJ-related symptoms. Interestingly, nicotine exhibits dual effects on inflammation; while it often exacerbates inflammation, it has also been found to reduce it under certain conditions. For example, in rheumatoid arthritis, nicotine inhibits specific immune responses, particularly those mediated by Th17 cells, which are critical in inflammatory diseases [6]. Additionally, in neurological disorders, nicotine has been observed to modulate immune responses and reduce inflammation, highlighting its complex and context-dependent role in mental health and inflammatory processes [7]. Further research is required to elucidate the effects of smoking on TMD and its underlying mechanisms.

Thus, the relationship between smoking and osteoarthritis (OA) is complex, especially concerning inflammatory responses. Although smokers tend to show a lower incidence of radiographic OA, they frequently experience heightened musculoskeletal pain and other inflammation-related complications [8]. This paradox highlights the nuanced effects of smoking on joint health and inflammation, suggesting that while smoking may influence certain pathways that mitigate OA development, it simultaneously exacerbates pain and inflammation in other musculoskeletal contexts [9].

Overall, the inflammatory response to smoking in OA reflects a balance between potential protective effects against joint degeneration and increased risks of musculoskeletal pain and joint deterioration. This complexity suggests that further research is essential to fully elucidate these dynamics and to clarify how smoking influences the inflammatory pathways that impact joint health and pain outcomes [10].

Smokers frequently experience elevated levels of stress and muscle tension, especially in the jaw and neck regions. This heightened muscle tension places additional strain on the TMJ, potentially contributing to the onset of TMDs or exacerbating existing conditions. The increased stress on the TMJ due to muscle tension highlights another pathway through which smoking may influence TMD risk and severity [3]. Smoking contributes to muscle tension and stress through several mechanisms. Nicotine, the primary addictive component in tobacco, acts as a stimulant that elevates heart rate and blood pressure, creating physical tension throughout the body. This physiological response to nicotine can exacerbate muscle tension, particularly in areas prone to stress, such as the jaw and neck, thereby increasing strain on the TMJ and potentially heightening the risk or severity of TMDs [11]. This heightened physiological state often manifests as muscle tension, particularly in areas commonly affected by stress, such as the neck, shoulders, and jaw [12].

Smoking also disrupts the body’s natural stress response. Although nicotine may provide a temporary sense of relaxation, it often leads to withdrawal symptoms that elevate stress levels when not smoking [11]. This cycle can intensify anxiety and chronic stress over time, contributing to persistent muscle tension. Additionally, smoking impairs oxygen delivery to muscles and other tissues, which can hinder relaxation and recovery, leading to increased muscle stiffness and discomfort [13].

Smoking significantly hinders the body’s natural healing capacity through multiple mechanisms. It is well-documented that smoking impairs blood circulation, a crucial process for delivering oxygen and nutrients to tissues essential for repair and regeneration [14]. This restricted circulation can slow down the healing of musculoskeletal tissues, including those around the TMJ. This impaired circulation can result in prolonged recovery times and persistent symptoms for TMD patients, complicating efforts to manage or resolve their condition effectively. As a result, smoking not only delays healing but may also contribute to the chronicity of TMD [15].

Sørensen et al. [16] demonstrated that smokers frequently encounter complications after surgery, including delayed wound healing and a higher incidence of infection compared to non-smokers. These findings highlight how smoking can hinder postoperative recovery, adding further challenges for TMD patients who may require surgical interventions, as the delayed healing and increased risk of complications can contribute to prolonged discomfort and hinder successful outcomes.

Nicotine and other chemicals in cigarettes can affect pain perception and thresholds [17]. Smokers may experience increased sensitivity to pain, which could contribute to chronic pain syndromes associated with TMDs [2]. Smoking affects pain perception both immediately and over the long term [18]; while smokers often demonstrate higher pain thresholds and tolerance than non-smokers—suggesting that nicotine temporarily increases pain tolerance [19]—withdrawal from smoking can lead to heightened pain sensitivity and reduced tolerance [20]. Ditre et al. [21] observed that during smoking cessation, individuals may experience elevated pain intensity and lowered tolerance due to nicotine withdrawal.

Nicotine’s short-term effects include reducing anxiety, providing temporary relief from stress. However, this relief can lead to dependency, paradoxically increasing anxiety over time [22]. Nicotine also impacts neurotransmitter systems associated with mood and anxiety, so while it might momentarily alleviate symptoms, prolonged use may worsen them [23]. In addition, pain-related anxiety is strongly linked to smoking behavior [24]; individuals with high pain anxiety often experience early relapse, emphasizing the psychological dimensions influencing smoking and pain sensitivity [25].

Overall, while smoking initially alters pain sensitivity, likely by increasing tolerance through nicotine’s analgesic effects, cessation reverses these effects, rendering individuals more sensitive to pain.

In conclusion, while nicotine may offer temporary relief for anxiety and inflammation, its long-term effects significantly complicate its potential therapeutic applications. Given nicotine’s rapid systemic distribution following inhalation, a lifetime history of smoking may act as a fast-acting maladaptive pain behavior in individuals with chronic overlapping pain conditions. Smoking appears to represent a form of pain behavior in individuals predisposed to chronic pain, who may also be at an elevated risk for TMDs. To address this issue, the promotion of health-enhancing behaviors such as increased physical activity, attention diversion techniques, relaxation practices, and maintaining consistent work routines is recommended. These strategies could mitigate pain intensity, maladaptive pain behaviors, depression, and anxiety in patients with chronic pain. Over time, adopting these behaviors may reshape pain responses and coping mechanisms, reducing susceptibility to TMDs. Conversely, habitual smoking may maladaptively modify pain perception and tolerance, further exacerbating vulnerability to TMDs through its influence on the way pain is experienced and managed.

No potential conflict of interest relevant to this article was reported.

Data sharing is not applicable to this article.

None.

Conceptualization: QSA. Data curation: YHL, QSA. Formal analysis: YHL, QSA. Methodology: YHL, QSA. Project administration: QSA. Visualization: YHL, QSA. Writing original draft: YHL, QSA. Writing review & editing: YHL, QSA.