Oral Manifestations of the Allergic Conditions
Immunity : Is the ability of an organism to resist infections . The
immune system is a complex network of cells and proteins that defends the
body against infection
The immune system keeps a record of every germ (microbe) it has ever
defeated so it can recognise and destroy the microbe quickly if it enters the
body again.
Abnormalities of the immune system can lead to allergic diseases, immuno
deficiencies and autoimmune disorders
It is divided into :-
A- Innate immunity
B – Adaptive (acquired) immunity Ab development to destroy Ag
Bacteria and virus (Ag) are soluble proteins introduced into the host cell and
stimulate reticuloendothelial system (spleen, lymph nodes, bone marrow) to
produce Ab
Anti bodies (Ab), are altered serum globulin molecules when brought in
contact with protein or microbes (i.e. Antigen) their production would
be excited.
The Ag may be destroyed by : Each antibody has a unique binding site shape which
locks onto the specific shape of the antigen. The antibodies destroy the antigen
(pathogen) which is then engulfed and digested by macrophages sequence this could
be occur by the following
A. Agglutination
B. Precipitation
C. Lyses
D. Neutralization
E. Production of phagocytosis (the above procedure discussed clearly in the immunity )
Allergy:
Immunologic reactions are detrimental to the tissue or physiology of the host.
Antibodies are immunoglobulins produced by plasma cells and of 5 types :
IgA, IgD, IgE, IgG, IgM
The Ab are located either in :
1- Circulation (in blood stream).
2- Fixed (to cells).
Immunoglobulins
IgA can be found in areas containing mucus (e.g. in the saliva, gut, respiratory
tract and in the urogenital tract) and prevents the colonization of mucosal areas by
pathogens.
IgD functions mainly as an antigen receptor on B cells.
IgE binds to allergens and triggers histamine release from mast cells (the underlying
mechanism of allergy) and also provides protection against helminths (worms).
IgG (in its four forms) provides the majority of antibody-based immunity
against invading pathogens.
IgM is expressed on the surface of B cells and also in a secreted form with very
high affinity for eliminating pathogens in the early stages of B cell mediated
immunity (i.e. before there is sufficient IgG to do the job).
When the individual exposed to the same Ag two things happen:
1- Ag may be neutralized or destroyed in the blood stream, by circulating Ab
(person is immuine).
2- The circulating Ab are not enough to destroy Ag, later reach the tissue cells
where it reacts with fixed Ab.
Allergens
any substances may have come in contact with. For example, if you have a rash on hands,
the doctor may ask if you put on latex gloves recently.
a blood test and skin test can confirm or diagnose allergens
so we could simply have the following definition
Substances that stimulate the immune reactions
and divided into:-
A. Soluble proteins (e.g. those in bacteria and viruses).The condition is called
bacterial allergy as in tuberculin test.
B. Non bacterial substances (fresh fruits & vegetables, fish, feather, hair, pollen,
milk
C. Drugs…etc) this condition is called atopy (hereditary).
D. Animal products. These include pet dander, dust mite waste, and cockroaches.
E. Drugs. Penicillin and sulfa drugs are common triggers.
F. Foods. Wheat, nuts, milk, shellfish, and egg allergies are common.
G. Insect stings. These include bees, wasps, and mosquitoes.
H. Mold. Airborne spores from mold can trigger a reaction.
I. Plants. Pollens from grass, weeds, and trees, as well as resin from plants such as
poison ivy and poison oak, are very common plant allergens.
J. Other allergens. Latex, often found in latex gloves and condoms, and metals like
nickel are also common allergens.
Depending on the speed, allergy may be classified into :
1- Immediate (or anaphylactic ) reactions. Occur in seconds up to 30 minutes.
2- Accelerated reactions Occur in 1 hr to 72 hrs.
3- Delayed reactions Occur in days or weeks
Anaphylaxis typically presents many different symptoms over minutes or
hours with an average onset of 5 to 30 minutes. The most common areas affected
include:
Skin Symptoms typically include generalized hives, itchiness, flushing, or swelling.
Respiratory symptoms and signs that may be present include shortness of
breath, wheezes, or stridor.The wheezing is typically caused by spasms of
the bronchial muscles while stridor is related to upper airway obstruction secondary to
swelling .Hoarseness, pain with swallowing, or a cough may also occur.
Gastrointestinal, symptoms may include crampy abdominal pain, diarrhea, and
vomiting. There may be confusion, a loss of bladder control or pelvic pain similar to that
of uterine cramps.
. Dilation of blood vessels around the brain may cause headaches. A feeling
of anxiety
Heart and vasculature Coronary artery spasm may occur with;
Subsequent myocardial infarction, dysrhythmia, or cardiac arrest. Those
with underlying coronary disease are at greater risk of cardiac effects from
anaphylaxis. The coronary spasm is related to the presence of histamine-
releasing cells in the heart. While a fast heart rate caused by low blood
pressure is more common ,a Bezold–Jarisch reflex has been described in
10% of cases where a slow heart rate is associated with low blood
pressure.
The Bezold–Jarisch reflex–Jarisch reflex involves a variety of
cardiovascular and neurological processes which cause hypopnea
(excessively shallow breathing or an abnormally low respiratory rate)
hypotension (abnormally low blood pressure)
bradycardia (abnormally low resting heart rate).
a drop of blood pressure pressure or shock (either distributive or
cardiogenic) may cause the feeling of lightheadedness or loss of
consciousness .Rarely very low blood pressure may be the only sign of
anaphylaxis,
In sensitized person; allergic reaction of the oral tissues could be due to:
Systemic intake (drug eruption, stomatitis medicamentosa)
Direct contact (contact stomatitis, stomatitis venenata)
Materials used in dental practice that may stimulate allergic reactions are;
• Rubber or latex (gloves, rubber cups, rubber dams)
• Formalin (in endodontic therapy, tooth pastes)
• Fillings (isopaste, light cure, free mercury
of amalgam)
• Impression materials (rubber base, silicon)
• Lining materials
• Dentures (acrylics, chrome-cobalt, gold alloys)
• Other chemicals and materials (haptane, phenol, procaine, lip
sticks,
cinnamon, and flavors in mouth washes...etc)
Clinical Findings of the oral tissue reactions to the allergens:
1- Swellings (e.g. Angioedema)
2- Ulcerative Lesions (e.g. Allergic mucositis, Erythema Multiforme)
3-White lesions (e.g. Lichenoid eruptions)
4-Red lesions (e.g. Plasma cell gingivitis)
Knowing the principles of dealing with this complication is very important for
the dentist
Epinephrine (1 mg/ml aqueous solution [1:1000 dilution]) is the
first-line treatment for anaphylaxis and should be
administered immediately
In adults, administer a 0.3 mg intramuscular dose using a
premeasured or prefilled syringe, or an autoinjector, in the mid-
outer thigh (through clothing if necessary)
Adjunctive measures include airway protection, antihistamines,
steroids, and beta agonists.
Patients taking beta blockers may require additional measures.
1- Angioedema (Angioneurotic Oedema)
• Well demarcated localized bilateral painless swelling (edema) which makes it
different from periapical abscess of the anterior teeth.
• It involves the deeper layers of the skin including the subcutaneous tissue.
• The lips are the common site but may occur anywhere on skin or mucous
membrane.
• Recurrent episodes of urticaria and/or oedema
• if less than 6 weeks duration are considered acute attacks existed beyond
this period are designated chronic.
Causes of the reaction:
a- A significant cases are idiopathic
b- Ingestion of food drug or contact with allergen
c- A recurrent form is inherited as an autosomal dominant trait.
Management
Avoidance of the allergen (food, pollen, drug) and use of antihistamines,
cortisone and adrenalin in sever form.
Hereditary type does not respond to antihistamines, corticosteroids, or epinephrine
and in an emergency, fresh frozen blood plasma should be given i.v.
2- Allergic stomatitis
There are basically two types of hypersensitivity reactions involved in allergic
stomatitis, type I immediate hypersensitivity, and type IV delayed
hypersensitivity. The allergic stomatitis may present with clinical appearances
that mimic classic oral vesiculobullous and ulcerative lesions
an oral mucosal immune inflammatory disorder variably characterized clinically
by
erythematous plaques
vesiculation,
ulceration,
hyperkeratosis
pain
burning sensation
itchiness.
3- Lichenoid drug eruptions
Lichenoid drug eruption, also called drug-induced lichen planus, is an
uncommon cutaneous adverse effect of several drugs ,characterized by a
symmetric eruption of flat-topped, erythematous or violaceous papules
resembling lichen planus on the trunk and extremities
The incidence of oral lesions without skin eruptions is common.
The etiology is mostly due to drug intake
Medications commonly reported to trigger a lichenoid drug eruption include:
Antihypertensives – ACE inhibitors, beta-blockers, nifedipine, methyldopa
Diuretics – hydrochlorothiazide, frusemide, spironolactone
Non-steroidal anti-inflammatory drugs (NSAIDs)
Phenothiazine derivatives
Anti-convulsants – carbamazepine, phenytoin
Medicines to treat tuberculosis
Antifungal medication – ketoconazole
Chemotherapeutic agents – 5-fluorouracil, imatinib
Antimalarial agents such as hydroxychloroquine
Sulfa drugs including sulfonylurea hypoglycaemic agents, dapsone,
mesalazine, sulfasalazine
Metals – gold salts
Others – allopurinol, iodides and radiocontrast media, interferon-α,
omeprazole, penicillamine, tetracycline
Other medications that have been reported in association with lichenoid drug
eruptions include
Tumour necrosis factor antagonists such as infliximab, etanercept and
adalimumab
Vaccines (especially those for herpes zoster and influenza).
The clinical and the pathogenesis are identical to lichen planus.
4- Plasma cell gingivitis
It is a rare condition; the cause of which is still not fully understood and
is characterized by massive infiltration of plasma cells into the
subepithelial tissue.
Clinical complication due to contact allergy characterized by generalized
erythematous, edematous attached gingiva usually accompanied by
inflammation of the lip and tongue.
Plasma cell gingivitis appears as mild gingival enlargement and may extend from
the free marginal gingiva on to the attached gingiva. Sometimes it is blended with
a marginal, plaque induced gingivitis, or it does not involve the free marginal
gingiva. It may also be found as a solitude red area within the attached gingiva
In some cases the healing of a plaque-induced gingivitis or a periodontitis resolves
a plasma cell gingivitis situated a few mm from the earlier plaque-infected
marginal gingiva. In case of one or few solitary areas of plasma cell gingivitis, no
symptoms are reported from the patient. Most often solitary entities are therefore
found by the dentist.
The gums are red, friable, or sometimes granular, and sometimes bleed easily if
traumatised The normal stippling is lost . There is not usually any loss of
periodontal attachment. In a few cases a sore mouth can develop, and if so pain is
sometimes made worse by toothpastes, or hot or spicy food. The lesions can extend
to involve the palate.
5. Plasma cell cheilitis appears as well defined, infiltrated, dark red plaque
with a superficial lacquer-like glazing. Plasma cell cheilitis usually involves the
lower lip. The lips appear dry, atrophic and fissured. Angular cheilitis is sometimes
present.
Where the condition involves the tongue, there is an erythematous enlargement
with furrows, crenation and loss of the normal dorsal tongue coating.
Diagnosis
Histologically plasma cell gingivitis shows mainly plasma cells. The differential
diagnosis is with acute leukemia and multiple myeloma.
Hence, blood tests are often involved in ruling out other conditions.
A biopsy is usually taken, and allergy testing may also be used.
The histopathologic appearance is characterized by diffuse, sub-epithelial plasma
cell inflammatory infiltration into the connective tissue.
The epithelium shows spongiosis. Some consider that plasmoacanthoma (solitary
plasma cell tumor) is part of the same spectrum of disease as plasma cell cheilitis