Xerostomia is a commonly reported oral complaint in patients receiving GLP-1RAs. Its mechanism is likely multifactorial, involving reduced fluid intake associated with appetite suppression, gastrointestinal fluid loss, altered autonomic regulation and the concomitant use of xerogenic medications (21). Reduced salivary flow may increase the risk of developing dental caries, mucosal discomfort, candidal infection, dysphagia and impaired denture retention (22). Clinicians should therefore enquire about oral dryness and related functional symptoms during routine examinations. The mechanisms underlying xerostomia in patients receiving GLP-1RAs remain incompletely defined and are likely multifactorial. An indirect mechanism is clinically plausible as GLP-1RAs commonly cause nausea, vomiting, reduced appetite and gastrointestinal discomfort, which may reduce fluid intake and contribute to dehydration and diminished salivary flow. The concomitant use of other xerogenic medications in patients with diabetes, obesity and cardiovascular comorbidities may further contribute to subjective oral dryness. A potential direct effect on salivary-gland function has also been proposed. Experimental evidence has revealed GLP-1 receptor expression in major salivary glands, providing biological plausibility for receptor-mediated modulation of glandular function. Salivary secretion is regulated by coordinated autonomic signaling involving intracellular calcium and cyclic AMP pathways; therefore, modulation of these pathways by sustained GLP-1 receptor stimulation could theoretically influence secretory activity (6,7) Recent mechanistic research has proposed that prolonged GLP-1 receptor activation may involve cAMP-dependent signaling, β-arrestin recruitment, receptor internalization and altered cellular responsiveness (6). However, these mechanisms remain hypothesis-generating, and direct human evidence demonstrating GLP-1RA-induced salivary-gland dysfunction is currently lacking. Clinically, this distinction is critical as xerostomia should not automatically be attributed to a direct pharmacological effect of the GLP-1RA. Hydration status, gastrointestinal symptoms, concomitant medications and underlying systemic disease should also be considered (7,8). A 2023 case series reported hyposalivation in three patients receiving semaglutide, providing important clinical information but not definitive evidence of causality (7).

Management should include preventive strategies, including the reinforcement of meticulous plaque control, frequent hydration, the use of sugar-free chewing gum, the use of salivary substitutes and the use of topical fluoride, where indicated (9). Patients with persistent symptoms may require more frequent recall and better caries prevention.

Although GLP-1 receptor agonists share broadly similar pharmacological effects, their gastrointestinal adverse effects are not identical. A recent Bayesian network meta-analysis of randomized trials demonstrated differences among individual agents in nausea, vomiting, diarrhea and other gastrointestinal adverse events, with some agents exhibiting greater gastrointestinal intolerance than others (10). Real-world comparative data have similarly suggested differences in gastrointestinal adverse event patterns between individual GLP-1Ras (10,11). However, these findings cannot be directly extrapolated to adverse dental effects. Direct comparative evidence for xerostomia, dysgeusia, dental erosion or other oral manifestations remains very limited. Semaglutide-associated hyposalivation has been described in a small case series (7); however, causality and the underlying mechanism remain uncertain. Therefore, clinicians should avoid assuming that one GLP-1RA has consistently greater oral toxicity than another does. Dental assessments should instead consider the specific agent, dose, treatment duration, recent dose escalation, gastrointestinal symptoms, hydration status and individual oral findings (7,10,12).

Gastrointestinal adverse effects are the most common toxicity associated with the use of GLP-1RAs, particularly nausea and, in susceptible patients, vomiting during treatment initiation or dose escalation (2,11,13,14). Recurrent vomiting or gastroesophageal reflux may expose oral tissues to gastric acid, increasing the risk of dental erosion, dentin hypersensitivity and restorative deterioration (15). Erosive tooth wear typically affects the palatal surfaces of the maxillary anterior teeth and occlusal surfaces of posterior teeth and may progress insidiously; therefore, patients with persistent nausea, retching, vomiting or reflux should be assessed for erosive changes (15).

GLP-1RA-associated delayed gastric emptying may contribute to reflux symptoms in susceptible individuals (16,17). Reflux may also produce unpleasant taste, halitosis or oral burning. Management should focus on preventive counselling, dietary and reflux-related advice, monitoring for erosive tooth wear, and medical referral when symptoms are severe or persistent. Following vomiting, patients should avoid immediate toothbrushing as acid-softened enamel is more vulnerable to abrasion; rinsing with water, milk or a bicarbonate-containing rinse followed by delayed brushing with fluoridated toothpaste is recommended. Topical fluoride varnish and remineralizing agents may be considered for early erosive lesions (15,18).

Some patients treated with GLP-1RAs report dysgeusia or an altered taste perception; however, the prevalence estimates are poorly defined (19). Disturbances in taste can affect food preferences, oral hygiene habits and nutritional intake. Although symptoms are usually transient, if the disturbance persists, other causes should be excluded, e.g., nutritional deficiencies, polypharmacy and systemic disease. While the direct effects of GLP-1RAs on oral sensory pathways are speculative, it is crucial that clinicians are aware of these symptoms and provide appropriate reassurance and supportive care. Overall, a number of the oral manifestations associated with GLP-1RA therapy are relatively mild; however, their cumulative effects may have a marked effect on oral health, treatment outcomes and patient comfort. The critical roles of GLP-1RAs in early detection and the application of preventive strategies are incumbent upon those of dental practitioners.

Patients receiving GLP-1RAs frequently undergo routine dentoalveolar procedures, such as extractions, periodontal surgery and implant placement. This raises questions about the possible effects on wound healing and post-operative recovery. Delayed wound healing, post-operative infection and impaired periodontal regeneration are known to be associated with poor glycemic control (20). Theoretically, GLP-1RAs could improve glucose homeostasis, which can improve tissue repair and decrease postoperative complications (28). This concept is supported by experimental data demonstrating increased angiogenesis, reduced oxidative stress and the modulation of inflammatory responses in several tissue models upon GLP-1 receptor stimulation (22).

Preclinical studies have demonstrated that GLP-1 signaling promotes fibroblast proliferation, enhances collagen deposition and improves vascular function, all of which are important for oral wound healing (23). These anti-inflammatory effects may also benefit healing following periodontal or implant surgery. However, there is limited evidence from studies on oral surgery.

There is no current evidence available to support the routine discontinuation of GLP-1RA therapy prior to minor dental procedures under local anesthesia alone. Simple extractions, scaling and root surface debridement, restorative treatment and periodontal maintenance can usually be accomplished without any alteration of medication regimens as long as the medical condition f the patient is stable (29). However, clinicians should be aware of the possibility of gastrointestinal adverse effects that may affect post-operative care. Patients with marked nausea or vomiting may have difficulty tolerating post-operative analgesics, maintaining adequate nutrition or following oral hygiene instructions. Post-operative advice may also need to be reinforced.

The proposed effects of GLP-1RAs on wound healing remain biologically plausible, yet clinically uncertain in dentistry. Improved glycemic control could indirectly support tissue repair in patients with diabetes, while experimental studies suggest additional effects on inflammation, angiogenesis, oxidative stress and tissue remodeling. However, these mechanisms should not be interpreted as evidence that GLP-1RAs independently accelerate oral or periodontal wound healing. Recent non-dental surgical studies (30,31) have produced heterogeneous findings, with some retrospective analyses reporting favorable or neutral postoperative outcomes and others identifying possible wound-healing concerns. These studies are difficult to extrapolate to periodontal surgery or implant surgery due to differences in procedure type, diabetes severity, nutritional status, obesity, comorbidities and peri-operative management. Thus, there is currently insufficient evidence to recommend GLP-1RA therapy specifically to enhance oral wound healing (30).

The association between GLP-1RA therapy and dental implant outcomes remains inadequately characterized. Improved glycemic control may theoretically reduce some of the biological risks associated with diabetes, while experimental research suggests that GLP-1 signaling may influence bone turnover, inflammation and osseointegration (27). However, these mechanisms do not establish a clinical benefit for implant therapy. The available human evidence concerning peri-implant health is limited and predominantly observational. Differences in diabetes control, periodontal status, smoking status, obesity status, implant characteristics and concurrent medications introduce substantial potential confounding effects. Consequently, GLP-1RA therapy should neither be considered an indication for implant treatment nor viewed as an independent predictor of implant success or failure. For current clinical practice, implant risk assessments should continue to prioritize glycemic control, periodontal stability, smoking status, oral hygiene, bone quality, systemic comorbidities and adherence to maintenance therapy. The potential effects of GLP-1RAs on osseointegration and peri-implant inflammation remain key research questions rather than established clinical indications (27). A summary of the strength of current evidence for oral and dental effects of GLP-1RAs is presented in Table I.

Delayed gastric emptying is clinically relevant when dental treatment involves deep sedation or general anesthesia as residual gastric contents may increase the potential for regurgitation and pulmonary aspiration. However, the magnitude of this risk varies among patients, and perioperative recommendations have evolved rapidly. Current multisociety guidance generally favors individualized risk assessment rather than the routine discontinuation of GLP-1RA therapy for each patient. Prior to sedation or general anesthesia, the dental team should document the GLP-1RA agent, indication, dose, frequency, timing of the most recent dose, recent dose escalation and the presence of gastrointestinal symptoms, such as nausea, vomiting, abdominal pain, bloating or severe reflux. Patients in an active dose-escalation phase or those with substantial gastrointestinal symptoms may represent a higher-risk group and require additional assessment or modification of the planned procedure. There is no basis for applying a universal prolonged fasting period or medication-withholding rule to every patient receiving a GLP-1RA. Instead, the dental practitioner should follow the current institutional, national and anesthesia-provider guidance applicable to the planned level of sedation. For patients considered to have an increased risk of aspiration, risk-mitigation measures may include modification of the procedure, consideration of a liquid-only diet for an appropriate period, adjustment of the anesthetic technique, or postponement when clinically indicated (17,29). Decisions concerning temporary interruption of GLP-1RA therapy should be made collaboratively with the prescribing clinician and anesthesia team, particularly in patients receiving medication for diabetes, as interruption may adversely affect glycemic control. For procedures performed under local anesthesia without sedation, delayed gastric emptying is generally not a major procedural concern. Nevertheless, gastrointestinal symptoms, hydration and overall medical stability should still be considered (29,32,33).

Routine dental procedures performed under local anesthesia can be completed without altering GLP-1RA therapy when the patient is medically stable and has no critical gastrointestinal symptoms or other factors increasing the risk of aspiration. Patients with severe or poorly controlled nausea, vomiting, regurgitation, or reflux should undergo medical assessment before elective dental treatment. Elective procedures may be deferred until symptoms are adequately controlled, particularly when sedation is being considered (11,12). For procedures requiring deep sedation or general anesthesia, the dental team should follow the individualized perioperative risk assessment described above and coordinate with the sedation provider and prescribing clinician when indicated. Dentists should not independently discontinue GLP-1RA therapy; decisions regarding withholding or modifying treatment should be made collaboratively with the prescribing clinician and anesthesia team (11,12).

The key clinical message provided by the current evidence is the following: i) GLP-1RA-related oral effects are predominantly indirect, and direct evidence for specific oral adverse effects remains limited. ii) Preventive dental care should be individualized according to caries, erosion, periodontal and salivary risk. iii) Proposed periodontal, wound-healing and implant benefits remain preliminary and should not alter established periodontal or implant treatment protocols. iv) For deep sedation or general anesthesia, the risk of aspiration should be assessed individually according to treatment phase, gastrointestinal symptoms and current perioperative guidance.

Several limitations should be considered when interpreting the available evidence on GLP-1RAs and oral health. First, direct dental evidence remains relatively limited compared with the extensive systemic literature on these medications. A large amount of the available oral evidence consists of case reports, small observational studies, pharmacovigilance analyses or extrapolation from gastrointestinal and systemic research (7,24,36). Second, patients receiving GLP-1RAs commonly have diabetes, obesity, cardiovascular disease or multiple concomitant medications, rendering it difficult to separate medication-specific effects from underlying disease and treatment-related confounding effects. Third, differences among individual GLP-1RAs, doses, treatment duration and routes of administration limit direct comparisons between studies. Fourth, experimental evidence demonstrating anti-inflammatory, bone-modulating or tissue-repair effects cannot be assumed to predict clinical periodontal, implant or wound-healing outcomes. Finally, perioperative recommendations have evolved rapidly as new evidence has emerged, and differences between professional guidance documents mean that recommendations should be interpreted in the context of local anesthesia, sedation and surgical protocols. These limitations highlight the need for prospective dental studies using standardized measures of salivary function, dental erosion, periodontal inflammation, peri-implant bone levels and postoperative healing. Future research is warrant to also investigate whether specific GLP-1RAs differ in their oral effects and whether any observed periodontal benefits persist after adjustment for glycemic control, weight reduction and other metabolic factors.