Gastrointestinal Diseases and Their Oral Manifestations

Lecture given 10/6/2025

inflammatory bowel disease

chronic idiopathic intestinal inflammation

what are the major types of inflammatory bowel disease?

ulcerative colitis, crohn’s disease, indeterminate colitis

is there a specific population that IBD affects more often?

yes, jewish populations

lower in hispanic and black populations

what is the etiology of IBD?

genetics, immune dysregulation, and external triggers

what defines genetic susceptibility to IBD?

high concordance in twins, increased risk in first degree relatives, genome wide association studies identified >200 distinct susceptibility loci

what defines immune dysregulation in the etiology of IBD?

dysregulated or inappropriate immune response to luminal bacteria / other trigger in a susceptible patient

what defines external triggers in the etiology of IBD?

smoking- increased CD risk, decreased UD risk

appendectomy- decreased UC risk

altered gut microbial flora, gut infection

medications- OCPs, NSAIDs

urban>rural

developed>underdeveloped

north climates>south

ulcerative colitis

continuous pattern of inflammation, mucosa only, rectum + variable length of colon involved

what is the break down of the most common types of UC?

30% proctitis

30% pancolitis

40% distal colitis

what are the symptoms of UC?

diarrhea, rectal bleeding, tenesmus, passage of mucous, crampy abdominal pain

extraintestinal manifestations

severity of symptoms correlates with the extent of disease

what are the characteristics of mild UC?

<4 BMs per day, ± blood in stool, no systemic signs, normal inflammatory markers

what are the characteristics of moderate UC?

4-6 BMs per day, ++ blood in stool, minimal systemic signs

what are the characteristics of severe UC?

>6 BMs per day, +++ blood in stool, systemic signs present

in UC, where is the inflammation found?

the mucosal layer of rectum/colon

crohn’s disease

segmental pattern of inflammation, transmural layers involved, can involve any sites from mouth to anus

what is the break down of the most common types of CD?

5% gastroduodenal

25% colon only

30% small bowel only

40% ileocolitis

what are the symptoms of CD?

fever, abdominal pain, vomiting, fatigue, weight loss, diarrhea, bleeding

perianal disease

strictures, bowel obstruction

fistulae

abdominal mass, intra-abdominal abscess

if you are visualizing a microscope slide of a colon and you see granulomas, should you suspect UC or CD?

crohn’s disease

what are some extraintestinal manifestations of crohn’s disease (not oral manifestations)?

erythema nodosum, pyoderma gangrenosum, sweet’s syndrome, episcleritis, uveitis, peripheral arthritis, ankylosing spondylitis, sacroiliitis

what are the extraintestinal oral manifestations of crohn’s idease?

aphthous stomatitis, mucogingivitis, cobbelstoning, deep fissuring ulcers, mucosal tags, cheilitis, pyostomatitis vegetans

what are the oral manifestations of IBD?

lip swelling, fissures, cobbelstoning, linear ulceration, mucosal tag, mucogingivitis, gingival hyperplasia, granulomatous inflammation on biopsies, tonsillar crohn’s disease, pyostomatitis vegetans

usually parallel bowel activity

are oral manifestations of IBD more common with UC or CD?

crohn’s disease

what could be a cause of recurrent aphthous stomatitis?

inflammatory bowel disease, celiac disease, vitamin and mineral deficiencies (B vitamins, iron, folic acid, zinc), behcet’s disease, stress, hormonal factors, food sensitivity, infections, familial tendency

what are some GI complications associated with IBD?

colon cancer (risk related to extend and duration of disease), perforation, hemorrhage (can lead to anemia), stricture formation, bowel obstruction, fistula, toxic megacolon

what are the medical treatments for IBD?

anti-inflammatory (mesalamine), steroids, immunomodulators, biologics, small molecules

mesalamine

anti-inflammatory

topical or oral

induction/maintenance of remission for mild/moderate UC

steroids

oral, topical, or IV

useful for induction of remission but NOT for maintenance therapy (no long term use)

high side effect profile

immunomodulators

azathioprine, 6-MP, MTX

bone marrow suppression, risk of infection, malignancy

biologics/small molecules

target various points in inflammatory pathway

most are potent immune suppressants, risk of serious infections, risk of malignancy (TNF antagonists)

when treating IBD patients, what should dental providers keep in mind?

caution with NSAIDs- can exacerbate IBD in some patients

risks of IBD therapy- more prone to infection (candidiasis), thrombocytopenia (with immunomodulators), or poor wound healing (steroids)

optimal dental care could reduce supply of pathogenic oral bacteria to the gut which can potentially give innovate methods to reduce risk and severity of IBD

GERD

symptoms or complications caused by the abnormal reflux of gastric contents into the esophagus

impairment of lower esophageal sphincter competence, transiet LES relaxation, esophageal clearance mechanisms, gastric emptying, or mucosal integrity

what conditions are associated with GERD?

hiatal hernia, pregancy, obesity, scleroderma, lifestyle and iatrogenic

what foods are potential causes of GERD?

coffee, chocolates, mints, fatty/fried foods, tomatoes, citrus fruits, black pepper

what habits are potential causes of GERD?

smoking, alcohol, late night snacks/meals and then lying supine, large meals

what medications are potenital causes of GERD?

COPD and high blood pressure medications

what are some symptoms of GERD?

heartburn, acid regurgitation, water brash (hypersalivation), dysphagia, extraesophageal manifestations like laryngitis, hoarseness, cough, asthma, chronic bronchitis, chest pain, dental erosion

what are some complications of GERD?

erosive esophagitis, peptic structure, barrett’s metaplasia, esophageal adenocarcinoma

what are the oral manifestations of GERD?

burning/itching mouth sensations, tongue sensitivity, halitosis, impaired tase (dysgeusia), water brash

dental erosion, painful oral ulcers, dental hypersensitivity, loss of VDO, TMJ pain, esthetic disfigurement

how common is dental erosion in patients with GERD?

very- up to 55% of patients

what is the main mechanism of dental erosion in GERD patients?

direct contact of acid (pH of 2-3)

hydroxyapatite crystals in enamel dissolve with pH less than 5.5

what does dental erosion look like when it is caused by GERD?

erosion distribution on posterior teeth, lingual and occlusal surfaces

what does dental erosion look like when it is caused by extrinsic sources?

erosion distribution on anterior teeth, labial surfaces with severity decreasing posteriorly

how is GERD managed?

aim at relief of symptoms, prevention of complications

begin with lifestyle modifications

medications like antacid therapy, H2RA therapy, and proton pump inhibitor (PPI) therapy

surgery

what are some lifestyle modifications that can be made to manage GERD?

avoid lying down for 3 hours after eating, raise the head of the bed 6 inches, avoid foods that induce symptoms, lose weight, avoid overeating, stop smoking, drinking

antacids

for infrequent symptoms

H2 blockers

for mild cases, longer relief

block histamines (histamines increase gastric acid production)

proton pump inhibitors (PPIs)

for frequent/severe symptoms

inhibit proton pump of gastric parietal cells (final pathway of acid secretion), acid-activated prodrugs, dose should be given 30 minutes prior to a meal, not effective if taken prn or not followed by eating/drinking

PCABs

novel class of acid-suppressing drugs

block potassium-binding site on proton pump, can be taken independently of meals, longer duration compared to PPIs

surgery for GERD

nissen fundoplication

stomach wrapped around LES

90% experience symptomatic improvement, but 10-65% still require medications

when treating GERD patients, what should dental providers keep in mind?

antacids with calcium can interfere with fluoride absorption, omeprazole inhibits metabolism of diazepam- increases sedative effect

patients may develop GERD symptoms in the fully supine position

familial adenomatous polyposis

rare autosomal dominant condition (mutation of APC gene)

prevalence 1/10,000

main clinical feature is multiple (hundreds to thousands) of colorectal adenomas

average age of polyp formation is 16 years

cancer risk is 100%, life expectancy is 42 years without treatment

gardner’s syndrome

FAP with prominent extraintestinal manifestations like- bony tumors (osteomas, frequently on jaw/skull), CHRPE, pancreas, thyroid, liver tumors, epidermal cysts, abdominal desmoid tumors, dental abnormalities (may precede colonic polyps)

what are the oral manifestations of gardner’s syndrome?

supernumerary teeth, unerupted teeth, odontomas, osteomas

what are the hamartomatous polyposis syndromes?

peutz-jeghers syndrome, cowden syndrome

peutz-jegher’s syndrome

rare autosomal dominant disorder (germline STK11)

multiple hamartomatous polyps in GI tract (intussusception, obstruction, bleeding)

significant risk of GI and non GI malignancies (93% by age 65)- small intestine, stomach, colon, pancreas, testicular, ovarian, uterine, cervical, and breast

what are oral signs of peutz-jegher’s syndrome?

flat, blue/gray-brown spots, 1-5mm size, mostly located on lips/perioral region, also buccal mucosa, hands, and feet

spots typically fade after puberty, except for buccal mucosa lesions

cowden syndrome

rare autosomal dominant condition (germline mutation in PTEN gene (tumor suppresor))

characterized by multiple hamartomatous lesions on skin, oral mucosa, intestine, and breast

increased risk for breast (25-50%) and thyroid cancers (10%)

what are some oral manifestations of cowden syndrome?

papillomas on lips and mucous membranes, cobblestoning of tongue

what is important for dental professionals to note about oral manifestations of hamartomatous polyposis syndromes and gardner’s syndrome?

they may be the presenting sign of a syndrome that carries signficant risk for malignancy

detection of any of these signs should prompt thorough history, physical examination, and genetic consultation

what is your lifetime risk of developing colorectal cancer?

~4%

what is the primary risk factor for sporadic colorectal cancer?

age

what age are people most commonly diagnosed with colorectal cancer?

65-74, median age is 66

t/f rates of new cases of CRC and deaths from CRC are falling

true HOWEVER incidence in patients under 50 has been increasing

what are the potential reasons for increases in incidence in CRC in patients under 50?

excess body weight, diabetes, western-style diet, increased antibiotic usage

what are strong risk factors for CRC?

advanced age, FAP/HNPCC (lynch syndrome), long standing IBD

what are moderate risk factors for CRC?

personal or family history of adenoma or CRC, pelvic irradiation

what are modest risk factors for CRC?

high fat diet, red meat diet, smoking, alcohol consumption, cholecystectomy, diabetes mellitus, obesity

what are protective factors against CRC?

NSAID/asprin use, high physical activity, high fiber/fruit/vegetable diet, high calcium intake, folate, hormone replacement therapy

what are clinical manifestations of CRC?

rectal bleeding, iron deficiency (occult bleeding), change in bowel habit/stool caliber, obstruction, may be asymptomatic until advanced/metastatic

t/f CRC can metastize to the oral cavity

true- most commonly to the posterior mandible, may present with jaw or tooth pain, paraesthesia, or loosening of teeth

neoplasm may be found in a nonhealing extraction socket

when treating CRC patients, what should dental providers keep in mind?

associated with oral pathogen F. nucleatum (may have procarcinogenic effect)

periodontal disease linked with increased risk for CRC

t/f more frequent dental visits directly associated with presence of percancerous polyps

false- inversely associated

celiac disease

inflammatory conditions of the small intestine in genetically susceptible individuals, immune mediated injury in response to ingested gluten, occurs primarily in whites of northern european ancestry

prevalence of 1:200-300 in europe and north america

what are clinical manifestations of celiac disease?

classically presents in infancy but often presents later

malabsorption resulting in diarrhea/steatorrhea, weight loss, and signs of nutritional deficiencies

symptoms can be very mild (subclinical celiac disease) or absent (asymptomatic iron deficiency)

what are the oral manifestations of celiac disease?

dental enamel defects (enamel hypoplasia that is bilateral and symmetrical), recurrent aphthous stomatitis, delayed tooth eruption, smaller teeth, signs of nutrient deficiencies like cheilitis, atrophic glossitis, and gingivitis 

what are the methods of diagnosis for celiac disease?

serologic testing- IgA anti-tissue transglutaminase antibody

endoscopy- scalloped mucosa, flattened villi

histologic- small bowel biopsy (gold standard), intra-epithelial lymphocytes, crypt hyperplasia, and villous atrophy

how is celiac disease treated?

dietary counseling, education, gluten-free diet, correction of nutritional deficiencies, prevention of bone loss

when treating celiac disease patients, what should dental providers keep in mind?

evaluation prior to invasive dental procedures- patients may have coagulopathy secondary to vitamin K deficiency

prophy paste, fluoride treatments may contain gluten

what does alcohol abuse predispose a person to?

poor oral hygiene, caries, periodontal disease, xerostomia, oral squamous cell carcinoma, greater loss of attachment

cirrhosis

late stage of progressive hepatic fibrosis

caused by- alcohol abuse, hep C, hep B, MASLD, primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis, hereditary hemochromatosis, wilson’s disease, alpha-1-antitrypsin deficiency

what are potential complications of cirrhosis?

portal hypertension (ascites, gastroesophageal varices, hepatic encephalopathy, hypersplenism, thrombocytopenia)

impaired synthetic function (hypoalbuminemia, coagulopathy)

hepatocellular carcinoma (HCC)

what are some oral manifestations of cirrhosis?

scleral/oral/sublingual icterus, gingivitis, gingival bleeding, petechiae, bruising, glossitis, cheilitis, sialdenosis (enlarged parotids)

HCV- xerostomia, lichen planus, sialdenitis

HCC- metastasis to jaw/oral cavity

when treating cirrhosis patients, what should dental providers keep in mind?

risk of infection (HBV, HBC), risk of bleeding, altered drug metabolism

analgesics- acetaminophen (limit to 1-2g per day), NSAIDs (caution, can precipitate kidney failure, GIB), opioids (increase dose interval, short term)

anesthetics- lidocaine, mepivacaine, prilocaine (limit dose)

sedatives- BZDs, reduce dosage, increased intervals, or avoid if possible

list the general categories of dental drugs that are metabolized by the liver

local anesthetics, analgesics (like acetaminophen and ibuprofen), sedatives, and antibiotics

when treating pre-liver transplant patients, what should dental providers keep in mind?

comprehensive dental evaluation, extraction of infected/non-restorable teeth, oral hygiene instruction

when treating post-liver transplant patients, what should dental providers keep in mind?

no elective dental treatment for 3 months after surgery