Article Type : Research Article
Authors : Shunmugavelu K
Keywords : rheumatoid arthritis; lupus; asthma; diabetes
The oral cavity is a reflection of the gastrointestinal
(G.1) system and oral changes are an expression of gastrointestinal diseases.
Alterations within the oral cavity can be the first sign of systemic diseases
and may allow early diagnosis and treatment.
The oral cavity is a reflection of the gastrointestinal
(G.1) system and oral changes are an expression of gastrointestinal diseases.
Alterations within the oral cavity can be the first sign of systemic diseases
and may allow early diagnosis and treatment. G.l. disturbances cause a decrease
of essential vitamins which can several affect the growth and development of
growing tissues. There is a change in the quality of dental tissues along with
delayed eruption of teeth and jaws. Studies prove that the oral cavity changes
like dental erosion is seen in about 22°/c of children aged 4 years and 44°/c
aged 12 years. In Europe and North America, 9 out 15 children have gingivitis
and adolescents show prevalence of about 60°/c (Italian ministry of health,
Guidelines 2013). In USA, enamel hypoplasia is seen in 10 to 49°/c of primary
dentition (Stayton). 33°/c children show at least one tooth with enamel
hypoplasia or opacities. A comprehensive review of G.l. diseases with their
manifestation is illustrated below.
It is an inflammatory bowel disease which affects any
part from mouth to anus including perianal and perioral skin. The etiology is
yet unknown. It may be autoimmune, pathogenic or due to allergens’. It is seen
more in males than females from late childhood to middle age'. Only 0.5°/c patients
developed oral lesions. The characteristic features involves skip lesions from
the mucosa to full thickness of bowel wall resulting in inflammatory exudate on
serosal surfaces. There are noncaseating granulomas in bowel wall. The lesions
outside G.l. are on the eyes, legs and are known as erythema nodusa'. It may be
related to immune conditions like rheumatoid arthritis, lupus, asthma and diabetes.
The symptoms include recurrent abdominal pain, diarrhea, mucus and blorxl in
stools. Recurrent bleeding causes iron deficiency anemia. The inflammation of
the bowel wall causes narrowing of the lumen leading to blackage. Depending on
the affected areas nutritional deficiencies like B 12 are seen if terminal ileum
and ileocecal region is involved. Duodenu m and jejunu m involvement causes
generalized malabsorption and nutritional deficiency. Adhesion and fistula
formation are common [1-5].
The oral manifestations show as lip swelling, angular
cheilitis, oral ulceration, mucosal cobblestoning, full width gingivitis,
geographic tongue and stomatitis. Granulomas go deep in muscle layer and biopsy
may involve a risk of facial perforations. Fecal Calprotectin test is used for
monitoring. Endoscopy and biopsy if used to confirm the diagnoses. The
management of the disease is done with steroids like prednisone along with
azathi opine, NSAlDS, enemas based on 5ASA. lmiximab and adalimimab are used
for more specific therapy targeted at cytokine TNF-alpha. Steroids should be
used in reduced doses for children as it affects growth. Bowel resection is
done to treat blr›ckage of the bowel wall.
It is an inflammatory bowel disease which involves the
rectum and progresses towards the upper part of the colon. It can happen at an
y age but more specifically seen in between 15 to 25 years of age and a small
peak is seen from 55 to 65 years of age. The median age is around 32 years.
Europeans have a higher incidence with 24.3 new cases per 100000 persons each
year. It is difficult to differentiate from Crohn’s disease and sometimes is
called indeterminate colitis. The characteristic feature of ulcerative colitis
is Pyostomatitis vegetans. It involves multiple military white or yellow
pustules that coalesce in snail track ulcers with an erphematous and edernatous
base in mucosa. The symptoms are weight loss, fatigue, and bloody diarrhea with
mucus and negative stool cultures. It is mainly mucosal inflammation and hence
superficial. The oral manifestations include glossitis, cheilitis, stomatitis,
lichen planus, mucosal ulcers, diffuse pustules and nonspecific gingivitis. It
is seen in 5 to 10°/c population.
The treatment involves use of oral steroids, Dapsone,
SASA based drugs, mesalazine, sulphasalazine and olsalazine. Ileostomy is
needed in some cases. Antiseptic mouth rinse is given to avoid Candida
infections such as dilute chlorhexidine or topical sugar-free nystatin.
It is an event which allows backflow of acids in
esophagus and pharynx due to defective relaxation of lower esophagus sphincter.
It can be associated with Helicobacter pylori, bulimia, hiatus hernia or
chronic alcoholism”. There is repeated regurgitation, nausea, heartburn,
coughing, laryngitis, asthma and pneumonia. Infants and young children show
irritability and arching of the back while feeding, feed refusal and show poor
growth. Hemorrhage, Baretts esophagus and adenocarcinoma are complications of
Gerd. Perimyolysis is seen in 17°/c children of 2 to 16 years of age group in a
cohort study by O’S ullivan et al in 1998. It is due to acidic food, beverages
or contarilinant, salivary flow, eating disorders and acid regurgitation.
The oral manifestations are erosion, sour taste,
burning mouth, ulcers, mucositis, halitosis and xerostomia. 83.3*/c dental
erosions related to GERD is seen in children. Erosion is seen mostly on palatal
surfaces of posterior and anterior teeth. Ruled surfaces are smooth and shiny.
Yellow color of the dentin is visible as enamel thins out or is worn off.
Severe cases may require dental restorative treatment'. Diagnosis is confirmed
through PH impedance or endoscopy. Treatment involves lifestyle changes like
regular diet, weight loss, and correct sleeping position, avoid smoking, no
late night eating. Proton pump Inhibitors are useful for suppressing tooth
erosion.
It is an autosomal dominant disorder with defective
chromosome. The characteristics feature is intestinal hypnosis which has a high
risk of malignant transformation to adenocarcinoma. It affects other organ
systems including skin, skeleton and soft tissues. The head and neck
manifestations are seen in child hand and adolescence. It involves epidermoid
cysts of skin of head and neck.
The oral manifestations include enostosis of jaw which
is seen as bone expansion in radiographs. There are increased incidence of supernumerary
and interrupted teeth. They show an increased risk of cdontomas. Osteornas
showing focal expansion of the jawbone can be felt over the skin and mucosa. It
is clinically visible. The treatment involves surgical removal of osteomas,
odontomas and cysts. It can cause cosmetic and functional issues'.
It is an autosornal dominant disorder showing mutation
of LKB I gene. It shows hamartomatous polyposis of small intestine'. Oral
manifestations include non-sun exposed freckles near lips and verinilion
border. There are flat, brown, painless, pigmented intra oral lesions seen on
the buccal and labial mucosa as well as the tongue' '. Lesions show mild
acanthosis with elongation of rete pegs and increased pigmentation in keratinocytes
and melanocytes without an increase in number of melanocytes. No specific
treatrilent is required until cosmetic intervention is needed. Lasers is the
treatment of choice.
Excess bilirubin in the blood results in the
accumulation of bilirubin in tissues, including the oral mucosa causing a
yellow discoloration. The severity of the yellow discoloration depends on the
blood concentration of bilirubin and the duration of the problem. Bilirubin has
an affinity for elastin, thus the mobile oral tissues with higher elastic
content such as the lingual frenum and the soft palate are more severely
affected. A yellowish to greenish pigment (biliverdin deposition) occurs in the
teeth of children with hyperbilirubinemia during calcification, as may be seen
in the primary teeth of biliary atresia patients. This is not seen in adults as
teeth have already calcified. However care should be taken in assessing a
yellowish discoloration of the sofi palate in patients receiving or eating
large amounts of vitamin A, which is stored in fat of small intestine'.
GI diseases related to protein-caloric malnutrition or
micronutrient malabsorption may have an effect on the oral tissues. The
classical examples are iron malabsorption inducing iron deficiency anemia and
vitamin B12 malabsorption in pernicious anemia. The first oral manifestation is
atrophic glossitis in which the filiform and fungi form papillae on dorsurn of
the tongue becomes atrophied. It’s accompanied with burning sensation
(glossopyrosis). In milder cases, the atrophy is patchy, but more severe cases
show involvement of the entire dorsurn. ln very severe cases, there may be
shallow, round to oval-shaped, persistent ulcers with bright red borders,
clinically resembling aphthous ulcers but often responsive to appropriate
replacement therapy. Affected patients are predisposed to developing angular
cheilitis that can be treated with antifungal medication. The
gastroenterologist may use atrophic glossitis as an indicator of moderate to
severe nutrient malabsorption. Treatment involves iron and B 12 supplements.
Malignant neoplasms of the liver and Gl tract
occasionally metastasize to the oral region, most commonly to the posterior
mandible and usually through the hematogenous route. Patients with mandibular metastasis
may be asymptomatic, or may complain of jaw or tenth pain, paraesthesia
(unilateral or bilateral numbness of the chin) or loosening of teeth.
Initially, the neoplasm is sometimes found in a non-healing extraction socket
afire a tooth has been extracted because of unexplained looseness. Less
commonly, metastases may involve the maxilla or oral soft tissues.
Coeliac disease is a small bowel disease usually seen
in the jejunum. It is also known as gluten-sensitive enteropathy. It is an
immune reaction to the alpha-gliaden component of gluten resulting in mucosal
villous atrophy and loss of a large absorptive surface area in the small bowel.
It can occur at any age but is most obvious in children.
Celiac disease is more common in patients with Down
syndrome and type 1 diabetes, autoimmune thyroid disease, and in some racial
groups. Northern European and Celtic populations seem particularly susceptible.
This relates to the prevalence of HLA -DQ2 and 14 HLA-DQ8 genes in the
populations affected.
An individual without coeliac disease has a 10°/e risk
of the disease if it is present in a sibling or direct family member and is at
85°/c risk if it is in their identical twin. Gluten containing food should
ideally be withheld until 6 months of age to reduce the risk of disease.
Oral conditions such as aphthous ulcers, angular
cheilitis, recurrent herpetic, lesions, caries, enamel hypoplasia, atropic
glossitis and glossodynia are seen. Investigation involves testing for
antibodies in the blend. A positive test should lead to more specific tests for
anti-gliadin antibodies and antiendomysial antibodies. Positive results in
these are significant. Endoscopy with jejunal biopsy is the most accurate test,
but it is not usually performed unless there is evidence of growth failure
together with an antibody profile which suggests coeliac disease.
Treatment Involves avoiding gluten in the diet
completely which can enable proper functioning and reverse the adverse effects
of malabsorption in the small bowel. Other than diet care must be taken as some
lipsticks and medications can have gluten as fillers.
Cystic fibrosis (CF) is a disease of the pancreas
which significantly upsets normal digestion and absorption of nutrients. CF is
caused by abnormal function of the CFTR protein, which regulates sodium and
chloride movement across cell membranes resulting in highly viscous mucous
secretions. The genetic abnormality underpinning CF is found in 1 in 25 people
of European descent, but as it is a recessive condition, the condition is only
found in 1 in 2500 live births in the European Union.
Thickened secretions cause ductal blockage in the
pancreas and the bile duct leading to pancreatitis and cirrhosis of the liver.
This damage is irreversible and can also lead to a form of diabetes unique to
CF. Fat and the fat-soluble vitamins, such as A, D, E, and K often not absorbed
well. The malabsorption of vitamin K can lead to bleeding issues in older
patients with CF. Child patients with CF traditionally needed a high
carbohydrate-rich diet to keep their calorie intake at adequate levels as
fat-based energy sources were not absorbed.
The treatment involves introduction of oral pancreatic
enzyme supplements. Therapy to allow a normal CFTR protein to be synthesized by
the body’s cells has been achieved with virus carriers inserting the gene into
cells’.
These diseases clearly indicate a comprehensive
knowledge of G.l. diseases and symptoms is needed to detect any disorders and
make correct differential diagnosis which will serve as a helpful guide for
both the dentist and the gastroenterologist in early diagnosis, treatment plan
and management of these challenging manifestations to improve the health and
well-being of the patient. The severity, progress and prognosis of the disease
can be monitored in the presence or extent of oral manifestations and
successful enlargement of G.l. diseases may be reflected in response of oral
tissues.