Crohn's Disease and Dental Practice

01

Epidemiology and Pathophysiology

Definition and nosological framework

Crohn's disease (CD) is a chronic granulomatous inflammatory disease of the gastrointestinal tract, whose etiology remains partially understood. It belongs, together with ulcerative colitis (UC), to the group of inflammatory bowel diseases (IBD). Inflammation is transmural (affecting all parietal layers) and segmental (alternating healthy and diseased areas).

The immunological mechanisms involve T helper cell stimulation leading to massive secretion of pro-inflammatory cytokines: IL-1, IL-12 and above all TNF-α — the primary target of modern biological therapies.

Key epidemiological data

Prevalence and demographic distribution

Incidence: 4 to 6 new cases / 100,000 inhabitants / year (France)
Prevalence: ~150,000 people in France; rising globally
Two age peaks: 15–35 years and beyond 60 years
Smoking: major well-documented aggravating factor

Prevalence of oral manifestations

An underestimated diagnostic challenge

Adults: 8% to 14.2% oral manifestations
Children: 50% to 80% in pediatric cohorts
Oral signs precede intestinal symptoms: 5% to 30% of cases
Possible interval before digestive symptoms: up to 9 years

The sentinel role of the dental practitioner The oral cavity constitutes the proximal end of the digestive tract. Oral manifestations are not merely secondary complications — they can precede the intestinal diagnosis by several years. The dental practitioner is often the first clinician to suspect the disease when faced with suggestive oral lesions.

02

Specific Oral Manifestations

Shared histological substrate

Specific lesions share the same non-caseating epithelioid and multinucleated giant cell granulomatous substrate as intestinal lesions. Diagnostic confirmation relies on mucosal biopsy revealing epithelioid granulomas. These lesions are pathognomonic of CD and their identification requires gastroenterological collaboration.

The four specific oral lesions — Clinical presentation

1

Cobblestone appearance

Mucosal edema traversed by deep fissures creating an irregular relief, primarily on the inner surface of the cheeks and in the vestibules.

Results from underlying granulomatous inflammation distending the connective tissue. The most iconic presentation of oral CD.

2

Linear ulcerations

Deep ulcers located in the mucosal reflection folds (vestibular sulci), bordered by hyperplastic ridges (mucosal tags or pseudopolyps).

Particularly painful, they impair eating and compromise oral hygiene.

3

Macrochelia and orofacial edema

Persistent diffuse swelling of the lips (Miescher's granulomatous cheilitis) or cheeks. Firm swellings on palpation with vertical labial fissures.

Without known intestinal involvement: orofacial granulomatosis (OFG) framework — a significant proportion eventually progresses to systemic CD.

4

Granulomatous gingivitis

Erythematous, swollen, granular-appearing gingiva with hyperplasia of the attached gingiva extending to the mucogingival junction.

Fragile and bleeding tissues even in the absence of significant plaque accumulation — an important differential criterion.

Pyostomatitis vegetans — Marker of severe disease activity Multiple small whitish or yellowish pustules fusing into a "snail track" pattern on an erythematous and friable mucosa. A rare lesion considered a cutaneomucous marker of severe IBD activity. Its presence mandates urgent gastroenterological reassessment.

03

Non-Specific Oral Manifestations

Reflecting systemic activity and nutritional deficiencies

Non-specific manifestations are generally more frequent than granulomatous lesions. They reflect the activity of intestinal disease and the consequences of ileal malabsorption. Their presence should systematically prompt a search for vitamin and mineral deficiencies.

Non-specific manifestations — Pathophysiological links

Manifestation	Pathophysiological mechanism	Clinical signs
Recurrent aphthous stomatitis	Systemic inflammation / Iron deficiency	Painful round or oval ulcers, correlated with flares
Hunter's glossitis	Vitamin B12 / Folate deficiency	"Glazed" tongue, depapillated, oral burning
Angular cheilitis	B2, B6, B12 deficiency / Dry mouth	Fissures and erythema at the labial commissures
Gingival bleeding	Vitamin K deficiency	Spontaneous gingivorrhagia without excess plaque
Burning mouth syndrome	Zinc or Magnesium deficiency	Oral burning sensation without visible lesion

Recurrent aphthous stomatitis — Do not underestimate Although resembling minor or major aphthae in the general population, these ulcers in CD patients are often more numerous, more persistent and closely correlated with digestive flares. Their presence mandates systematic investigation for anemia or vitamin deficiency, and communication with the treating gastroenterologist.

04

Caries Risk and Xerostomia

Significantly elevated DMFT index

Crohn's disease patients present a significantly higher DMFT index than healthy controls (Brito et al.). This increased susceptibility results from a convergence of biological and behavioral factors specific to the disease.

Xerostomia — Multiple origins

Central aggravating factor for caries risk

Direct involvement of salivary glands by granulomas
Frequent drug-induced cause: antidepressants, immunosuppressants
Chronic dehydration during diarrheal phases
Consequence: reduced mechanical cleansing of tooth surfaces and impaired salivary buffering — prolonged enamel exposure to acid attacks

Cariogenic dietary behavior

Diet modification during flares

During active phases: preference for refined carbohydrates better tolerated intestinally
Increased meal frequency to maintain body weight
Enhanced proliferation of Streptococcus mutans and Lactobacilli
Avoidance of fibrous foods in favor of simple sugars = ideal cariogenic environment

Prevention

Xerostomia management and enamel protection

Individualized preventive strategy — central axis of dental management

Salivary substitutes

Hydrating sprays or gels, especially before bedtime. Xylitol gums or lozenges to stimulate natural saliva production after meals.

Enhanced fluoride prophylaxis

Standard fluoride toothpaste (1450 ppm) routinely. High caries risk: prescription 5000 ppm toothpaste. Custom fluoride trays for persistent hyposalivation.

Dietary counseling

Avoid sticky, sugary and acidic foods. Regular water intake in small amounts. Limit frequency of sugar exposures between meals.

05

Periodontitis and Implant Risks

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Bidirectional relationship — IBD and periodontal disease

CD worsens periodontitis

Circulating TNF-α and IL-1β lower the tolerance threshold of periodontal tissues to dental plaque, accelerating attachment loss and alveolar bone resorption — independently of oral hygiene levels.

Periodontitis worsens CD

Chronic periodontitis, as a permanent inflammatory focus, sustains systemic inflammation and may influence CD activity. Early periodontal treatment = double benefit for patient outcomes.

Implant failure risk — Odds Ratio = 7.95 Crohn's disease patients present an early implant failure risk approximately eight times higher than healthy patients. This risk is particularly marked during active disease phases or in patients on high-dose corticosteroids. A rigorous benefit-to-risk analysis is mandatory before any implant project.

Prerequisites for an implant project in a Crohn's patient

Disease in documented stable remission — minimum 6 months
Absence of systemic corticosteroids or at the minimum possible dose
Complete prior periodontal debridement and excellent plaque control
Coordination with the gastroenterologist regarding biologic therapy windows
Full informed consent regarding the residual elevated risk of osseointegration failure

06

Impact of Systemic Treatments

Corticosteroids — Specific risks

Prednisone · Hydrocortisone · Budesonide

Suppression of the hypothalamic-pituitary-adrenal axis — adrenal insufficiency risk during any stressful dental procedure
Delayed tissue healing
Increased susceptibility to opportunistic infections (oral candidiasis)
Risk of osteoporosis and osteonecrosis of the jaw (rare, less frequent than with bisphosphonates)

NSAIDs and Aspirin — Contraindicated

Absolute prohibition in Crohn's patients

COX-1 inhibition → disrupts protective prostaglandins of the digestive mucosa
Arachidonic acid shunted to 5-lipoxygenase pathway → pro-inflammatory leukotrienes
Can trigger or aggravate an intestinal inflammatory flare
Reference analgesic: Paracetamol. Alternative: Tramadol or Codeine with monitoring

Biological therapies — Therapeutic windows before invasive surgery

Class	Drug	Recommended stop interval	Postoperative resumption
Anti-TNF	Infliximab / Adalimumab	4 weeks	After complete healing
Anti-integrin	Vedolizumab	2 to 4 weeks	14 days postoperatively minimum
Anti-interleukin	Ustekinumab	4 weeks	After mucosal healing
Anti-JAK	Filgotinib	2 days	Rapid resumption possible

Oral surgery should ideally be performed at the end of the dosing interval, when serum concentration is at its lowest. Shared decision-making with the referring gastroenterologist is required.

07

Dental Antibiotics and CDI Risk

Clostridioides difficile — Incidence 3x higher in Crohn's patients CDI incidence is approximately three times higher in Crohn's patients than in the general population (32.9 vs 9.3 per 1,000 patients). Any dental antibiotic can trigger CDI or a disease relapse. This risk entirely governs antibiotic prescribing choices in the dental office.

CDI risk stratification by antibiotic class

Antibiotic	CDI Risk	Use in Crohn's patients
Clindamycin	Very high	Formally prohibited — even in penicillin allergy
Cephalosporins	High	Avoid systematically
Fluoroquinolones	High	Avoid systematically
Amoxicillin / Augmentin	Moderate	Use with caution when necessary
Metronidazole	Very low	Drug of choice for anaerobic odontogenic infections
Azithromycin / Clarithromycin	Low	Preferred alternative in penicillin allergy

Penicillin allergy — Alternative protocol In confirmed penicillin allergy, the recommended alternatives are azithromycin or clarithromycin. Clindamycin must be avoided absolutely, even in this context — its CDI risk profile is incompatible with an IBD background.

08

Chairside Management

Systematic medical history — 5 points to evaluate

Current disease phase: remission or active flare?
Intestinal surgical history: strictures, fistulas, resections
Complete medication list: corticosteroids, immunosuppressants, biologics
Extra-intestinal manifestations: joint, ocular, cutaneous involvement
Perianal complications or frequent diarrhea (restroom access needed)

Active Flare

Treatment during an active phase

Minimal interventions only — pain and infection control exclusively

Permitted procedures

Non-invasive conservative care, symptomatic treatment of mucosal lesions (topical anesthetics, topical corticosteroids), light supragingival scaling.

Procedures to defer

All oral surgery, non-urgent extractions, invasive periodontal treatment, implant placement. Defer until documented remission is achieved.

Remission

Treatment during remission

Optimal therapeutic window for planned invasive procedures

Positioning and session length

Short appointments to limit patient fatigue. Semi-reclined position if associated GERD or joint pain. Restroom access if needed.

Local anesthesia

Vasoconstrictors generally permitted. If sulfite sensitivity suspected in severe corticosteroid therapy: plain mepivacaine without vasoconstrictor.

Oral surgery

Optimal asepsis. Atraumatic suture technique. Avoid non-resorbable membranes in high-risk patients. Antibiotic prophylaxis if severe immunosuppression confirmed.

Topical treatment of painful mucosal lesions

Viscous Lidocaine

Topical contact anesthetic

Topical application before meals

Immediate relief of painful ulcerations. Do not swallow in large quantities.

Triamcinolone / Clobetasol

Topical corticosteroid — gel or paste

Apply to ulcers 2–3×/day

For linear ulcerations and major aphthae. Limited duration — monitor for candidiasis.

Topical Tacrolimus

Topical immunomodulator

Topical application — per prescription

For OFG forms resistant to topical corticosteroids. Specialist use only.

Paracetamol (Acetaminophen)

Systemic analgesic — first-line

1 g × 3/day — oral route

Reference analgesic in Crohn's patients. Tramadol or Codeine for intense pain under digestive monitoring.

09

Pediatric Considerations

Pediatric CD — Often more severe and extensive

In children and adolescents, Crohn's disease directly interferes with growth and maturation processes. Chronic inflammation and nutritional deficiencies induce growth retardation in 10% to 40% of pediatric cases, with a negative correlation between growth velocity and inflammatory markers (CRP, orosomucoid).

Impact on craniofacial development

Cephalometric studies — morphological trends

Reduction in posterior facial height and cranial base length
Shortening of the mandibular body and ramus height
Significant delay in permanent tooth eruption (first molars and incisors ++)
Osteopenia and increased risk of enamel hypoplasia

Implications for the clinician

Orthodontics and pediatric dentistry

Pubertal delay impacting orthodontic treatment planning
Residual growth potential is unpredictable — dependent on systemic disease control
Elevated caries risk linked to nutritional deficiencies and dietary changes
Oral manifestations often precede intestinal diagnosis in children

Orthodontist — Integrate delays into treatment planning Residual growth potential may be unpredictable in a child with CD. Delayed eruption and altered mandibular morphology require flexible orthodontic planning in close coordination with the pediatrician and gastroenterologist. No permanent fixed appliance should be placed without prior systemic stabilization.

10

Prevention and Multidisciplinary Care

Pre-therapeutic dental clearance — Before any biologic or heavy immunosuppressive therapy

Complete dental assessment is mandatory before initiating immunosuppressive treatment.

Initial assessment

Systematic panoramic radiograph (OPT) + supplementary views as needed
Comprehensive periodontal probing and plaque index

Elimination of infectious foci

Teeth with no conservative solution → extraction
Cysts and periapical lesions → endodontic treatment or extraction
Active periodontitis → complete debridement before immunosuppression

Post-clearance verification

Clinical reassessment at 4–6 weeks to validate complete healing
Dental health certificate transmitted to the gastroenterologist

Dental recall frequency

Biannual follow-up — minimum standard

Professional prophylactic cleaning at each visit
Monitoring for new mucosal lesions signaling a disease flare
Adaptation of hygiene and fluoride advice according to disease evolution
Annual radiographic monitoring (bite-wing) for proximal caries detection

Multidisciplinary communication

Mandatory care network

Gastroenterologist: coordination of biologic therapy windows
Pediatrician (children): monitoring of growth and pubertal delay
Rheumatologist: if joint involvement affects patient positioning
General practitioner: corticosteroid management and systemic risks

11

Clinical FAQ

Antibiotic choice must account for the elevated CDI risk. For anaerobic odontogenic infection, metronidazole is the drug of choice — it has a very low CDI risk profile and is commonly used to treat Crohn's flares itself. Amoxicillin can be used with caution when necessary. Clindamycin is absolutely prohibited, even in penicillin allergy — in that case, prefer azithromycin or clarithromycin. Cephalosporins and fluoroquinolones also carry high CDI risk and should be avoided.

No. NSAIDs and aspirin are absolutely contraindicated in Crohn's disease patients. COX-1 inhibition disrupts the synthesis of protective prostaglandins of the digestive mucosa, which can trigger or aggravate an intestinal inflammatory flare. Additionally, shunting of arachidonic acid toward the 5-lipoxygenase pathway increases production of pro-inflammatory leukotrienes. The reference analgesic is paracetamol (acetaminophen) (1 g × 3/day). For more intense pain, tramadol or codeine may be considered under digestive side-effect monitoring.

Infliximab ideally requires a 4-week stop before planned invasive surgery, with surgery performed at the end of the dosing interval (minimum serum concentration). For a non-deferrable emergency: contact the referring gastroenterologist for advice, perform the procedure under optimal aseptic conditions with atraumatic technique, consider antibiotic prophylaxis if the patient is considered severely immunosuppressed, and do not resume biologic therapy before complete mucosal healing — generally 14 days postoperatively as a minimum.

Several presentations should alert the practitioner: (1) Cobblestone appearance of the cheek or vestibular mucosa; (2) Linear ulcerations deep in the vestibular sulci with hyperplastic borders (mucosal tags); (3) Macrochelia — firm persistent lip swelling without obvious local cause (Miescher's granulomatous cheilitis); (4) Granulomatous gingivitis resistant to standard hygiene; (5) Severe recurrent aphthous stomatitis correlated with digestive symptoms. These signs can precede the intestinal diagnosis by years — biopsy and gastroenterological referral are mandatory.

Long-term corticosteroid therapy suppresses the hypothalamic-pituitary-adrenal axis, preventing the patient from responding physiologically to procedural stress with increased cortisol production. For simple local anesthesia procedures, the risk is generally low. For heavier or anxiety-inducing procedures: (1) contact the treating physician to assess adrenal function; (2) consider perioperative hydrocortisone supplementation if indicated (dose-doubling rule); (3) minimize session length and procedural stress; (4) if sulfite sensitivity in anesthetic solutions is suspected, use plain mepivacaine without vasoconstrictor.

It is possible but requires strict precautions. The implant failure risk is approximately 8 times higher (OR = 7.95) in Crohn's patients. Favorable conditions include: documented stable remission for at least 6 months, no or minimum-dose corticosteroids, no ongoing biologic therapy or respected therapeutic window, excellent prior periodontal debridement, and full informed consent regarding residual elevated risk. The decision must be made jointly with the gastroenterologist and documented in the patient record. Active disease phases and high corticosteroid doses represent absolute temporary contraindications.

Ref

References

Oral manifestations of Crohn's disease

1

Systematic review Katz J, Shenkman Z, Stavropoulos F, et al. Oral manifestations of Crohn's disease: a systematic review. PMC / J Oral Pathol Med. 2023.
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2

Review Fatahzadeh M. Oral manifestations of inflammatory bowel disease: two case reports. Clin Med Res. 2017.
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3

Review Lankarani KB, Sivandzadeh GR, Hassanpour S. Oral manifestations in inflammatory bowel disease. Swiss Dental Journal SSO. 2013.
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4

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5

Review Losurdo G, et al. Oral manifestations as the first presenting sign of Crohn's disease in a pediatric patient. PMC. 2020.
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6

Review Vavricka SR, Schoepfer A, Scharl M, et al. Oral manifestations of inflammatory bowel disease: a guide to diagnosis and management. Frontline Gastroenterol BMJ. 2020.
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7

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Periodontitis, implantology and CDI risk

8

Review Crohn's disease and periodontal manifestations: a review of current evidence. Fortune Journals. 2023.
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9

Clinical study Gomes C, et al. Association of periodontal disease with activity of Crohn's disease. PMC / J Crohns Colitis. 2021.
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10

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11

Epidemiological study Gisbert JP, et al. Patients with Clostridioides difficile infection following dental antibiotic prescription. PMC / Open Forum Infect Dis. 2023.
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12

Guideline NICE. Clostridium difficile infection: risk with broad-spectrum antibiotics. National Institute for Health and Care Excellence. 2015.
nice.org.uk — CDI risk with broad-spectrum antibiotics

Biological therapies, corticosteroids and surgical management

13

Guideline NNUH NHS. Joint guidelines for the management of interruption of biologic therapies for elective surgery. 2022.
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14

Review Daubländer M, et al. Application of corticosteroids in dentistry: a review. PMC / Clin Oral Investig. 2020.
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15

Review Becker DE, Reed KL. Selection of the safest local anesthetic for dental treatment in medically compromised patients. PMC / Anesth Prog. 2021.
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16

Guideline HAS. Dental management of patients at high risk of infective endocarditis. Haute Autorité de Santé. 2011.
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Pediatric CD, growth and dental development

17

Review Pigneur B, Seksik P, Viola S, et al. Crohn's disease in children. FMC-HGE. 2019.
fmcgastro.org — Crohn's disease in children
18

Clinical study Dental eruption patterns and their relationship to systemic health conditions in children. IJCMPH. 2023.
ijcmph.com — Dental eruption patterns and systemic conditions
19

MDPI study Variability in permanent teeth eruption in children with growth hormone deficiency and idiopathic short stature. MDPI. 2024.
mdpi.com — Teeth eruption in children with GH deficiency

Caries prevention, xerostomia and guidelines

20

Guideline HAS. Dental caries prevention strategies — Evaluation report. Haute Autorité de Santé. 2010.
has-sante.fr — Caries prevention strategies
21

Register study Eriksson C, et al. Consumption of dental treatment in patients with inflammatory bowel disease, a register study. PMC / BMC Oral Health. 2022.
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22

Review IBD and periodontal disease — analysis of the bidirectional relationship. Oral-B Professional.
oralbprofessional.fr — IBD and periodontal disease
23

Thesis Crohn's disease: the need for multidisciplinary collaboration in dentistry. Université de Lille.
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