Dental considerations in
MALABAR DENTAL COLLEGE
• CONCEPT OF IMMUNITY AND AUTOIMMUNITY
• Human body has got capacity to resist almost all types of organisms or toxins that tend to damage the
tissues and organs.
• Immunity present at birth or as apart of general process-innate immunity
• Immunity aquired against specific invading organism-acquired immunity(b-cell & t-cell mediated)
• Failure of the immune system to tolerate self
• It is a condition in which structural or
functional damage is caused by the
immunologically competent cells or antibodies
against normal components of body.
Classification of autoimmune diseases
Ferguson A 1995
• 1.ORGAN SPECIFIC AUTOIMMUNE DISEASES
• Hashimottos thyroiditis
• Primary myxedema
• Pernicious anemia
• Addison’s disease
• Type 1 diabetis mellitus
• Myasthenia gravis
• Good pastures syndrome.
• Sjogrens syndrome
• Non organ specific
• Rheumatoid arthritis
• Systemic sclerosis
• Chronic inflammatory autoimmune disorder
which is charecterized by dimnished lacrimal
and salivary gland secretion(sicca
complex),resulting in keratoconjunctivitis sicca
• Primary sjogrens syndrome-xerostomia & xerophthalmia.
• Secondary sjorgrens syndrome-triad of
xerophthalmia,xerostomia& a connective tissue
• ORAL MANIFESTATIONS
• Unpleasant taste sore mouth
• Difficulty in eating dry food(cracker sign)
• Mouth mirror or tongue blade adheres to buccal
mucosa(tongue blade sign)
• Shed epithelial cells on the labial surface of maxillary
• Parotid enlargement in 80% patients.
• Tongue may appear lobulated ,usually red with partial or
• Diagnosis of sjogrens syndrome
• Laboratory findings
• 75% of patients with primary sjogrens syndrome
have polyclonal hyperglobulenemia.
• Antisalivary duct antibodies
• Rhematoid factor
• Antinuclear antibodies.
• Normocytic normochromic anemia
• Sialometry-salivary flow rate estimation
• Sialography-cherry blossom appearance
• MRI –salt & pepper appearance
• investigation for occular signs
• 1.Schimmers test-check lacrimation
• 2.Ocular staining-cornea stained using rose
Bengal dye & examined microscopically.
• Slit lamp examinationclearly reveals the stained
corneal cells with their devitalised nuclei
• Such stained areas represents corneal damage
from inadequate lacrimation.
(benign lymphoepithelial lesion)
• Symmetric or bilateral chronic ,painless
glands attributed to chronic infection.
• Goodwin 1952 introduced the term benign
• Exact etiology unknown
• Inflammatory or autoimmune or neoplastic
• Related to sjigrens syndrome in which antisalivary gland antibodies
• CLINICAL FEATURES
• Unilateral or bilateral salivary gland enlargement.
• Mild pain,local discomfort, & xerostomia.
• Onset associated with fever,respiratory disorders,oral
infection,tooth extraction etc
• The enlargement in size can be varied but generally the size
increases by a few centimetres.
• Occassionally lacrimal glands are enlarged.
• Incisional & excisional biopsy
• Focal infiltrates of small lymphocytes that expands
to replace glandular epithelium.
• Hyperplasia & metaplasia of ductal epithelium.
• Lymphoid follicles & germinal centres may or may
• Appropriate assesment of patient for the presence
of ocular or systemic components of sjogrens
• Surgical excision or radiation
• Mild cases no treatment
• Some cases swelling regresses,persistent
disease may be treated by surgical excision.
• Radiation is not adviced due to possibility of
radiation induced malignancy.
ulcers,canker sores,recurrent aphthous
stomatitis)• Most common cause of oral ulcerations.
• Elevated levels of IgA & IgG in sera of patients with RAS.
• T-lymphocytes from RAS patients had increased
cytotoxicity to oral epithelial cells.
• Suggests autoimmune origin
• 1.minor RAS
• 2.major RAS(suttons disease,periadenitis necrotica mucosa)
• 3.Herpetiform ulcer.
• 4.oral ulcers associated with Behcets syndrome.
• CLINICAL FEATURES
• Onset of disease marked by burning sensation, 2-48 hours before
• Initially localized area of erythema develops within hours,a small
white papule forms,ulcerates and enlarges in next 48-72hrs.
• Ulcers are usually regular and well defined,rimmed by an
• Covered by yellowish gray fibrinous pseudo membrane.
• Usually seen on non keratinized oral mucosa(buccal & labial
mucosa),rare on heavily keratinized palate or gingiva.
• MINOR RAS
• Commonest variety
• Round or oval ulcers measures less than 5mm
• Heals within 10-14days without scarring
• MAJOR RAS
• Severe form
• Large painful ulcers, 1cm-3cm
• Lips,soft palate,faucial pillars mostly affected
• Severe pain and dysphagia.
• Pesist upto 6weeks,heals with scarring
• Recurrent Herpetiform Ulcers
• Crops of multiple small,shallow ulcers often upto
100 in number.
• Numerous small lesion on intraoral mucosal
• Begin as pinhead sized erosions that gradually
enlarge & coalse
• More painful than suspected by its size.
• Present almost continuesly for one to three years.
• Based on history of patients complaint & clinical findings.
• Patients reports of bouts of oral ulceration on mobile oral
• Lasts for few weeks.
• Patients are healthy inspite of ulceration
• Mouth rinses(Chlorhexidine gluconate,benzydamine
• Topical steroids(hudrocortisone hemisuccinate
pellets,triamcinalone acetonide in adhesive paste)
• Antibiotics-topical tetracyclines
• Immuno modulators-levimasole
• For almost 2decades the concept of autoimmune
pathogenesis for periodontal disease were considered.
• Alphonse VG etal(1981) detected rheumatoid factor in
subgingival plaque,inflamed gingival tissue,stimulated
pooled saliva & serum of patients suffering from
chronic moderate periodontitis.
• Increased levels of antibodies to type1 collagen in
patients with periodontal diseases.
• All these suggested autoimmunity may contribute to
pathogenisis of this common disease.
• Anusaksathien O and Dolby AE (1991) postulated
possible explanations to explain the presence of
autoantibodies in periodontal disease.
• 1.enhanced presentation of self antigens through
increased expression of the molecule associated with
antigen presentation namely Ia antigen.
• Altered T-helper or T-suppressor cells.
• Bacterial or viral cross reactivity with self antigen
leading to production of cross reactive antibodies.
• Genetic predisposing factors
• Immunologic predisposition
• Blisters in pemphigus vulgaris is associated with
binding of IgG (G1 and G4)autoantibodies to
keratinocyte cell surface molecules
• PV antibodies bind to keratinocyte
• Binding results in loss of cell cell adhesion
• Pemphigus vulgaris -70% cases
• Rapid appearance of vesicles or bullae
• Lesions contain thin watery fluid which later
• When bullae rupture they form eroded areas.
• Nikolsky sign-loss of epithelium occassioned by
rubbing apparently unaffected skin.
• Asboe hansen sign-or bullae spread phenomenon
• Oral manifestations
• First to come last to go.
• Oral lesion begins as a bullae on a non inflamed base
• Ruptures to form a shallow ulcer with tissue tags on
• Common sites are buccal mucosa ,gingiva and palate
• Ulcers extend peripherally over a period of time until
they involve large portions of oral mucosa.
• Distal extension from oral cavity causes involvement of
esophagus,pharynx,and larynx causes dysphagia and
hoarseness of voice
• Pemphigus vegetans is an uncommon variant of
• Occurs in 1-2% pemphigus vulgaris
• Two types 1.Neumann type-pustules
• 2.Hallopeaue type-bullae and
• Cerebriform tongue –charecterised by a pattern
of sulci and gyri on the tongue
• Cytology-TZANK CELLS..
Epithelial cells that are free in vesicular spaces and are
charecterised particularly by degenerative changes
which include swelling of nuclei and hyperchromatic
• In PV the antibody will bind the immunoglobulin
deposits in the intercellular substance and exhibit
positive fluorescent under fluorescent microscope.fish
net pattern of binding
• Topical therapy
• Painful skin lesions and foul odour managed
by 0.01%pottasium permangnate or 0.5 %
• Topical corticosteroids or procaine
• Chlorhexidine mouth rinses
• A.control phase
• Initial high dose of corticosteroids to a point of clinical
• Lever suggests 180-360 mg of prednisolone daily for 6-
• B.consolidation phase
• In this phase the dosage is reduced.
• C.Maintanence phase
• Dose gradually tapered down to alternate day dose and
• Immunosuppressive agents-Azathioprine 100-
200mg in conjunction with prednisolone
• Plasmapherisis-patients who are refractory to
• Photopherisis-administration of 8-
methoxypsoralen followed by exposure of
peripheral blood to uv radiation.causing
photoinactivation of WBC
• Immunomodulators –levimasole(100mg/week)
pemphigus or fogo selvagum)
• Benign variety of pemphigus.
• Manifested as early bullous lesions which rapidly
rupture and dry to leave masses of flakes or
scales suggestive of exfoliative dermatitis or
• Brazilian wildfire pemphigus
• Endemic form of pemphigus foliaceus
• Occurs commonly in children.
• Oral lesions are rare.
• Anhalt et al first described paraneoplastic pemphigus
Tumour antigens evoke an immune response that leads
to development of an autoimmune response to
• This autoantibody response leads to blistering in
mucosa and other epithelia.
• Often fatal.
• Most common malignancy associated is NON
• GIANT CELL LYMPHOMA
• BRONCHOGENIC SCC
• Oral erosions and ulcers are common
• Benign mucous membrane pemphigoid,ocular
• The word cicatrical means scarring
• Chronic subepidermal blistering and scarring
autoimmune disease with a predilection for
stratified squamous mucous membrane and
• Charecterized by vesicles that heals by scar
formation.generally occurs on mucous
membrane of oral cavity and conjunctiva.
• Oral lesions have two clinical presentations
• 1.erosions on the non-keratinized
mucosa/keratinized gingiva or desquamative
• Oral lesions have distinct margins..heals by
• Nikolsky sign positive
• Spontaneous gingival bleeding
Sub conjunctival scarring leads to blindness in 15%
• Rarely involves mucous membrane
• Elderly people
• Appears as rashes commonly on limbs urticarial
• Remains for several weeks before appearance of
vesicles and bullae.
• Vesicles are thick walled and rupture occurs
• Oral lesions
• Small bullae,rarely painful
• Buccal mucosal gingiva more commonly involved.
• Generalized edema and inflammation of gingiva.
• Remissions are common
• Use of systemic steroids
• Group of inherited bullous disorders
charecterized by blister formation in response
to mechanical trauma.
• 3 types of presentation
• Bullous pemphigoid
• Cicatrical pemphigoid
• Classical presentation is non inflammatory bullous
disease heals with scarring
• Patients have erosions blisters and scars over trauma
• The bullous pemphigoid like presentation is
widespread inflammatory vesiculobullous eruption
involving the trunk,central body,skin folds and
• 10% patients exhibit severe mucous membrane
involvement may present a picture clinically similar to
cicatrical pemphigoid with erosions and scarring in the
oral cavity,conjunctiva,upper oesophagus anus and
• Prevention of trauma
• Antibiotics for secondary infection
Systemic lupus erythematosis
• Autoantibodies ,immune complex formation and
immune dysregulation resulting in damage to any
organ including kidney,skin,bloodcells,and CNS
• Environment all these leading to immune
• Low grade fever and malaise
• Erythematous rash over malar region,refered
to as butterfly rashes
• Pain on joints,rheumatoid arthritis.
• Renal involvement-nephritis
• Cardiopulmonary-pleuritic chest pain
• CNS-neuropathy,sensory motor incoordination
• Oral lesions
• Multiple white plaques with dark reddish purple
• Hyperemia and edema are marked
• Bleeding and superficial ulceration
• Dental caries
• Use of corticosteroids
• Dental consideration
• Platelet count measured before oral surgical
• Prophylaxis against bacterial endocarditis
• Shafers textbook ot oral pathology
• Burkets oral medicine