The interplay between oral health and gastrointestinal disorders: a comprehensive narrative review of emerging links and clinical implications

Summary

: Emerging evidence suggests a bidirectional relationship between oral health and gastrointestinal (GI) disorders, yet this connection remains inadequately understood in clinical practice. This comprehensive narrative review examines the current evidence linking oral microbiome dysbiosis, periodontal disease, and other oral health parameters with various GI disorders. Our review identified significant associations between periodontal disease and increased risk of inflammatory bowel disease (IBD) and colorectal cancer. Oral microbiome dysbiosis, characterized by increased abundance of pathobionts including Porphyromonas gingivalis and Fusobacterium nucleatum, was linked to exacerbation of IBD symptoms and intestinal inflammation. Additionally, gastroesophageal reflux disease (GERD) demonstrated significant correlations with dental erosion, periodontitis, and oral mucosal lesions. Mechanistic studies suggest that oral-gut translocation of bacteria, systemic inflammatory mediators, and shared immune dysregulation may underlie these associations. Conclusions: This review highlights the significant interplay between oral health and GI disorders, emphasizing the potential for integrated clinical approaches. Recommended clinical implications include comprehensive oral health assessment in patients with GI disorders, periodontal therapy as an adjunctive treatment strategy, and interdisciplinary collaboration between gastroenterologists and dental professionals. Further prospective longitudinal studies and clinical trials are warranted to establish causality and develop evidence-based integrated treatment protocols.

Keywords:

ulcerative colitis – Crohn’s disease – gastrointestinal disorder – oral manifestations

Introduction

The gastrointestinal (GI) tract extends from the mouth to the anus. It plays an essential role in food digestion by propelling bolus into the esophagus and stomach, absorbing nutrients in the small intestine through enzymatic secretion and water in the large intestine, protecting the body from microbial invasion, and expelling feces [1].

Gastrointestinal disorders (GIDs) are among the most common problems in health care. Despite being often misdiagnosed, oral and gastrointestinal diseases can affect each other. The major role of the oral cavity is biting, chewing, and mixing food particles with saliva to form a “bolus” ready for swallowing and passing through the pharynx and esophagus onto the stomach [1].

Oral lesions may occur earlier, during, or after the development of GI diseases. Oral lesions may be similar to GI lesions or induced by systemic changes in GI disorders such as malabsorption [2].

To provide safe and appropriate dental care, dentists are typically concerned with the proper diagnosis of oral manifestations of GI disorders, homeostasis, risk of infection, drug actions and interactions, and many times, this could be a warning alarm for diagnosing a systemic disorder of the patient. The present article offers a detailed review of the oral manifestations of various GI diseases or conditions [3].

The classification given by Jajam et al. represents a systematic approach to understanding the complex relationship between gastrointestinal disorders and their oral manifestations, highlighting the importance of interdisciplinary medical investigation (Tab. 1) [4].

Inflammatory bowel diseases

Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic inflammatory diseases with primary intestinal involvement. Generally, it is assumed that IBD is a multifactorial disease in which the immune system, genetics, and environmental factors all play a role [5]. Oral manifestations could also occur in these patients due to other causes, such as drug reactions, infections, and unrelated diseases. Patients with IBD may present with these oral manifestations years before the appearance of intestinal disease [6]. Recognizing these patterns may assist physicians and other caregivers in making a timely diagnosis of IBD while avoiding unnecessary workups.

Crohn’s disease

Crohn’s disease is a relapsing systemic inflammatory disease, mainly affecting the gastrointestinal tract with extraintestinal manifestations and associated immune disorders. Although it has long been recognized that Crohn’s disease (CD) can affect any part of the body from the mouth to the anus, a detailed understanding of the specific lesions manifesting in the mouth and their clinical importance has evolved relatively recently.

Although the exact cause remains unknown, it is a complex interaction between genetic predisposition, environmental risk factors, and immune dysregulation in intestinal microbiota. Clinical features include diarrhea, which is the most common symptom and is present in 70–80% of cases; other symptoms include abdominal pain, which is most common in the right lower quadrant, weight loss, anorexia, and fatigue (Fig. 1). Patients may also report, or even present, with extra-intestinal manifestations such as arthritis, uveitis, or erythema nodosum [7].

Oral lesions have been detected years before clinically apparent disease. Some lesions may persist for ten or more years, while others show spontaneous healing. Several authors suggest that exacerbating aphthous ulcers may mark an impending intestinal flare-up. E. coli has been found in the mouths of some patients, perhaps due to diminished IgA secretion, use of antibiotics, or steroid administration. It has been postulated that lymphocytes may release damaging tissue mediators after exposure to enterobacterial extracts. This explanation attempts to link activity in the mouth with that in the intestines, as a common response to low IgA levels and lack of mucosal defense against foreign antigens [8]. Oral CD can be detected in the buccal mucosa, lips, tongue, hard and soft palate, salivary glands, gingiva, and teeth with alterations that can either be typical and pathognomonic, and in most cases, this can be associated with or highly suspicious of inflammatory bowel disease or nonspecific bowel disease [9].

Another typical finding in CD is the frank granulomatous invasion of the buccal mucosa. Raised smooth surfaced nodules or a “cobblestone appearance,” are created by marked mucosal hypertrophy, with deep-surfaced fissuring or linear ulceration. In the mucobuccal folds, hyperplastic ridges may be seen and resemble denture-induced granulomas [8].

Mucogingivitis appears as an edematous, granular, and hyperplastic gingiva with or without ulceration. Other specific lesions are lip swelling with vertical fissures, deep linear ulcerations (usually in the buccal sulci with hyperplastic folds), and midline lip fissuring, all with minimal or no association with intestinal CD activity [10]. Tab. 2 describes specific and nonspecific oral lesions in CD.

The oral findings are clinically silent and asymptomatic in the majority of CD patients. Oral lesions in these patients do not require special care; instead, they will disappear on their own as the gastrointestinal disease is treated with immunosuppressive medications, biological agents, and/or anti-inflammatory drugs (5-ASA) if needed [11].

The arsenal of therapeutic interventions comprises of topical and systemic steroids, 5-ASA drugs, biologic therapies, immunosuppressive medicines, and even antibiotics such as tetracycline [2].

Controlling colonic illness is the first and most important step in treating oral lesions [2]. One possible treatment for CD would be to try food restriction [12].

Ulcerative colitis

An illness of unknown cause that is characterized by repeated episodes of bloody diarrhea in a clinical setting and diffuse inflammation of the large intestine wall in a pathological setting. Colonic and rectal mucosa are where inflammatory alterations are limited to, or most severe in, and extend proximally from the rectum [13].

The rectum is affected distally in ulcerative colitis (UC), extending proximally for a variable distance with an abrupt demarcation between inflamed and non-inflamed mucosa [4]. This causes ulcerations of the colon‘s and rectum‘s lining, which exacerbates constipation, dehydration, fever, exhaustion, and bloody stools. UC patients typically go through periods of remission and recurrence. It has been linked to several genetic variables. IBD is linked to 163 susceptibility disease-associated loci. Thirty are linked to CD, twenty-three to UC, and most of the remaining ones are shared by both UC and CD. The sharp rise in UC cases in recently industrialized countries suggests that environmental factors play a part in the onset of the disease. Urban lifestyles, pollution exposure, dietary modifications, access to antibiotics, better sanitation, and a decrease in illnesses are all linked to industrialization and are seen as general contributing factors [14]. The exact cause of UC is unknown; however, many factors have been implicated such as immune dysfunction, tobacco, NSAIDs, psychological stress, milk intake, etc. [4]. Fig. 2 explains UC‘s risk factors and disease symptoms.

Males are more likely to develop ulcerative colitis, which occurs twice as frequently as CD [15]. UC is typically diagnosed in slightly older adults, with a mean age of 32 years, in contrast to CD. A bimodal pattern characterizes the prevalence of UC, with the maximum occurring in early adulthood and between the sixth and seventh decade of life [16]. Prevalence has been ascribed to the Westernized lifestyle.

UC may be characterized by a series of specific and nonspecific oral lesions, as described in detail below in Tab. 3 [17]. In UC, common oral lesions include aphthous stomatitis and ulcers, although ulcers are observed less frequently compared to those with CD. Additional oral manifestations may include angular cheilitis. Cheilitis might manifest alongside scaly perioral skin and significant cervical lymphadenopathy. Pyostomatitis, also known as pyoderma vegetans, is considered a highly specific marker of UC which presents as a nonspecific destructive eruption with burrowing pustules that later evolve into large ulcers, typically found on the lower lip. These lesions may occur in various areas except the tongue. Pyostomatitis tends to improve when colitis is effectively managed but flares up during exacerbations. Some patients may develop lesions of pyoderma gangrenosum, characterized by progressive necrosis leading to deep ulceration, which can affect the tongue [18]. Some patients may experience nonspecific lesions like dry mouth, taste change, halitosis, and periodontitis. These nonspecific oral lesions in UC are observed to be more prevalent than specific lesions [17].

In the treatment of UC, the primary approach involves administering systemic corticosteroids, typically effective in alleviating oral manifestations. Additionally, immunosuppressive and biological agents are frequently employed in treatment.

Disease associated with genetics

Peutz-Jeghers syndrome

Peutz-Jeghers syndrome (PJS) is an autosomal dominant syndrome characterized by multiple hamartomatous polyps in the gastrointestinal tract, mucocutaneous pigmentation, and an increased risk of gastrointestinal and non-gastrointestinal cancer mostly in the small bowel. PJS was first reported in a pair of identical twins with melanotic macules described by Connor in 1895 and illustrated by Hutchinson in 1896 [19].

PJS is mainly caused by gene mutation and inheritance. The serine/threonine kinase 11 (STK11) tumor suppressor gene, which is found on chromosome 19p13.3. is mutated in PJS cases. This gene is sometimes referred to as the LKB1 gene, and it is hypothesized that the inactivation of this gene contributes to the development of many malignancies. Inheritance involves autosomal dominance patterns meaning that an individual with PJS has a 50% chance of passing the mutated gene to each of their offspring [20]. PJS is considered rare, with an estimated prevalence of about 1 in 50,000 to 200,000 individuals. Symptoms of PJS often manifest in childhood, with the appearance of characteristic mucocutaneous pigmentation and gastrointestinal symptoms, and affect both males and females equally. Individuals with PJS have an increased risk of developing various cancers, particularly gastrointestinal cancers, including colorectal, small bowel, stomach, pancreatic, and breast cancers [19,20].

The most prominent oral manifestation of PJS is the presence of pigmented lesions on the lips, buccal mucosa (inner lining of the cheeks), and perioral area (around the mouth). These pigmented lesions typically appear as well-defined brown to black macules or patches [2].

Zaheri et al. highlighted that treatment for pigmented lesions is generally unnecessary unless there are specific cosmetic or social reasons to intervene [21]. Their study demonstrated positive outcomes with the use of potassium-titanyl-phosphate laser ablation for pigmented lesions, showing mild acanthosis with elongation of rete pegs and increased pigmentation in melanocytes and adjacent keratinocytes.

Gardner syndrome

Gardner syndrome (GS) is a genetic disease with autosomal dominant transmission, representing a phenotypic variant of familial adenomatous polyposis (FAP). The study on genome sequencing highlights the diagnostic utility of identifying multiple risk variants contributing to the severity of phenotypes in genetic diseases such as GS [22]. It is marked by a high risk of malignancy caused by many adenomatous polyps lining the gut mucosal surface. In 1951, Gardner provided the syndrome‘s first description. He reported having malignancies outside the colon in addition to several polyps inside the colon.

The development of GS is primarily linked to genetic mutations within the adenomatous polyposis coli (APC) gene on chromosome 5q21, a critical tumor suppressor gene responsible for regulating cell growth. Mutations in this gene lead to uncontrolled cell proliferation, with additional genetic factors such as loss of DNA methylation, RAS gene mutations, and alterations in other cancer-related genes potentially contributing to the syndrome‘s progression [23]. GS is a rare inherited disorder that is inherited in an autosomal dominant manner. The incidence of GS is between 1 in 4,000 and 1 in 12,000, depending on the region [24].

The dental abnormalities associated with this condition may include impacted or unerupted teeth, congenitally missing teeth, supernumerary teeth, hypercementosis, dentigerous cysts, fused molar roots, long and tapered molar roots, hypodontia, compound odontomes, and multiple caries. Difficulties in extraction due to ankylosis have also been reported [25]. Preventive measures are often the primary approach to managing individuals who are aware of familial inheritance or upon its discovery. This treatment regimen typically involves maintaining a healthy diet, utilizing NSAIDs like sulindac, or COX-2 inhibitors such as celecoxib, which can help impede polyp growth in the colon. This is particularly crucial for individuals with Gardner syndrome, who face an increased risk of developing colon cancer. Regular surveillance through lower GI endoscopies is also advised to monitor polyp growth and detect any progression to malignant tumors. If more than 20 polyps are identified, surgical removal of the colon may be recommended to mitigate the risk of colon cancer development [24].

Disorder associated with hypersensitivity

Celiac disease

Celiac disease is a systemic autoimmune-mediated disorder triggered by the ingestion of gluten, a protein found in wheat, barley, and rye, in individuals with specific genetic predispositions. The condition is characterized by small intestinal enteropathy, systemic symptoms related to malabsorption and/or immune activation, and autoantibodies to tissue transglutaminase (TTG). Removal of gluten from the diet results in the resolution of symptoms and enteropathy in most patients, making it unique among autoimmune diseases, as the trigger has been identified and its removal can effectively manage the condition [25,26]. It is a hereditary disorder, with a genetic predisposition identified in the major histocompatibility complex region. People with certain gene mutations (HLA-DQ2 or HLA-DQ8) are more susceptible to developing celiac disease [25].

The reported prevalence is 0.5 to 1% in the general population. Over the past 10 to 20 years, the true prevalence, detection, and diagnosis have increased. The prevalence of celiac disease is higher in first-degree celiac disease relatives of 10–15% and in other at-risk groups, particularly patients with Down syndrome, type 1 diabetes, or IgA deficiency. Females are more susceptible than males with a ratio of 2 : 1 [27].

Oral manifestations of celiac disease include several symptoms that can affect the mouth and teeth. These manifestations are not limited to the digestive system and can be a diagnostic clue for the disorder. The key oral manifestations of celiac disease are dental enamel defects that can include enamel pitting, grooving, and sometimes complete loss of enamel. Recurrent aphthous ulcers, delayed tooth eruption, caries, geographic tongue, angular cheilitis, atrophic glossitis, burning tongue, and dry mouth are the common oral manifestations that can be a diagnostic clue for celiac disease, especially when combined with other symptoms such as digestive issues, fatigue, and weight loss [28,29]. The primary treatment for celiac disease involves adhering to a gluten-free diet, which means avoiding foods containing wheat, rye, or barley. Typically, symptoms improve within 1 to 2 weeks of starting this diet, but even small gluten exposures can hinder recovery or trigger a relapse [30].

Repeating a small bowel biopsy after 3 to 6 months of being on a gluten-free diet is recommended to assess progress. If abnormalities persist, other potential causes such as lymphoma should be considered. Improvement in symptoms and small-bowel health usually coincides with a decrease in specific antibody levels [26,28].

Supplementary vitamins, minerals, and hematinics may be prescribed based on individual deficiencies. This personalized approach helps address any nutrient gaps and supports overall health during the management of celiac disease [28,30].

Disorders associated with infections

Peptic ulcer disease

Peptic ulcer disease (PUD) is sores that develop on the stomach lining, small intestine, or esophagus due to excessive gastric acid secretion or pepsin activity. This disruption extends into the muscularis propria layer of the gastric epithelium, commonly affecting the stomach and proximal duodenum. It can also affect the lower esophagus, distal duodenum, or jejunum. Peptic ulcers come in two main types: gastric ulcers and duodenal ulcers. In individuals with a gastric ulcer, epigastric pain typically arises within 15–30 minutes after eating, while those with a duodenal ulcer usually experience pain 2–3 hours post-meal [31].

Infection with Helicobacter pylori (H. pylori) bacteria is the most common cause of peptic ulcers, and non-steroidal anti-inflammatory drugs (NSAIDs) are the leading culprit for ulcers that develop in people without H. pylori infection or both [32]. H. pylori is a gram-negative bacterium that infects the gastric mucosa, leading to gastritis and potentially peptic ulcer disease and gastric cancer. H. pylori affects a significant portion of the population; however, only a small subset will develop clinical disease (Fig. 3) NSAID use, such as aspirin, is widespread and increases the risk of gastrointestinal adverse events, including peptic ulcer disease. While H. pylori and NSAID use are responsible for the vast majority of peptic ulcers, other less common causes have been identified, including gastrinoma (e. g., Zollinger-Ellison syndrome) and other medications [33].

PUD is a global problem with a lifetime risk of development ranging from 5% to 10% [30]. A higher occurrence of PUD has been linked to the male gender, smoking, and chronic medical conditions. Additionally, PUD has been connected to advancing age. In recent years, a notable decline in the diagnosis of PUD and its related complications has been observed due to enhanced hygienic and sanitary conditions, along with efficient treatment and careful administration of NSAIDs [33]. Duodenal ulcers are four times more prevalent than gastric ulcers [31].

Peptic ulcers themselves don‘t cause direct oral manifestations. However, some studies suggest a connection between peptic ulcers and certain oral conditions, possibly due to nutritional deficiencies or changes in taste perception. These oral signs can be caused by other underlying conditions as well. Here are some possible oral manifestations that might be associated with peptic ulcers: burning mouth syndrome, aphthous ulcers, angular cheilitis, changes in taste, and a dark erythematous tongue with a slimy yellowish coating. There may also be congestion and dilatation of sublingual veins [4].

PUD is generally managed through a combination of medications and lifestyle modifications, with the treatment strategy tailored to the ulcer‘s underlying cause. Antisecretory medications for PUD include H2-receptor antagonists and proton pump inhibitors (PPIs). It may be advisable to include calcium supplements, as prolonged use of PPIs can elevate the risk of bone fractures. For NSAID-induced PUD, the approach involves either discontinuing NSAID use or reducing the dosage. If feasible, corticosteroids, bisphosphonates, and anticoagulants should also be stopped. Prostaglandin analogs, such as misoprostol, may be utilized as a preventive measure against NSAID-induced peptic ulcers. The first-line treatment for H. pylori-related PUD consists of a triple therapy regimen that includes two antibiotics and a proton pump inhibitor. Commonly prescribed combinations include pantoprazole with clarithromycin and either metronidazole or amoxicillin, administered for 7 to 14 days. Should the initial treatment prove ineffective, a quadruple therapy involving bismuth and alternative antibiotics is recommended [31].

Gastroesophageal reflux disease

The physiological process known as gastroesophageal reflux (GER) is frequently seen. It is linked to the lower esophageal sphincter‘s (LES) relaxation occurring at a different time from swallowing, which permits the stomach contents to pass into the esophagus. After meals, episodes often last up to three minutes in healthy persons and are either asymptomatic or cause only a few symptoms [15,34].

Gastroesophageal reflux disease (GERD) is distinguished from GER by its chronic, long-lasting, and more serious complications. This involves unusual reflux of gastric ingredients into the esophagus at least once a week, leading to heartburn and acid regurgitation, causing macroscopic impairment of the esophagus that finally influences the quality of life. Other organs such as the pharynx, larynx, respiratory system, and oral cavity can also be affected. When this happens, it is known as extraesophageal syndrome. GERD‘s classical symptoms are heartburn and sour taste, but dysphagia, sore throat, odynophagia, globus sensation, and nausea are also commonly reported (Fig. 4) [34].

GERD occurs when stomach acid flows back up into the esophagus, causing heartburn and other symptoms. The primary cause is a weakened or malfunctioning lower esophageal sphincter (LES). This valve normally prevents stomach contents from flowing back up, but other causes include increased intra-abdominal pressure, delayed gastric emptying, esophageal motor dysfunction, and other factors like medications (such as NSAIDs, antidepressants, and beta-blockers), diet (high-fat, spicy, or acidic foods), lifestyle factors (smoking, alcohol consumption), and certain medical conditions (such as scleroderma or diabetes) [15].

It‘s important to note that the exact cause of GERD in any individual may vary, and often a combination of factors is involved. GERD, a common gastrointestinal disorder, affects approximately 20% of adults in western cultures. While it is more prevalent in men than women, both genders are susceptible [34].

GERD patients are at an increased risk of dental erosion, severe periodontitis, halitosis, and oral mucosal lesions. Studies have shown lower buffering capacity, salivary flow rate, and pH in GERD patients, with reduced micro-crystallization of saliva in children with GERD. A strong link exists between GERD and bisphosphonate-induced osteonecrosis of the jaw (ONJ), associated with Sjogren‘s syndrome, adrenal insufficiency, and vitamin C deficiency. Pathogen-induced acidosis, hypoxia, and insufficient antioxidant defenses contribute to ONJ [1].

Many patients with GERD seek dental treatment for hypersensitivity, only to discover the underlying condition, which requires further medical attention. Proton pump inhibitors are the preferred treatment for GERD, offering a non-invasive and cost-effective approach. They can also aid in diagnosing GERD. However, in some cases, drug therapy alone may not be sufficient to manage symptoms, necessitating anti-reflux surgery [8].

Plummer-Vinson syndrome

Plummer-Vinson syndrome (PVS) is characterized by a combination of microcytic hypochromic anemia, atrophic glossitis, and esophageal webs or strictures. This condition is also referred to by various names, including Paterson-Kelly syndrome, Paterson-Brown-Kelly syndrome, and sideropenic dysphagia [35]. The precise etiology of PVS is not clearly defined. Nonetheless, several contributing factors have been identified, such as iron deficiency anemia, nutritional deficiencies (including vitamin B12 and folic acid), genetic predispositions, and autoimmune factors. The specific interplay of these elements leading to the syndrome remains inadequately understood [36]. Data regarding the incidence and prevalence of PVS are scarce, primarily due to its rarity, with most information derived from case reports. Predominantly, the affected individuals are women aged between their fourth and sixth decades of life, although cases have also been reported in adolescents and children, albeit infrequently [36].

Patients with PVS exhibit various oral manifestations associated with iron deficiency anemia, including stomatitis, glossitis, angular cheilitis, erythematous mucositis, recurrent aphthous stomatitis, pale oral mucosa, oral candidiasis, dry mouth (observed in 49.3% of patients), and burning mouth syndrome (reported in 76–100% of patients). Other findings include lingual varicosity (56%), oral lichen planus (33.3%), recurrent aphthous ulceration (25.33%), and early tooth loss. Nutritional deficiencies lead to the initial disappearance of filiform papillae, followed by fungiform papillae, with regeneration occurring in reverse order; however, vallate and foliate papillae in the posterior third remain unaffected. This condition can also result in taste dysfunction [15].

Primary treatment for PVS involves oral iron supplementation to correct iron deficiency anemia, which often resolves dysphagia and esophageal webs. In cases where dysphagia persists, endoscopic dilatation of the esophageal webs may be necessary. Long-term monitoring is essential to prevent recurrence and screen for esophageal carcinoma. Dietary modifications to increase iron intake and regular follow-up are also recommended [36].

Pernicious anemia

Is a type of anemia characterized by a deficiency in vitamin B12, essential for the production of red blood cells. This deficiency is primarily due to an autoimmune disorder that interferes with the absorption of vitamin B12 from the small intestines [1].

Pernicious anemia is an autoimmune condition characterized by the destruction of gastric parietal cells or intrinsic factors, leading to impaired absorption of vitamin B12 (cobalamin). This results in megaloblastic anemia, neurological complications, and gastrointestinal issues [1]. It primarily affects older adults, particularly those of Northern European descent, and is more common in women than men. Prevalence increases with age, typically presenting in individuals over 60 years old [1].

Common oral signs include glossitis (smooth, beefy-red tongue), recurrent aphthous ulcers, mucosal atrophy, and a burning sensation in the mouth. Patients may also experience angular cheilitis and pallor of the oral mucosa [8]. Management involves lifelong vitamin B12 supplementation, typically through intramuscular injections or high-dose oral tablets. Regular monitoring of vitamin B12 levels and addressing any neurological symptoms or related conditions are crucial for long-term care [1].

Tab. 4 lists the treatment regimen recommended by the British National Formulary [37].

Hiatal hernia

Hiatal hernia is the protrusion of intra-abdominal contents into the thoracic cavity through an enlarged esophageal hiatus of the diaphragm. A hiatal hernia occurs when the upper part of the stomach pushes through the diaphragm into the chest cavity. It is primarily caused by weakening of the diaphragm, increased intra-abdominal pressure (due to obesity, heavy lifting, or chronic coughing), or congenital abnormalities [38]. Hiatal hernias are common, especially in people over 50 years of age. Risk factors include obesity, pregnancy, smoking, and conditions that increase abdominal pressure. It is more prevalent in women than in men [38]. Indirect oral manifestations may arise from GERD, commonly associated with hiatal hernia. These include dental erosion (especially of the posterior teeth), halitosis, and a sour taste in the mouth (Fig. 5). Patients may also report xerostomia due to medications or chronic reflux [39]. Management involves lifestyle changes (weight loss, diet modification, avoiding lying down after meals), medications (antacids, H2 blockers, proton pump inhibitors), and in severe cases, surgical repair. Addressing GERD is crucial in preventing oral complications [40].

Considerations for oral health for dentists and GI clinicians

For both dental and GI clinicians, it‘s crucial to consider the systemic health of patients with conditions such as vertebral compression fractures, long-term steroid use, and gastrointestinal issues. These patients face heightened risks such as delayed healing, increased infection due to anemia, and the side effects of corticosteroids, including hypertension and hyperglycemia. Dental procedures should be approached with caution, especially in the dental chair, which should be positioned at a 45-degree angle to minimize acid regurgitation and reduce stress [3].

Patients on prolonged steroid therapy may experience adrenal suppression and require careful monitoring. NSAIDs should be avoided due to their association with gastrointestinal bleeding, with acetaminophen being a safer alternative. Caution is also needed for patients with perforations, as this can exacerbate anemia, and long-term use of cimetidine or ranitidine may lead to thrombocytopenia. Additionally, H2 antagonists may interact with lidocaine, and interfere with the absorption of antifungal medications, potentially altering their efficacy [3].

In patients who have had bowel surgery or suffer from conditions like Plummer-Vinson syndrome, malabsorption of vitamin K is a concern, and prolonged healing or susceptibility to infections may require the use of saliva substitutes to address dry mouth. A collaborative, multidisciplinary approach involving the patient’s healthcare team –⁠ including primary care physicians, hematologists, and gastroenterologists –⁠ is essential to create a comprehensive treatment plan [5].

Dental professionals should monitor for oral infections, delayed healing, and lesions, which may indicate systemic issues. Patients with hiatal hernia or GERD should be monitored for enamel erosion and advised on appropriate fluoride treatments and dietary modifications to mitigate acid damage. Consistent dental care, iron supplementation, and good oral hygiene are vital for maintaining oral health and preventing complications.

Conclusion

Oral health and gastrointestinal (GI) disorders are intricately connected, with each influencing the other in significant ways. GI disorders, such as gastroesophageal reflux disease (GERD), celiac disease, Crohn‘s disease, and irritable bowel syndrome (IBS), can manifest with oral signs and symptoms, including enamel erosion, aphthous ulcers, xerostomia, and mucosal lesions. These manifestations often serve as early indicators of underlying systemic conditions, highlighting the importance of oral examinations in detecting and managing GI disorders.

Conversely, poor oral health, including periodontal disease and dental caries, may contribute to or exacerbate GI conditions. The shared pathogenic mechanisms, such as inflammation and microbial dysbiosis, underscore the need for a multidisciplinary approach in managing patients with concurrent oral and GI issues. Dental and medical clinicians must collaborate closely to ensure comprehensive patient care, recognizing that optimal oral health can significantly impact overall digestive health.

Further research is essential to deepen our understanding of the bidirectional relationship between oral health and GI disorders, paving the way for improved diagnostic, preventive, and therapeutic strategies. In conclusion, integrating oral health considerations into managing GI disorders is vital for enhancing patient outcomes and fostering a holistic approach to healthcare.