14.1 Gastrointestinal Disease and Intrinsic Dental Erosion
Key Takeaways
- Gastric hydrochloric acid has a pH of 1.0 to 2.0, well below the critical pH of 5.5 for enamel and 6.2 to 6.7 for dentine and cementum.
- Intrinsic erosion classically affects the palatal surfaces of maxillary anterior teeth and the occlusal surfaces of mandibular molars.
- Restorations standing proud of the eroded surface, described as amalgam islands, indicate chemical rather than mechanical tissue loss.
- The Basic Erosive Wear Examination scores each sextant 0 to 3 and sums them to stratify risk from none through low and medium to high.
- Orofacial granulomatosis and cobblestone buccal mucosa can be the first presentation of Crohn's disease.
1. Gastrointestinal Pathology: GORD, Inflammatory Bowel Disease, and Coeliac Disease
Gastro-Oesophageal Reflux Disease (GORD)
GORD is a chronic digestive disorder caused by transient or permanent incompetence of the lower oesophageal sphincter (LOS), sliding hiatal hernia, or impaired gastric clearance. This allows retrograde reflux of acidic gastric juice—containing hydrochloric acid ($HCl$) with a pH of $1.0-2.0$ and proteolytic pepsin—into the oesophagus and oral cavity.
- Dental Erosion (Intrinsic Acid Wear / Perimylolysis): Enamel dissolution commences when the oral environment falls below the critical pH of enamel (pH 5.5), while dentine and cementum demineralize below pH 6.2 to 6.7. In GORD, intrinsic acid contact produces characteristic smooth, silky, cupped-out erosive lesions with loss of anatomical surface morphology. Existing amalgam restorations appear elevated above the surrounding tooth surface ("amalgam islands").
- Characteristic Anatomical Distribution: GORD-induced erosion predominantly affects the palatal surfaces of maxillary anterior teeth and the occlusal surfaces of mandibular first and second molars. In contrast, extrinsic dietary erosion (citrus fruits, carbonated soft drinks, sports beverages) primarily damages the labial, buccal, and incisal surfaces.
- The Basic Erosive Wear Examination (BEWE): The BEWE is the validated scoring index endorsed in the UK for recording erosive tooth wear across six sextants (07–14, 13–23, 24–27, 37–34, 33–43, 44–47):
| BEWE Score | Visual Clinical Criteria |
|---|---|
| Score 0 | No erosive wear. |
| Score 1 | Initial loss of surface enamel texture (silky appearance). |
| Score 2 | Distinct defect; hard tissue loss affecting $< 50%$ of the tooth surface area. |
| Score 3 | Severe hard tissue loss affecting $\ge 50%$ of the tooth surface area (often exposing dentine). |
Risk Staging: The highest score in each sextant is summed to yield a cumulative score ($0-18$): None ($0-2$), Low ($3-8$), Medium ($9-13$), and High ($\ge 14$). For high-risk scores, clinical governance mandates prescribing 5,000 ppm sodium fluoride toothpaste (Duraphat), non-acidic remineralizing pastes (casein phosphopeptide-amorphous calcium phosphate, CPP-ACP), delayed post-reflux toothbrushing (rinse with water or sodium bicarbonate; wait $\ge 30-60\text{ minutes}$ before brushing), and urgent GP referral for medical acid suppression with proton pump inhibitors (PPIs: omeprazole, lansoprazole).
Inflammatory Bowel Disease (IBD): Crohn's Disease vs Ulcerative Colitis
Inflammatory bowel disease comprises two distinct chronic idiopathic relapsing inflammatory conditions:
Inflammatory Bowel Disease (IBD)
│
├── Crohn's Disease (CD):
│ ├── Transmural inflammation, skip lesions, entire GI tract ("gum to bum")
│ ├── Non-caseating epithelioid granulomas
│ └── Oral Manifestations (10–20%): Cobblestoning, Lip Macrocheilia (OFG),
│ Deep Linear "Knife-Cut" Ulcers, Mucosal Tags
│
└── Ulcerative Colitis (UC):
├── Mucosal/submucosal inflammation restricted to colon and rectum
└── Oral Manifestations: Pyostomatitis Vegetans ("Snail-Track" Microabscesses),
Aphthous Stomatitis
| Feature | Crohn's Disease (CD) | Ulcerative Colitis (UC) |
|---|---|---|
| Anatomical Distribution | Any segment from mouth to anus ("gum to bum"); terminal ileum predilection | Confined strictly to rectum and colon; extends contiguously proximally |
| Depth of Inflammation | Transmural (full thickness of intestinal wall); fissures, fistulae | Mucosal and submucosal only; continuous friable erythema |
| Histopathology | Non-caseating granulomas (~50–60% of cases); lymphoid aggregates | Crypt abscesses, crypt architectural distortion, no granulomas |
| Pathognomonic Oral Signs | Cobblestone buccal mucosa, lip swelling (Orofacial Granulomatosis), deep linear knife-cut vestibular ulcers | Pyostomatitis vegetans ("snail-track" pustules), non-specific aphthous ulceration |
- Crohn's Disease Oral Hallmarks: Oral lesions occur in 10% to 20% of patients and frequently precede gastrointestinal symptoms by months or years. Classical signs include:
- Cobblestone Mucosa: Submucosal lymphoedema and chronic non-caseating granulomatous inflammation creating a nodular, cobblestone appearance on the buccal mucosa.
- Orofacial Granulomatosis (OFG) / Macrocheilia: Persistent, painless, firm, non-pitting swelling of the lips (predominantly the lower lip), histologically characterized by non-caseating granulomas.
- Deep Linear Ulcerations: Painful, elongated, "knife-cut" ulcers in the buccal or labial vestibule, often bordered by hyperplastic mucosal tags.
- Ulcerative Colitis and Pyostomatitis Vegetans: The pathognomonic oral manifestation of ulcerative colitis is pyostomatitis vegetans. It presents as multiple tiny, yellowish-white, friable microabscesses or pustules arranged in linear, serpentine, or branching patterns across an intensely erythematous, folded mucosa, classically termed a "snail-track" pattern (lesions en escargot). Rupture leaves shallow erosions. Its appearance strongly mirrors active colonic disease.
Coeliac Disease
Coeliac disease is a systemic autoimmune enteropathy triggered by dietary ingestion of gluten (specifically the ethanol-soluble protein fraction gliadin in wheat, secalin in rye, and hordein in barley) in genetically predisposed individuals expressing HLA-DQ2 or HLA-DQ8. Autoantibodies against tissue transglutaminase (anti-tTG) and endomysium drive chronic duodenal and jejunal mucosal inflammation, intraepithelial lymphocytosis, crypt hyperplasia, and villous atrophy, leading to profound malabsorption.
- Oral Manifestations:
- Recurrent Aphthous Stomatitis (RAS): Atypical or severe recurrent aphthous-like ulcerations occur in up to 30% to 40% of coeliac patients. In paediatric patients, recalcitrant RAS may be the sole presenting sign.
- Chronologically Distributed Dental Enamel Hypoplasia: Permanent teeth developing during active childhood coeliac disease (central incisors, lateral incisors, and first permanent molars) exhibit symmetrical, chronologically matched enamel defects (horizontal grooves, deep pits, or severe structural hypoplasia) resulting from hypocalcaemia and autoimmune damage to ameloblasts during amelogenesis.
- Atrophic Glossitis and Angular Cheilitis: Depapillated, smooth, erythematous tongue resulting from malabsorption of iron, folate, and vitamin $B_{12}$.
Recognising and Grading Erosive Tooth Wear
The dental consequence of gastro-oesophageal reflux and of eating disorders is erosive tooth wear, and the examinable skill is distinguishing its pattern from attrition and abrasion. Intrinsic acid from regurgitation classically affects the palatal surfaces of upper anterior teeth and the occlusal surfaces of lower molars, producing cupping of cusps and restorations that stand proud of the surrounding tooth surface. Extrinsic acid from diet affects labial and occlusal surfaces in a pattern determined by how the drink is consumed. In the UK, wear is recorded using the Basic Erosive Wear Examination (BEWE), which scores the most affected surface in each sextant from 0 to 3 and sums the sextants to give a risk level guiding management. Management is prevention first — identifying and treating the acid source, advising against brushing immediately after an acid challenge, fluoride and desensitisation — with monitoring by study casts or photographs, and restoration reserved for progression, sensitivity or aesthetic need.