1. Describe the causes, the clinical features and course of traumatic oral ulceration.

● Traumatic oral ulcers are the most common type of oral ulcers in both children
and adults. The exact cause of these ulcers is not known, but several factors can
contribute to their development, including minor tissue injury from dental work,
accidentally biting the cheek or tongue, wearing orthodontic braces or retainers,
and vitamin deficiencies. [3]
● The clinical features of traumatic oral ulcers include painful, round or oval-shaped
sores that are white, gray, or yellow in color with a red border. These ulcers may
appear on the gums, tongue, lips, palate, or buccal mucosa. They usually heal on
their own within 1-2 weeks, and treatment is aimed at reducing the pain and
discomfort associated with the ulcers. [2]
● The course of traumatic oral ulcers is usually benign, and the ulcers heal without
any complications. However, in some cases, these ulcers can become recurrent
and may require further investigation to rule out any underlying systemic
conditions. It is important to seek medical attention if the ulcers are persistent,
unusually large, or accompanied by other symptoms such as fever, swollen
glands, or difficulty swallowing
2. List and explain the possible aetiological factors for recurrent aphthae to peers
and patients
● Recurrent aphthous stomatitis (RAS), commonly known as recurrent aphthae, is
a condition characterized by the recurrence of round or ovoid painful ulcers on
the oral mucosa [1]. The exact cause of RAS is still unclear, but several factors
have been proposed as possible aetiological factors, including
○ Genetic factors: Studies suggest that genetic factors play a role in the
development of RAS. A family history of RAS increases the risk of
developing the condition [3].
○ Local trauma: Minor injury to the oral mucosa, such as biting the cheek,
using dental appliances, or dental work, can trigger the onset of RAS
lesions [1].
○ Stress: Emotional stress or psychological factors have been proposed as
a possible trigger for RAS. Stressful events or anxiety can exacerbate the
condition [1].
○ Nutritional deficiencies: Deficiencies in iron, folic acid, vitamin B12, and
zinc have been linked to the development of RAS. A well-balanced diet
rich in these nutrients may help prevent the condition [1].
○ Immunological factors: Some evidence suggests that RAS may be an
autoimmune disorder, in which the immune system attacks healthy cells in
the mouth. This can lead to the formation of ulcers
3. List and describe the typical clinical features of the three types of recurrent
aphthae that distinguish them from each other.
● There are three types of recurrent aphthae, namely minor, major, and herpetiform
ulcers. Here are the typical clinical features of each type:
a. Minor aphthae: These are the most common type of recurrent aphthae
and are typically less than 1 cm in size. They present as shallow ulcers
 with a yellowish-white center and a red border. They are usually painful
and heal within 1-2 weeks [2].
b. Major aphthae: These ulcers are less common but are typically larger and
deeper than minor aphthae, ranging from 1-3 cm in size. They have a
similar appearance to minor aphthae, but they may take several weeks to
heal and can leave scars. Major aphthae are usually more painful than
minor aphthae and may be associated with systemic symptoms such as
fever and malaise [2].
c. Herpetiform aphthae: This type of aphthae is rare and is characterized by
the presence of multiple small ulcers that are less than 1 cm in size.
These ulcers often cluster together and may resemble the lesions seen in
herpes simplex virus infection. Herpetiform aphthae are typically very
painful and can last for several weeks to months
4. Describe the pathology of aphthae and list the ancillary laboratory tests you would
require to determine a possible aetiology.
● Aphthae, or aphthous ulcers, are typically diagnosed based on clinical
examination and medical history, as there are no specific laboratory tests
available for diagnosing this condition [1]. However, in some cases, ancillary
laboratory testing may be performed to help determine the underlying cause of
recurrent aphthae.
● To determine the possible etiology of aphthae, laboratory tests may be ordered to
rule out underlying systemic conditions, such as nutritional deficiencies,
autoimmune diseases, and infections. Some of the laboratory tests that may be
used include blood tests for vitamin B12, folic acid, iron, and other nutrient
deficiencies, as well as testing for systemic diseases such as HIV, syphilis, and
inflammatory bowel disease. A biopsy may also be performed to help differentiate
between aphthae and other ulcerative lesions, as well as to rule out malignancy
● It is important to note that most cases of aphthae are idiopathic, and no
underlying cause can be identified. Therefore, ancillary laboratory testing is
typically reserved for patients with recurrent, severe, or atypical aphthae or those
with systemic symptoms such as fever or weight loss [1]. Additionally, some
laboratory tests, such as a urine pregnancy test or a blood glucose test, are
considered waived tests and can be performed in a point-of-care setting with
minimal interpretation and training
5. List the diagnostic criteria for Behcet’s disease and explain the difference
between Behcet’s disease and recurrent aphthae.
● Behcet's disease is a chronic inflammatory disorder that affects multiple organ
systems and is characterized by recurrent mouth sores, genital sores, and skin
lesions. The diagnostic criteria for Behcet's disease are based on clinical findings
and include recurrent oral ulcers, as well as two of the following: recurrent genital
ulcers, eye inflammation, skin lesions, or a positive skin prick test. Behcet's
disease can also affect other organs, such as the brain and spinal cord, leading
to neurological complications, including stroke and meningitis [[2]].
 ● Recurrent aphthae, on the other hand, are a common condition of the oral
mucosa characterized by the recurrent formation of round or ovoid ulcers with
circumscribed erythematous margins and a grayish-yellow base [[1]][[3]]. Unlike
Behcet's disease, recurrent aphthae typically occur in patients who are otherwise
healthy, and their etiology is unclear. While both conditions share the
characteristic of recurrent oral ulcers, Behcet's disease is distinguished by its
involvement of other organ systems and its more systemic nature. Additionally,
the diagnosis of Behcet's disease requires the presence of other clinical findings
beyond just oral ulcers
6. Recognise drug-related and HIV-associated oral ulceration from idiopathic
ulceration.
● Recurrent aphthous ulcers are the most common type of oral ulcer, and mucosal
ulceration could be related to malignancy such as oral squamous cell carcinoma
[1]. Drug-induced oral ulcerations have also been reported, particularly with drugs
used for the treatment of chronic disorders like diabetes, angina pectoris,
rheumatoid arthritis, and osteoporosis [3]. In contrast, HIV-associated oral
ulceration is one of the most common oral manifestations of the disease [2].
Diagnostic criteria for idiopathic recurrent aphthous ulcers are based on their
clinical presentation, including the presence of painful ulcers with a diameter of
less than 5 mm and a white-yellowish fibrinous membrane, with or without
erythema surrounding the lesion. In contrast, HIV-associated oral ulcers tend to
be larger, have irregular borders, and may be accompanied by systemic
symptoms. Diagnosis of drug-induced oral ulcers requires a detailed medical
history, including medication use
7. List the typical features of oral lichen planus.
● Oral lichen planus is a chronic inflammatory condition that affects the mucous
membranes inside the mouth [1]. The typical features of oral lichen planus are
white, lacy patches, red and swollen tissues, or open sores in the oral cavity [1],
and white patches or lacy threads on the inside of the cheeks [2]. These lesions
may cause burning, pain or other discomfort [1]. It is not contagious and cannot
be passed from one person to another
8. Explain the putative aetiology and pathogenesis of oral lichen planus.
● Oral lichen planus (OLP) is a chronic inflammatory disorder that affects the
mucous membranes inside the mouth, as well as other parts of the body like the
genital mucous membranes, skin, nails, and scalp [1]. The exact cause of OLP is
uncertain, although there is evidence to suggest that it may be related to an
autoimmune process. It has been proposed that OLP may arise from a T
cell-mediated autoimmune response against antigens within the epithelial cells of
the oral mucosa. This results in damage to the epithelium and lamina propria of
the oral mucosa [3]. Other factors such as genetic predisposition, viral infections,
drugs, and stress have also been suggested to contribute to the development of
OLP [2]. Overall, the pathogenesis of OLP is complex and not fully understood,
but it is believed to be multifactorial in nature
9. List the clinical types of oral lichen planus and describe the symptoms.
 ● Reticular oral lichen planus is the most common form and is characterized by
white, lacy or web-like patches on the inside of the cheeks. This type of OLP may
also appear as thin, white lines on the tongue, gums, or lips [1].
● Erosive oral lichen planus, on the other hand, may present as red, swollen, or
ulcerated areas inside the mouth. Patients with this type of OLP may experience
pain, burning, or other discomfort when eating or drinking [1]. Bullous OLP is a
rare form of OLP that causes blisters to form in the mouth
10. List and recognise the typical histological features of hypertrophic and atrophic
oral lichen planus.
● Hypertrophic OLP is characterized by hyperkeratosis and acanthosis, with a
thickened epithelium that may form papillomatous or verrucous projections. The
subepithelial inflammatory infiltrate is usually mild to moderate and composed
mainly of lymphocytes and histiocytes. [1]
● Atrophic OLP is characterized by a thinning or loss of the epithelium,
accompanied by a more intense subepithelial inflammatory infiltrate, which can
include plasma cells, eosinophils, and neutrophils. This subtype can be divided
into two types: the first one is a homogeneous form with a smooth, shiny, and
erythematous surface, while the second one presents with erosions or
ulcerations
11. Explain the nature of lichenoid reactions and what the difference is with lichen
planus.
● Lichenoid reactions and lichen planus are related but different conditions.
Lichenoid reactions refer to a rash that looks similar to lichen planus but is
caused by a reaction to a medication or other substance, rather than being an
autoimmune disorder like lichen planus. Lichenoid drug eruption is a type of
lichenoid reaction that is caused by medications and can affect the skin or oral
mucosa [3].
● Lichen planus, on the other hand, is a chronic inflammatory condition that can
affect the skin, scalp, nails, genital area, and the mucous membranes inside the
mouth [1][2]. It is an autoimmune disorder, which means that the body's immune
system mistakenly attacks its own tissues. The resulting rash can appear as
purplish, itchy, flat bumps that develop over several weeks [2]. In the mouth,
lichen planus can cause white, lacy patches; red, swollen tissues; or open sores
12. Recognise clinical features that suggest a lichenoid reaction.
● The clinical features of lichenoid reactions vary depending on the underlying
cause.
○ Lichenoid keratosis: Lichenoid keratosis is an inflammatory reaction that
arises in a regressing solar lentigo or seborrheic keratosis. The clinical
features include a papule or plaque with a keratotic surface, a
reddish-brown to gray color, and a lacy white pattern on dermoscopy [1].
○ Lichenoid drug eruption: Lichenoid drug eruptions can look much like
idiopathic lichen planus, but the rash is more extensive and distributed
symmetrically over the trunk and limbs. They can also present with
blisters, erosions, or purpura. The oral mucosa may also be affected.
 Lichenoid drug eruptions may occur after taking a new medication or after
a dose increase, and they typically resolve after discontinuing the
medication [2].
○ Lichenoid granulomatous dermatitis: Lichenoid granulomatous dermatitis
is an unusual reaction pattern that can be caused by various triggers,
including medications, infections, or malignancies. The clinical features
include red to brown papules or plaques with or without scaling or
erosions. The lesions are typically symmetric and involve sun-exposed
areas such as the face, neck, and upper extremities. The diagnosis is
based on biopsy and histological examination
13. List a number of important drugs and materials that can elicit a lichenoid reaction.
● Blood pressure medications: ACE inhibitors and beta-blockers
● Nonsteroidal anti-inflammatory drugs (NSAIDs)
● Antibiotics: tetracycline, sulfonamides, penicillin, ampicillin, erythromycin,
ciprofloxacin, and others
● Antimalarials: hydroxychloroquine and chloroquine
● Anticonvulsants: phenytoin, carbamazepine, and lamotrigine
● Gold injections used to treat rheumatoid arthritis
● Dental materials: amalgam fillings, dental composites, and dental cement
● Topical agents: neomycin and bacitracin
● Metal implants: titanium, nickel, and cobalt
● Vaccines: hepatitis B, influenza, and tetanus toxoid
● Plant extracts: Ginkgo biloba and St. John’s wort
14. Explain the putative relationship between lichen planus and oral cancer and
recognise possible/suspicious risk signs for developing oral cancer.
● Lichen planus (LP) is a chronic inflammatory disease that can affect various
mucosal surfaces of the body, including the mouth, and can lead to oral lichen
planus (OLP) [1]. OLP is considered to be a potentially malignant disorder, and
studies have shown a link between OLP and the development of oral cancer [2].
However, the estimated risk of malignant transformation is controversial, with
some studies indicating a low risk of about 1% [3].
● Certain risk signs have been identified that may suggest the possibility of
malignant transformation in OLP. These include persistent ulcerations, erosions
or blisters, rough, thick or hardened areas, leukoplakia (white patches),
erythroplakia (red patches), and non-healing areas or nodules [1]. It is important
to note that the presence of these risk signs does not necessarily indicate
malignant transformation, but they should be closely monitored and evaluated by
a dental professional
15. Describe the nature of discoid lupus erythematosus and distinguish this lesion
clinically from lichen planus
● Discoid lupus erythematosus (DLE) is a chronic autoimmune disorder that
primarily affects the skin, but may also involve other organs in the body. DLE is
characterized by scaly, coin-shaped plaques that are usually red, but can also
appear brown or purple. These plaques tend to be well-defined and can be raised
 or flat. The lesions are typically found on the face, scalp, ears, and neck, but can
also appear on other parts of the body that are exposed to the sun.
● One key distinguishing feature of DLE lesions is that they often cause scarring
and pigment changes, especially in areas of the skin that have been repeatedly
affected. In contrast, lichen planus lesions do not typically cause scarring or
pigment changes. DLE lesions can also be distinguished from lichen planus by
their tendency to occur in sun-exposed areas of the skin, while lichen planus
lesions tend to be found on the trunk, limbs, and mucous membranes.
● Another clinical feature that can help differentiate DLE from lichen planus is the
presence of follicular plugging or scale within the plaques of DLE, which is not
typically seen in lichen planus. In addition, DLE may be associated with other
symptoms such as hair loss, nail changes, and oral ulcers, which are not
commonly seen in lichen planus.
● Overall, while both DLE and lichen planus are skin conditions that can cause
scaly, raised plaques on the skin, there are several key clinical features that can
help distinguish the two conditions. If you have concerns about a skin lesion, it is
important to consult with a healthcare professional for an accurate diagnosis and
appropriate treatment.
16. List the main histological differences of discoid lupus erythematosus from lichen
planus.
● Discoid lupus erythematosus (DLE) and lichen planus (LP) are two
dermatological conditions that can share some clinical and histological features.
However, there are several key differences between the two.
● Histologically, DLE is characterized by a predominantly lymphocytic infiltration in
the upper dermis and a perivascular and periadnexal distribution of the
inflammation, often with some degree of follicular plugging. [1] In contrast, LP
typically shows a band-like infiltrate in the upper dermis, sometimes with
"saw-tooth" rete ridges at the interface between the epidermis and dermis, and
the presence of Civatte bodies (dyskeratotic keratinocytes) in the epidermis. [1]
● Moreover, DLE usually affects sun-exposed areas such as the face, scalp, ears,
and neck, while LP can occur anywhere on the body, including mucous
membranes. [2] Additionally, DLE can lead to permanent scarring and
dyspigmentation if left untreated, and there is a rare but increased risk of
squamous cell carcinoma developing within longstanding DLE lesions

17. Formulate a differential diagnosis of oral lichen planus and conditions which
mimic it clinically.
● The differential diagnosis of OLP includes several conditions that may mimic it
clinically.
○ Pemphigus vulgaris
○ Lupus erythematosus
○ Chronic graft-versus-host disease
○ Candidiasis
○ Geographic tongue
 ○ Leukoplakia
○ Lichenoid drug eruption
○ Mucous membrane pemphigoid
18. Describe the nature of chronic ulcerative stomatitis; explain why it is different
from other forms of stomatitis and how it is diagnosed.
● Chronic ulcerative stomatitis is a rare autoimmune disease that causes painful
ulcers in the mouth [1]. It is characterized by recurrent oral mucosal ulceration,
and it has been primarily reported in older females [3]. Unlike other autoimmune
diseases that cause mouth blisters and ulcers, chronic ulcerative stomatitis does
not respond well to corticosteroids [1].
● The diagnosis of chronic ulcerative stomatitis is typically made clinically, based
on the appearance of the ulcers and the patient's history. Biopsy may also be
performed to confirm the diagnosis [1]. The ulcers may be seen on the lips,
buccal mucosa, tongue, and palate, and they tend to be painful, irregularly
shaped, and have elevated borders [3]. Chronic ulcerative stomatitis is
differentiated from other forms of stomatitis based on its unique clinical features,
as well as its lack of response to corticosteroids
19. Describe the clinical features and course of disease of pemphigus vulgaris.
● It is an autoimmune condition in which the body produces antibodies that attack
proteins in the skin and mucous membranes [1]. The blisters can occur anywhere
on the skin but are most commonly found in the mouth, throat, and genital area
[3]. The blisters can be painful, and when they break open, they leave open sores
that can become infected. The disease can progress rapidly and can be fatal if
left untreated [1]. Treatment typically involves immunosuppressive medications to
reduce the body's autoimmune response and prevent further damage to the skin
and mucous membranes [1]. With treatment, the disease can be managed, and
remission is possible, but it may take months to years to achieve [3]. Regular
follow-up with a dermatologist or other specialist is important to monitor disease
activity and adjust treatment as necessary.
20. Explain the pathogenesis of pemphigus vulgaris and how it is diagnosed
histologically
● Pemphigus vulgaris is an autoimmune disorder that causes blisters on the skin
and mucous membranes throughout the body, affecting the mouth, nose, throat,
eyes, and genitals [1]. Pemphigus vulgaris is caused by IgG autoantibodies that
bind to a protein called desmoglein 3 (dsg3) that is found in the desmosomes in
the keratinocytes near the bottom of the epidermis [3]. The binding of these
autoantibodies causes a loss of cell-to-cell adhesion and, as a result, the
formation of blisters in the skin and mucous membranes [1].
● Histologically, pemphigus vulgaris can be diagnosed through a biopsy of the
affected area. The biopsy specimen will show acantholysis, which is the
separation of epidermal cells from each other due to the breakdown of cell-to-cell
adhesion [3]. Direct immunofluorescence can also be used to identify the IgG
antibodies bound to the desmoglein 3 protein in the epidermis
21. Describe the immunofluorescence diagnostic methodology for pemphigus
vulgaris and compare this with the diagnostics for mucous membrane
pemphigoid.
● Pemphigus vulgaris is diagnosed through skin biopsy with direct and indirect
immunofluorescence and enzyme-linked immunosorbent assay (ELISA) testing
[1]. Direct immunofluorescence uses a fluorescent dye to detect antibodies on
the skin biopsy specimen, while indirect immunofluorescence measures
circulating antibodies in the blood [1]. ELISA testing can detect circulating
antibodies in the blood as well, and can be used to monitor disease activity and
response to treatment [1].
● Mucous membrane pemphigoid, on the other hand, is diagnosed through a
combination of clinical features, biopsy, and immunofluorescence testing [2].
Direct immunofluorescence testing is performed on a biopsy specimen to detect
the deposition of IgG and/or C3 at the basement membrane zone [2]. Indirect
immunofluorescence testing can also be used to detect circulating autoantibodies
against various basement membrane zone antigens [2]. However, mucous
membrane pemphigoid can have a more diverse set of clinical presentations,
which can make diagnosis more challenging than pemphigus vulgaris

22. Mention the other variants of pemphigus vulgaris.

● The other main subtypes of pemphigus are:
○ Pemphigus foliaceus and allied disorders
○ Pemphigus erythematosus (an overlap of pemphigus foliaceus and lupus
erythematosus)
○ Pemphigus herpetiformis
○ IgA pemphigus
○ Pemphigus vegetans
○ Paraneoplastic pemphigus
23. Describe the typical features and clinical course of benign mucous membrane
pemphigoid.
● Benign mucous membrane pemphigoid, also known as cicatricial pemphigoid, is
an autoimmune disease that affects the mucous membranes of the body,
particularly the oral mucosa and conjunctiva [2, 3]. The condition is characterized
by blistering lesions on the mucous membranes that can be erosive and cause
scarring over time. It is a rare condition, and the exact cause is not well
understood.
● The clinical course of benign mucous membrane pemphigoid is usually chronic,
with periods of remission and relapse. The disease typically progresses slowly
and affects both sexes equally, with an average age of onset in the sixth to
seventh decade of life. The lesions may first appear as small blisters or erosions,
which can become larger and more extensive over time, leading to scarring and
tissue damage. In severe cases, the disease can cause vision loss, difficulty
swallowing, or breathing problems if the mucous membranes in the respiratory
tract are involved
 ● The treatment of benign mucous membrane pemphigoid typically involves the
use of immunosuppressive medications to reduce the activity of the immune
system and prevent further damage to the mucous membranes. Treatment may
also involve the use of topical or systemic steroids, as well as other
anti-inflammatory medications, depending on the severity of the disease and the
extent of mucous membrane involvement. Patients with benign mucous
membrane pemphigoid require close monitoring and long-term follow-up care
due to the chronic nature of the condition and the risk of complications
24. Describe the pathology and immunofluorescence diagnostic methodology for
benign mucous membrane pemphigoid and compare with pemphigus vulgaris.
● Mucous membrane pemphigoid (MMP) is an autoimmune subepithelial blistering
disease with predominant involvement of mucosal surfaces. The disease affects
various mucosal surfaces of the body including the mouth, eyes, nose,
nasopharynx, hypopharynx, larynx, esophagus, genitals, and/or anus [1] [2]. The
diagnosis of MMP is usually made by direct immunofluorescence microscopy of
frozen biopsies. This demonstrates linear deposits of complement, IgG or IgA
along the basement membrane
● In contrast to MMP, Pemphigus vulgaris (PV) is an autoimmune disease
characterized by intraepithelial blister formation on the skin and mucous
membranes. It is diagnosed by direct immunofluorescence microscopy of
perilesional skin, which shows a characteristic "fishnet" pattern of intercellular
IgG deposition between keratinocytes
25. Explain the nature of desquamative gingivitis and list the clinical differential
diagnosis.
● Desquamative gingivitis (DG) is a clinical condition characterized by the presence
of erythema, ulceration, erosion, blistering, or desquamation of the attached and
marginal gingivae [3]. Patients with DG may complain of mucosal sloughing,
gingival bleeding, and oral discomfort, especially when consuming foods or
beverages that may be acidic or spicy [1]. The differential diagnosis for DG is
broad and includes various conditions such as chemical and electrical burns,
allergic reactions, hormonal disorders, and mucocutaneous diseases [2].
Additionally, the use of mouthwashes, chewing gums, cosmetic products, or
drugs can also cause similar clinical patterns [2]. Therefore, it is important to
perform a thorough evaluation of the patient's medical and dental history, as well
as a comprehensive oral examination, to establish an accurate diagnosis and
appropriate treatment plan
26. Describe the typical clinical features of erythema multiforme and the course of the
disease.
● Erythema multiforme (EM) is a self-limited, immune-mediated mucocutaneous
condition [1]. The condition is characterized by the development of "target"
lesions on the skin, which are often accompanied by erosions or bullae involving
the oral, genital, and/or ocular mucosae [2]. The lesions are round, raised, and
red with a central blister or crust, giving them the appearance of a target [3]. The
lesions are typically symmetrical and are distributed on the extremities and trunk
 [1]. The mucosal involvement of EM can range from mild redness and ulceration
to severe mucositis with extensive blistering and sloughing of the affected tissue,
which can make eating and drinking very painful and difficult [3]. The disease
course can be acute, recurrent, or persistent [1]. The self-limited form of EM is
usually mild and resolves within 2-6 weeks without any specific treatment [3].
However, the severe form of the disease, known as EM major, can be
life-threatening due to extensive mucosal involvement, and requires prompt
management [2]. Recurrent episodes of EM may occur in some patients, and a
thorough evaluation for possible underlying causes may be necessary
27. Identify the aetiological agents of erythema multiforme.
● Erythema multiforme is a condition that can have various triggers, including
infections, medications, and other factors. According to a study, infections are
associated with 90% of cases of erythema multiforme [1]. Among the most
commonly identified infectious agents are herpes simplex virus (HSV) type 1 [1].
● In addition to infections, some medications may trigger erythema multiforme.
Antibiotics such as erythromycin, nitrofurantoin, penicillins, sulfonamides, and
tetracyclines, anti-epileptics, and non-steroidal anti-inflammatory drugs have
been implicated in some cases of erythema multiforme [3]. Vaccinations are also
known to cause erythema multiforme in infants
28. Identify/recognise the histological features of erythema multiforme.
● Erythema multiforme (EM) is a type of skin condition that can be recognized by
its characteristic target-like skin lesions. [3] A skin biopsy of erythema multiforme
may show several histological features. These include apoptotic individual
keratinocytes (cellular self-destruction), hydropic degeneration of basal
keratinocytes (swollen degenerating cells at the base of the epidermis), and
intercellular oedema (spongiosis). [1] The underlying cause of EM is believed to
be a cell-mediated immune response, and infections are associated with 90% of
cases
29. Describe the relationship and the clinical differences between erythema
multiforme and herpetic stomatitis
● Erythema multiforme (EM) and herpetic stomatitis are two different conditions
with distinct clinical features. EM is an acute, immune-mediated condition that is
characterized by the appearance of distinctive target-like lesions on the skin,
often accompanied by erosions or bullae involving the oral, genital, and/or ocular
mucosae. [1] On the other hand, herpetic stomatitis is a viral infection caused by
the herpes simplex virus (HSV) that causes painful blisters and sores on the lips,
mouth, tongue, and gums. [2]
● One of the major differences between the two conditions is their causative
agents. EM is caused by a cell-mediated immune response, and infections are
associated with 90% of cases. Although HSV type 1 is the most commonly
identified infectious agent, other infections such as Mycoplasma pneumoniae,
cytomegalovirus, and other herpesviruses have also been implicated in EM. [1] In
contrast, herpetic stomatitis is caused by the herpes simplex virus, and the
infection is highly contagious
 ● Additionally, the clinical presentations of the two conditions differ. EM lesions are
typically symmetric, and their characteristic appearance is of concentric rings with
alternating areas of normal and erythematous skin, creating a "target" or "iris"
pattern. The lesions may be raised or flat and can occur on the limbs, trunk,
palms, and soles. Oral, genital, and ocular mucosae may also be involved,
causing pain, swelling, and irritation. [1] In contrast, herpetic stomatitis usually
presents with clusters of small, painful, fluid-filled blisters that break open and
form sores. These sores can occur on the lips, mouth, tongue, and gums and
may be accompanied by fever and swollen lymph nodes
30. Explain the relationship and differences between allergic stomatitis and dermatitis
● Allergic stomatitis and dermatitis are both conditions that involve inflammation,
but they affect different areas of the body. Allergic stomatitis, also known as
contact stomatitis, is a type of delayed hypersensitivity reaction that occurs when
an allergen comes into contact with the lining of the mouth. This can cause
redness, swelling, and sores in the mouth, as well as itching and burning
sensations [3]. Allergic dermatitis, on the other hand, is a type of skin
inflammation that occurs when the skin comes into contact with an allergen or
irritant. It can cause redness, itching, and sometimes blistering or cracking of the
skin [2].
● The underlying causes of allergic stomatitis and dermatitis are also different.
Allergic stomatitis is caused by exposure to an allergen in the mouth, such as
certain foods, dental materials, or medications, whereas allergic dermatitis is
caused by exposure to an allergen or irritant on the skin, such as soaps,
detergents, or metals
31. Explain the nature of the traumatic eosinophilic ulcer, its clinical appearance and
course of the disease.
● Traumatic eosinophilic ulcer (TEU), also known as traumatic ulcerative
granuloma with stromal eosinophilia (TUGSE), is a benign and self-limiting lesion
that typically occurs on the tongue but can also affect other oral mucosal sites [3].
The most common presentation of TEU is an asymptomatic or mildly tender,
solitary, non-healing ulcer that varies in size from a few millimeters to several
centimeters [1]. It typically appears as an elevated, erythematous lesion with a
white or yellow fibrinous center surrounded by a red halo, which may resemble a
malignancy, such as squamous cell carcinoma, or a viral infection, such as
herpes simplex virus [1][2]. However, the lesion is not infectious or malignant and
usually resolves spontaneously within a few weeks to a few months, without
treatment
● TEU is considered a reactive lesion caused by an inflammatory response to local
trauma or irritation, such as accidental biting, sharp edges of teeth or
restorations, and dental procedures [1][2]. Histologically, TEU is characterized by
a mixed inflammatory infiltrate, including numerous eosinophils, histiocytes,
lymphocytes, and plasma cells, which invade the adjacent stroma and create a
pseudo-invasive appearance [2]. The diagnosis of TEU is primarily based on the
clinical features and histopathological findings [2]. However, it is important to
 differentiate TEU from other benign or malignant lesions, such as squamous cell
carcinoma, Kaposi sarcoma, or lymphoma, which may have a similar appearance
and require additional tests or biopsies [1]. Overall, TEU is a common and benign
lesion that may mimic other more serious conditions, but it typically resolves
spontaneously without treatment
32. Describe the nature of factitious ulceration/lesions.
● Factitious ulceration or lesions are skin injuries that are intentionally self-inflicted
by the patient, often due to a psychological disorder such as Munchausen
syndrome or factitious disorder imposed on self (FDIS) [1]. These lesions can
vary in appearance and may not resemble any known dermatitis [1]. Factitious
ulceration/lesions are often located on areas that are easily accessible to the
patient and can be bilateral and symmetrical or primarily within reach of the
dominant hand. The face and breasts are common locations for these lesions [1].
Diagnosis of factitious ulceration/lesions can be difficult as patients may deny
active participation and are often unwilling to admit to self-harm [2]. A thorough
examination and accurate description of the lesion is necessary for proper
diagnosis and management [3]. Treatment of factitious ulceration/lesions may
require a multidisciplinary approach including psychological evaluation and
management
33. Workout the differential diagnosis of recurrent ulcers and persistent ulcers.
● Recurrent ulcers:
○ Recurrent aphthous stomatitis (RAS)
○ Behçet syndrome
○ Cyclic neutropenia
○ Intraoral herpes infections
○ Immunobullous disorders (such as pemphigus vulgaris and bullous
pemphigoid)
○ Inflammatory bowel disease (such as Crohn's disease and ulcerative
colitis)
○ HIV infection
○ Certain medications (such as nonsteroidal anti-inflammatory drugs,
beta-blockers, and chemotherapeutic agents) [2]
● Persistent ulcers:
○ Arterial insufficiency
○ Venous hypertension
○ Peripheral neuropathy
○ Vasculitis
○ Pyoderma gangrenosum
○ Infection
○ Malignancy
○ Autoimmune disorders (such as lupus and rheumatoid arthritis)
○ Certain medications (such as bisphosphonates and nonsteroidal
anti-inflammatory drugs)