Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Sexually transmitted diseases

Definition:

Sexually transmitted diseases are a group of infectious diseases in which the

principle method of infection is sexual contact.

Syphilis
• Causative organism: A spirochaete known as Treponema pallidum
(T.P.).
• Incubation period: 2-4 weeks and may be up to 90 days.
• Mode of transmission: Mainly by direct contact with infectious lesions.
1. Sexual contact is the most common method o infection.
2. Accidental contact e.g. medical personnel.
3. Needle pricks and blood transfusion.
4. Transplacental infection from infected mother to her baby.
5. Indirect contact e.g. from WC is rare.
• Classification:
A) Acquired syphilis.
B) Congenital syphilis.

A) Acquired Syphilis

It is further subdivided into 4 stages:

1) Primary syphilis. 2) Secondary syphilis.
3) Latent syphilis. 4) Tertiary syphilis.

1) Primary syphilis

• Clinical features:
- The primary lesion of syphilis is known as chancre.
- It appears at the site of entry of T.P.
- 90% of chancres are seen at or near the genital area.
- 10% of chancres are extra genital and have been described on almost every
part of the body e.g. on the lips, tongue, tonsils, breast, fingers ….etc
- Typical chancre is: solitary, painless, indurated, well-defined, circular or oval
and exudes clear serum.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

- Regional lymph nodes become enlarged one week after appearance of chancre.
They are discreet, firm to rubbery in consistency, neither painful nor tender and
freely mobile.

• Natural course of primary syphilis:

- Even without treatment, chancre undergoes spontaneous healing within 2-4
weeks leaving a thin scar.
- 75% of patients enter phase of latency i.e. complete freedom from symptoms
and signs in the presence of +ve serological tests. It lasts from 2 weeks to 6
months.
- 25% of patients develop manifestations of secondary syphilis while the
chancre is still present.

2) Secondary syphilis
- The lesions appear 1-6 months after the appearance of the primary lesion.
- Any organ of the body can be affected, although skin and mucous membranes
are mainly affected.

• Clinical manifestations of 2ry syphilis:

1. Skin lesions. 2. Mucous membrane lesions.
3. Lymphadenopathy. 4. Alopecia.
5. Generalized constitutional symptoms e.g. fever, headache, malaise, anorexia
weight loss.

1- Skin lesions.
- The lesions may be macular, papular or maculopapular. However, the
commonest and most characteristic is the papule.
- Skin rashes appear as generalized, symptom less, rosy macules and papules.
2- Mucous membrane lesions:
- Mucous membrane lesions “Mucous patches”: appear as shallow white
erosions on mucosal surfaces e.g. oral mucosa, palate, pharynx, larynx, vagina
or urethra. After sometime, the mucous patches show confluence giving “Snail-
track ulcers”.

• Natural course of secondary syphilis:

- It may consist of a single episode lasting for several weeks or a series of
recurrent episodes. In untreated cases, secondary manifestations cease to occur
2-3 years after infection.

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3)Tertiary Syphilis

• Clinical manifestations of tertiary syphilis include:

1- Benign late syphilis: Gumma.
2- Cardiovascular syphilis.
3- Neurosyphilis.

1. Benign Late Syphilis “Gumma”

- It affects mainly: skin, mucous membranes, subcutaneous tissue & submucosal
tissue. It may also affect: muscles, bones and sometimes internal organs.
I- Skin lesions
- The lesions are: firm, painless with a characteristic arciform or serpiginous
outline. Healing occurs with thin, atrophic, tissue-paper like scar.
II. Mucosal lesions of the mouth, nose & throat
- Gumma may originate in the submucosa of the palate, pharynx, larynx or nasal
septum. It begins as painless swelling that may breakdown to give an ulcer with
a characteristic punched-out appearance. Perforation of the palate, destruction of
the uvula, laryngeal stenosis and nasal deformity may occur.
- The tongue may be involved with deep interstitial glossitis causing
“macroglossia” and latter on “deep fissured tongue”. Leukoplakia may occur
especially on the tongue, inner aspect of cheeks and lips. 50% of these lesions
undergo malignant change.

2- Cardiovascular syphilis:
It is the result of endarteritis obliterans of the vasa vasorum supplying the major
vessels e.g. aorta and coronary arteries. Damage to the wall of these vessels
results in: Aortitis, aortic aneurysm, aortic incompetence and angina pectoris.

3- Neurosyphilis:
- It is the result of inflammation of meninges and endarteritis obliterans of the
vasa vasorum supplying blood vessels of the brain and/or spinal cord.
- Clinical presentations include:
1- Syphilitic meningitis: Localized or diffuse.
2- Tabes dorsalis: Due to damage of the dorsal nerve roots.
3- General paralysis of the insane: Due to degeneration of the brain itself.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

B) Congenital Syphilis
• Mode of infection: Transplacental.
• Clinical manifestations: are similar to the 2ry stage of syphilis in adults.

1) General symptoms & signs:

- Failure to thrive.
- Thrombocytopenia, bleeding and anaemia (due to affection of blood forming
organs).
- Pneumonia or gastroentritis.

2) Skin lesions:
- Generalized macular or maculopapular rash.
- Bullous lesions may occur.
- Condylomata lata may be seen.
- Skin lesions have a predilection for certain areas: face, around mouth, napkin
area, the palms and soles.

3) Mucous membrane lesions:

- Rhinitis and nasal snuffles are common.
- Destructive changes of nasal supportive structures causing perforation of the
nasal septum and depression of the nasal bridge “Saddle-shaped nose”.
- Mucous patches may occur in the pharynx and larynx causing hoarse cry.
4) Bone lesions:
- Epiphysitis is common ulna and radius.
- Bilateral osteomyelitis of the inner aspect of the tibia is pathognomonic.

(5) Other organs:

- There may be generalized lymphadenopathy, hepatospleno-megally,
meningitis, choroidoretinitis or nephrotic syndrome.

Stigmata of congenital syphilis

These are the residual manifestations of congenital syphilis throughout life.
They include:
1) Dental changes.
2) Other stigmata.

1) Dental changes: Due to invasion of the tooth germ with T.P. causing
endarteritis. These changes include:
a) Hutchinson’s teeth: Affect central incisors, which become notched
and the cutting edge is narrower than the gingival edge.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

b) Moon’s molar: Affect molar teeth where the 4 cusps tend to be

packed together in the center instead of being at the corners.

2) Other stigmata:.
- Interstitial keratitis. - Perforation of the hard palate
- Saddle nose. - 8th nerve deafness
- Rhagades: Linear lesions around the mouth and anus.
- Sabre tibia.

Diagnosis of Syphilis
1. History and clinical examination.
2. Demonstration of T. pallidum by dark-ground microscopy “DG
test”.
3. Serological tests of syphilis.

Dark-ground microscopy “DG test”: It is positive mainly in samples collected

from:
- Chancre. - Regional L. N. “Gland puncture”.
- Mucous patches of 2ry syphilis. - Condylomata lata

Serological Tests of Syphilis “STS”

- When T.P. invades human tissue, a complex antibody response is stimulated.
The various STS detect one or more of these antibodies using treponemal
antigens. STS may be classified according to the type of antigen used into:
I- Non-treponemal antigen tests “Non-specific STS”: They include:
1) Complement fixation tests e.g. Wasserman reaction.
2) Follocculation tests: e.g. VDRL and RPR.
The VDRL and RPR tests, although not specific for syphilitic antibodies, are
economical and simple to perform. Thus they are used as screening tests.
Moreover, they can be quantitated and thus the titer can give a measure of the
progress of a treated case. The tests usually become +ve about 2-4 weeks after
appearance of chancre.
II- Treponemal antigen tests “Specific STS”:
Treponemal tests utilize T.P. as antigen. Consequently, they are more specific
than the "Non-specific STS" and are generally used as confirmatory tests. They
include:
1- Treponema pallidum immobilization (TPI) tests.
2- Fluorescent treponemal antibody absorption (FTA-ABS) test.
3- Treponema pallidum haemagglutination (TPHA) tests.
4- Reiter protein complement fixation test (RPCFT).

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Treatment of Syphilis

• Penicillin, being the cheapest and most effective is the drug of choice.
• The serum level of penicillin required for treatment of syphilis is low but
needed to be maintained for a long period, hence long-acting penicillins
are used.

• The ones available are:

1) Procaine penicillin: Single injection is effective for 24 hs.

1) Benzathine penicillin G: Single injection is effective for 2 weeks.

Stage of S. Benzathine penicillin G Procaine penicillin G

(1) Early S. 2.4 million units I.M. 600,000 units I.M. daily
single dose for 10 days
(2) Late latent & benign 2.4 million units I.M. 600,000 units I.M. daily
late S. once a week for 3 weeks for 15 days
(3) Cardiovascular S. ---------------- 600,000 units I.M. daily
for 20 days
(4) Neurosyphilis ----------------- 600,000 units I.M. daily
for 20 days

For those allergic to penicillin, one of the following regimens may be used:
1) Tetracycline HCl: 500mg/6hs for 15 days (Early syphilis) or 30 days (Late
syphilis)
2) Doxycycline: 100mg/8hs (Early syphilis) or 21 days (Late syphilis)
3) Erythromycin: 500mg/6hs for 15 days (Early syphilis) or 30 days (Late
syphilis)

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Acquired Immunodeficiency Syndrome "AIDS"

Aetiology:
• Human immunodeficiency virus (HIV).
• Two types are known: HIV-1 and HIV-2.
• Both are retroviruses belonging to lentivirus subfamily.

Epidemiology:‫معدالت اإلنتشار‬
• HIV infection is a world wide epidemic.
• Tens of millions are infected with HIV and the number of AIDS cases is
increasing dramatically.
• Patients are commonly young but any age from intra-uterine to
senescence may be affected.

Established modes of transmission: ‫طرق العدوى‬

1. Sexual intercourse: ‫ اإلتصال الجنسي‬Vaginal or anal
2. Contaminated blood and blood products: ‫نقل الدم الملوث بالفيروس‬
3. Contaminated needles and syringes: a‫اإلبر والمحاقن الملوثة بالفيروس‬
4. Mother to child: ‫ من األم للطفل‬In-utero, during birth or milk
5. Organ or tissue donation: ‫نقل األعضاء و األنسجة‬
However, the virus is minimally infectious and casual contact is insufficient for
transfer.

Pathogenesis:
• The cellular receptor for HIV is the CD4 molecule.
• Many cells within the immune system bear this molecule specially
CD4+ve T -helper cells (T-4 cells), which are most affected.
• The T-helper cells perform a regulatory role in immune response and are
responsible for stimulating the production of antibodies and the
maturation of several types of cells of the immune system.
• The overall effect of HIV infection on the immune system is gradual
depletion of T-helper cells.
• Consequently, depletion of T-helper cells results in immune deficiency.
• N.B.: The number of CD4+ve T-helper cells in normal adults is 1000/µL

Clinical picture of HIV infection

I. Primary HIV infection. II. Asymptomatic carrier.
III. AIDS-related complex “ARC”. IV. Symptomatic HIV infection “AIDS”.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

I. Primary HIV infection “Acute retroviral syndrome”:

• It appears after an incubation period of 3-6 weeks.
• Fever, myalgia, arthralgia, urticaria, meningitis, oral & esophageal ulcers.
• It lasts 1-3 weeks.

II. Asymptomatic carrier stage “Latent period”:

• It is characterized by freedom from symptoms and signs but the patient is
infectious and serological tests are positive.
• It lasts 3- 10 years after infection.

III. AIDS-related complex “ARC”:

• It refers to the period between “Latent period” and development of
“AIDS”.
• ARC is diagnosed: If any of the following persist for 3 months
1. Weight loss more than 10% ‫نقص الوزن‬
2. Fever more than 38 Cº ‫إرتفاع درجة الحرارة‬
3. Diarrhea ‫إسهال مزمن‬
4. Persistent generalized lymphadenopathy ‫تضخم الغدد الليمفاوية‬
5. Profound malaise ‫إعياء مزمن‬
6. Multidermatomal herpes zoster ‫حزام نارى منتشر‬
7. Oropharyngeal candidiasis ‫فطريات الفم والبلعوم‬
8. Oral hairy leukoplakia.
9. CD4+ve T-helper cells <500/µL but >200 /µL

Oral hairy leukoplakia:

• Firm, white, asymptomatic proliferation on the tongue that cannot be
peeled off.
• It is caused mainly by Epstein-Barr virus with secondary involvement of
Human Papilloma Virus and candida.
• It is rarely seen in patients with renal transplantation and congenital
immunodeficiency.
• It can be treated by zidovudine or acyclovir.

IV. Symptomatic HIV infection “AIDS”

• This is the final and uniformly fatal end stage of HIV infection.
• It is characterized by:

1. Constitutional symptoms: General lassitude, weight loss, night sweats &

diarrhea.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

2. Neurological disease: Sensory polyneuropathy, progressive myelopthy,

intellectual and cognitive impairment.

3. AIDS-defining conditions. These can be used as indicators for AIDS

providing other causes of immunodeficiency are excluded:
• CD 4+ve T-helper cells below 200/µL
• Candidiasis (oropharyngeal, trachea, bronchi).
• Kaposi sarcoma and lymphoma.
• Disseminated or extrapulmonary coccidiodomycosis.
• Extrapulmonary cryptococcosis.
• Disseminated or extrapulmonary histoplasmosis.
• Disseminated or extrapulmonary M. avium complex.
• Disseminated or extrapulmonary tuberculosis.
• Pneumocystitis carinii pneumonia.
• Toxoplasmosis of the brain.
• Recurrent salmonella infections
• Chronic cryptosporodiosis with diarrhea.
Death: Due to opportunistic infections.

Diagnosis of HIV infection

1. Clinical history: To detect high risk groups e.g. IV drug addicts,
homosexuals, haemophilics.
2. Detection of IgG antibodies to envelope components (gp120): Using
ELISA & Western blots assays.
3. Detection of p24 antigen.
4. Detection of antibodies to p24 antigens.
5. Isolation of HIV virus in cultured T lymphocytes.

Prevention and treatment of HIV infection

1) Prevention of HIV infection “AIDS” ‫الوقاية خير من العالج‬
1. Testing of blood & blood products.
2. Using sterile needles & disposable syringes.
3. Limiting the number of sexual partners.
4. Using condoms and practicing safe sex.
2) Treatment of HIV infection “AIDS”
Anti-retroviral drugs:
The FDA-approved anti-retroviral drugs fall into two main groups:
I. Reverse transcriptase inhibitors:

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

a) Neocleoside analogues: Zidovudine, didanosine, zalcitabine, stavudine

and lamivudine
b) Non-nucleoside analogues: Nevirapine and delavirdine.
II. Protease inhibitors: Saquinavir, ritonavir and nelfinavir.

Yeast Infections
"Candidiasis, Candidosis, Moniliasis"

 Causative organism: Candida albicans is the most common cause (80%

of cases).

 Epidemiology: All ages and both sexes can be affected.

 Mode of infection: - Autoinfection - Direct contact.

 Predisposing factors:
- Lack of local bacterial flora.
- Local tissue damage e.g. ill-fitted denture.
- Low cell mediated immunity.
- Saturated serum transferrin (In infants).
- Pregnancy & Oral Contraception.

 Common Clinical types:

1. Oral candidiasis: Oral thrush, hypertrophic type, atrophic type, cheilosis,
glossitis and black-hairy tongue.
2. Intertriginous: e.g. napkin candidiasis.
3. Interdigital: e.g. in house wives due to prolonged hand emersion in
water.
4. Candidal paronychia: e.g. in house wives due to prolonged hand
emersion in water.
5. Genital: male and female.
6. Congenital cutaneous candidisis.
7. Systemic candidiasis.
8. Chronic mucocutaneous candidiasis.

Oral thrush
• Creamy-white soft plaques on the oral mucosa. Removal of this material
reveals a red base. It may progress to ulceration of the mucosa.
• In adults oral candidiasis may present as red sore mouth.
• The infection may spread to the esophagus and trachea in AIDS patients.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Chronic hyperplastic type (Candidal leukoplakia):

• It is a disease of middle aged adults.
• Firm irregular plaques are seen on the oral mucosa that can not be easily
removed.

Diagnosis of Yeast Infections

1. History & clinical examination.

2. Scrape and 10% KOH smear: Budding yeasts and slender filaments are
seen.
3. Fungal culture: Using Sabouraud’s glucose-peptone agar medium OR
4% malt extract medium. White colonies of Candida albicans are seen.
4. Serum tube test: Candida albicans produces filaments when grown on
serum or 2-3 hours at 37Cº.

Prevention of Yeast Infections

Avoidance of predisposing factors: ‫الوقاية خير من العالج‬e.g.

- Careful mouth hygiene.
- Wearing well-fitted denture.
- Avoid long courses of antibiotics, whenever possible.
- Personal hygiene with drying & increased ventilation of skin.
- Using cotton underwear.

Treatment of Yeast Infections

Mild cases: Topical antifungal agents e.g. Nystatin, miconazle,

clotrimazole, tioconazole…etc.

Extensive cases: Systemic antifungal drugs e.g. Fluconazole,

Ketoconazole, Itraconazole…etc.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Lichen Planus

 Background: Oral lichen planus (OLP) is a chronic inflammatory

disease that causes bilateral white striations, papules, or plaques on
the buccal mucosa, tongue, and gingivae.

 The lichen planus antigen is unknown, in which case lichen planus

would be a true autoimmune disease.

 The role of autoimmunity in the pathogenesis is supported by many

autoimmune features of OLP, including its chronicity, onset in adults,
predilection for females, association with other autoimmune diseases,
occasional tissue-type associations, depressed immune suppressor
activity in patients with OLP, and the presence of autocytotoxic T-cell
clones in lichen planus lesions.

 Internationally: OLP affects approximately 1-2% of the general adult

population, although the prevalence of the disease is unknown in
many areas. OLP is a common noninfectious oral mucosal disorder
among adult patients who are examined at oral pathology and oral
medicine clinics.

Mortality/Morbidity:

 Oral squamous cell carcinoma (SCC) developed in fewer than 5% of

patients with OLP who did not use tobacco

History
 In many patients, the onset of OLP is insidious, and patients are
unaware of their oral condition. In such instances, the referring
medical or dental practitioner identifies the clinical changes in the
oral mucosa.
 Some patients report a roughness of the lining of the mouth,
sensitivity of the oral mucosa to hot or spicy foods or oral hygiene

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

products, painful oral mucosa, sore gums, red or white patches on

the oral mucosa, red gums, or oral ulcerations.
 Approximately two thirds of patients with OLP report oral discomfort,
especially in association with atrophic and erosive lesions.
 Erythematous and erosive lesions are often sensitive or painful.

 Symptoms vary from mucosal sensitivity to continuous

debilitating pain.

 Oral mucosal lichenoid lesions may occur after the administration of

systemic drugs such as nonsteroidal anti-inflammatory drugs
(NSAIDs), sulfonylureas, antimalarials, beta-blockers, and some
angiotensin-converting enzyme (ACE) inhibitors.

 In rare cases, oral mucosal lichenoid lesions occur after a dental

restoration is performed or after the patient starts using a denture;
the lag period varies. Patients with an associated allergy to metals or
components of the appliance should be evaluated by means of patch
testing.

 Up to 44% of patients with OLP develop coincident skin lesions.

Conversely, more that 70% of patients with cutaneous lichen planus
develop coincident OLP.

 Oral mucosal lesions are variable and present as white striations

(Wickham striae), white papules, white plaques, erythema (mucosal
atrophy), erosions (shallow ulcers), or blisters.

 The lesions predominantly affect the buccal mucosa, tongue, and

gingivae, although other oral sites are occasionally involved.
 The lesions are usually bilateral.
 The lesions may appear as a mixture of clinical subtypes. For
example, white streaks and gray streaks may form a linear or
reticular pattern on an erythematous background. Alternatively,
a central area of shallow ulceration (erosion) may have a
yellowish surface (fibrinous exudate) surrounded by an area of
erythema.

 In most patients, telltale white striations or papules are evident

on the buccal mucosa or on the lateral margin of the tongue,
either alone or in combination with other lesions.

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 Gingival lesions commonly appear with a fiery red erythema

that affects the entire width of the attached gingiva, a
condition previously called desquamative gingivitis.
 In patients predisposed to pigmentation, OLP lesions may be
associated with patchy brown melanin deposits in the oral
mucosa (inflammatory melanosis).
Diagnosis:
 Biopsy may be required to exclude malignancy or to differentiate
between OLP and other white or chronic ulcerative oral lesions,
including reactive keratoses, chronic hyperplastic candidosis,
epithelial dysplasia, discoid lupus erythematosus, gastrointestinal
disease (including oral Crohn disease), and anemic states.

 Etiology: Unknown, but the disease may be associated with:

1. Liver disease: e.g. chronic active hepatitis particularly due to hepatitis C.
2. Autoimmune diseases: e.g. Myasthenia gravis, dermatomyositis and
alopecia areata.
3. Ulcerative colitis.

 Clinical picture
The disease may affect skin, hair, nails and oral mucosa:

1. Skin lesion:
- Appear as pruritic, flat-topped, shiny, polygonal papules with a
characteristic violaceous color.
- These occur most commonly on the volar aspect of wrists, back of
hands, lumbar region, glans penis, shins and ankles.

2. Hair:
- Lichen planus may affect scalp hair causing cicatricial alopecia.

3. Nails:
- Thinning and longitudinal ridging may occur.

4. Oral mucosa:
- Oral lesions occur in 40%-60% of cases affecting buccal mucosa, tongue
and lips.
- Lesions consist of milky-white papules with white reticular streaks
arranged in a lace-like pattern.
- Ulcerative lesions may occur particularly in patients with hepatitis C.

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- Carcinoma may develop on top of oral lesion, particularly the ulcerative

type.

 Dermatopathology

The epidermis shows:

- Hyperkeratosis “Thickened horny cell layer”.
- Focal hypergranulosis “Thickened granular cell layer”.
- Irregular acanthosis “Thickening of epidermis”.
- Irregular elongation of rete ridges.
- Degeneration of basal cell layer.

The dermis shows:

- Band like inflammatory infiltrate of lymphocytes that closely
approximates the epidermis.
- Melanophages are seen due to pigment dropping after basal cell damage.

The oral lesions show:

- Parakeratosis and thinning of the epithelium.

 Differential diagnosis

The oral lesions must be differentiated from:

1. Candidiasis.
2. Leukoplakia.
3. Oral lesions of pemphigus.

Treatment of lichen planus:

Skin lesions:
1) Topical treatment: Potent topical corticosteroids are usually required to
treat skin lesions.
2) Systemic treatment: e.g. systemic steroids. This is indicated mainly in
severe or ulcerative cases.

Oral lesions:
1) Topical corticosteroids: e.g. triamicinolone acetonide in orabase may be
helpful in mild cases.
2) Intra-lesional injection: of corticosteroids is helpful in some cases.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

3) Systemic steroids: These are indicated in severe ulcerative cases. High

dose of oral steroid is usually required.
4) Oral retinoids: are also helpful in erosive oral lichen planus.
5) Surgical excision: of resistant oral lesions has been recommended to
guard against squamous cell carcinoma.

Pemphigus Vulgaris "P.V."

 Definition:
It is a severe, life-threatening, autoimmune, intraepidermal blistering disease
affecting skin and mucous membranes and is characterized by acantholysis of
epidermal cells.

 Epidemiology:
- It is a disease of adults (40-60years).
- Both sexes are equally affected.

 Etiology
- It is an autoimmune disease.
- Circulating IgG autoantibodies bind to intercellular adhesion molecules
(Desmogleins) between epidermal cells of skin and oral mucosa causing
loss of cellular adhesion (Acantholysis) resulting in blister formation.

 Clinical features
- P.V. affects skin and oral mucosa.
- The disease starts in the oral mucosa in 50%-70% of cases 6-12 months
before the appearance of skin lesions.
- More than 90% of patients will develop oral lesions at some time during
the course of the disease.

Skin lesions:
- Generalized flaccid bullae are seen that rupture easily leaving crusted
erosions.
- The erosions heal slowly leaving hyperpigmentation.

Oral lesions:
- Bullae occur anywhere in the oral cavity.
- They rupture easily and thus intact bullae are rarely seen.
- Patients usually present with persistent large painful erosions and ulcers
that heal slowly.

 Dermatopathology

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

- The major histologic feature is suprabasal acantholysis “Separation of

keratinocytes”.

 Diagnosis

1. Biopsy: From small bullae or erosions.

2. Tzanck smear: Swab from the base of erosions or freshly opened blisters
shows acantholytic cells.
3. Direct immunofluorescence: of perilesional skin shows intercellular
deposits of IgG and/or C3.
4. Indirect immunofluorescence: Circulating IgG autoantibodies against
desmoglein 3 are detected in 80%-90% of cases.

 Differential Diagnosis

Oral lesions must be differentiated from:

- Erosive lichen planus.
- Behcet’s disease.
- Oral lesions of Stevens-Johnson syndrome.

Treatment of Pemphigus Vulgaris

1) Patients with oral lesions only: Intralesional injection of triamicinolone

acetonide 10-20mg/ml can be helpful.

2) Patients with generalized disease:

- Patient must be hospitalized.
- Systemic corticosteroids are given orally in a dose of 1-3mg/kg body
weight/day (Usually 120-240mg/day) until cessation of new blister
formation. This is followed by gradual withdrawal of corticosteroids to
the minimally effective dose.
- Correction of water and electrolyte imbalance and prevention of
secondary infection are important.

 Course and prognosis

The mortality rate is 5% and it is mainly due to:
- Steroid-induced complications.
- Sepsis.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Herpes simplex infection

 Causative organism: Herpes simplex virus (HSV).

 There 2 types of the virus:

a) HSV-1: Usually associated with facial and oral infections.

b) HSV-2: Usually associated with genital infections.

However, there is a considerable overlap.

 Mode of transmission:

1- Direct contact with contagious secretions.

2- Droplet infection.

The virus can shed in saliva and genital secretions for days or weeks after a
single attack of the disease.

 Incubation period: 2-20 days

 Pathogenesis:

1. Viral entry: Through susceptible mucosa or breaks in the skin.

2. Viral spread & establishment of latency: Virus ascends through the
peripheral sensory nerves to the sensory or autonomic nerve root ganglia where
latency is established.
3. Recurrent attacks: Occur as a result of virus activation in the ganglia with
subsequent virus spread down the sensory nerves to reach skin and mucous
membranes.

Precipitating factors for recurrent attacks:

1. Exposure for UV radiation e.g. excessive sun exposure.
2. Febrile illness.
3. Common cold.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

4. Minor trauma.
5. GIT disturbances.
6. Psychological stress.
7. Premenstrual.
 Clinical picture

I-Primary herpes simplex:

- Occurs when the virus enters the body for the first time.
- 90% of cases with primary infection are subclinical (asymptomatic).
- Symptomatic primary infection is often associated with fever and regional
lymphadenopathy.

II-Recurrent herpes simplex:

- It usually results from activation of the latent virus.
- A prodrome of tingling, itching or burning sensation usually precedes the
appearance of lesions by 24 hours.
- Fever and regional lymphadenopathy are usually absent.

Clinical Types
1. Herpes labialis.
2. Herpetic gengivostomatitis.
3. Herpetic keratoconjunctivitis.
4. Herpetic whitlow.
5. Congenital herpes simplex.
6. Herpes simplex pneumonia.
7. Herpes simplex encephalitis.
8. Genital herpes simplex.
9. Disseminated herpes simplex (In immunocompromised subjects.
Most of the clinical types may occur as a primary or recurrent infection.

1. Herpes labialis: This is the most common clinical type.

 Primary herpes:
- An erythematous area appear initially followed by umbilicated vesicles that
turn into pustules.
- Pustules rupture leaving crusted erosions that heal within 2-4 weeks leaving
post inflammatory hypopigmentation or hyperpigmentation.
- The condition is associated with regional lymphadenopathy. Fever may also
occur.
 Recurrent herpes:
- Grouped vesicles on an erythematous base that turn into pustules.
- Pustules rupture leaving crusted erosions that heal within 1-2 weeks leaving
post inflammatory hypopigmentation or hyperpigmentation.
- Regional lymphadenopathy and fever are absent.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

2. Herpetic gengivostomatitis:
- This is the most common presentation in children between 1-5 years of age.
- The condition begins with fever, malaise, restlessness and excessive dribbling
with foul smiling of mouth. Regional lymph nodes are enlarged.
- The gums are swollen and bleed easily. Drinking and eating are painful.
- Vesicle present as white plaques on the oral mucosa. The plaques are followed
by ulcers with a yellowish pseudomembrane.
- Fever subsides within 3-5 days. Recovery is usually complete in 2 weeks.

3. Herpetic keratoconjunctivitis:
- Primary herpetic infection of the eye causes severe purulent conjunctivitis with
superficial erosion and opacity of the cornea.

4. Herpetic whitlow:
- It is due to direct inoculation of the virus into skin e.g. fingers of medical
personnel.
- Indurated papules, large bullae or scattered vesicles appear at the inoculation
site.
- The condition is easily confused with pyogenic infections.

5. Congenital herpes simplex:

- It is due to transplacental spread of the virus from the mother to the baby.
- Early intrauterine infection: causes disturbed embryogenesis, which is
incompatible with life.
- Late intrauterine infection: causes growth and psychomotor retardation with
recurrent vesicular eruption.

 Complications of herpes simplex

1. Secondary bacterial infection.
2. Cutaneous or systemic dissemination (In immunocompromised
patients).
3. Congenital herpes simplex secondary to maternal infection.
4. Erythema multiforme.

 Diagnosis of herpes simplex

1. History and clinical examination.
2. Tzanck smear (Stained with Giemsa’s stain): Multinucleated giant
keratinocytes are seen.
3. Biopsy: Ballooning and reticular degeneration of the epidermis together
with intraepidermal vesicles are seen.
4. Viral culture.
5. PCR: It identifies viral DNA in tissue samples.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Treatment of herpes simplex

1. Preventive measures: ‫الوقاية خير من العالج‬

- Avoidance of precipitating factors.
2. Antiviral therapy: e.g. oral acyclovir
a- Primary infection: acyclovir 200mg 5 times/day for 7-10 days.
b- Recurrent infection: acyclovir 200mg 5 times/day for 5 days.
c- Severe or complicated cases: I.V. acyclovir is given in a dose of
5mg/kg/8hours for 5-7 days.
N.B.: Acyclovir must be given very early at the beginning of symptoms to be
effective.
3. Local treatment: e.g. antiseptic cream.

Erythema Multiforme
 Definition:
It is an acute muco-cutaneous syndrome that represents a reaction of the
skin to different causes such as infections, drugs or systemic disease.

 Etiology:
1. Drugs (The most common cause): e.g. sulfonamides, barbiturates,
NSAIDs, penicillin….
2. Infections: e.g.
a. Viral infections: Herpes simplex, AIDS, Hepatitis B, Mumps.
b. Bacterial infections: Streptococcal infections.
c. Mycoplasma infections.
d. Mycobacterial infections: T.B. & leprosy.
3. Autoimmune diseases: e.g. Lupus erythematosus, Dermatomyositis.
4. Sarcoidosis.
5. Malignancies: e.g. Carcinoma, lymphoma & Leukemia.
6. Unknown cause: In 50% of cases the exact cause cannot be determined.

 Clinical picture
Two clinical types are recognized:
I-Erythema multiforme minor:
It is characterized by:

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

- Mild symptoms & signs.

- No bullae, no systemic symptoms.
- Little or no mucosal lesions.
- Lesions usually confined to extensor aspect of extremities.
- H. simplex is the most common cause.
Clinical features include:
- Skin lesions are dull red maculo-papules 1-2cm in diameter affecting
mainly extensor aspect of extremities, palms and soles.
- The center may be cyanotic or purpuric giving target-like lesions.
- Skin lesions may itchy or painful.
- Healing occurs within 1-2 weeks with hyperpigmentation.

II-Erythema multiforme major (Stevens-Johnson syndrome)

It is characterized by:
- Severe symptoms & signs.
- Bullae & systemic symptoms occur.
- Mucosal lesions are extensive.
- Lesions are generalized.
- Drug reaction is the most common cause.
Clinical features include:
- Fever, weakness and malaise.
- Skin lesions are generalized maculopapular and bullous lesions.
- Sever involvement of mucous membranes specially of the mouth, but
pharynx, larynx and even trachea may be involved.
- Mouth lesions are painful and tender.
- Other mucosal surfaces may be affected e.g. cornea, conjunctiva and
genital mucosa.

 Prognosis
I- Erythema multiforme minor: Self-limited and not fatal.
II- Erythema multiforme major: Death occurs in 10-20% of cases.

 Diagnosis
1. History and clinical examination.
2. Dermatopathology:
a. Epidermal changes:
- Focal necrosis of keratinocytes.
- Intercellular edema & vacuolar degeneration of basal cells resulting in
sub-epidermal bullae.
b. Dermal changes:
- Perivascular mononuclear cell infiltrate.
- Dermal edema & extravasation of RBCs.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

 Differential Diagnosis
Mucous membrane lesions must be differentiated from other causes of oral
ulcers e.g.:
- Oral lesions of pemphigus.
- Herpetic gengivostomatitis.
- Erosive lichen planus.

Treatment of erythema mutiforme

1. The precipitating cause: Must be eliminated.

2. Mild cases: Symptomatic treatment is enough in e.g. bland topical
applications or topical steroids.
3. In severely ill patients:
- Systemic corticosteroids are usually given e.g. prednisone 40-80mg/day.
- Bland topical applications or topical steroids.
- Control of secondary infection.

BehÇet's syndrome
"Oculo-oral-genital syndrome"

 Definition:
It is a chronic multisystem syndrome characterized by the triad of:
1. Recurrent aphthous stomatitis (RAS).
2. Recurrent genital ulcers.
3. Ocular lesions.

 Epidemiology
- It is more common between the 2nd to the 4th decades.
- It is more common in males than females.

 Clinical picture
1. Recurrent aphthous stomatitis (RAS):
- Recurrent oral ulcers occur in 90-100% of cases.
- They are painful, shallow or deep and have a yellow fibrinous base.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

- There may be single or multiple ulcers

2. Recurrent genital ulcers:

- These occur in 60-90% of cases.
- They are painful and tend to heal with scarring.

3. Ocular lesions:
- Occur in 70-85% of cases.
- These include uveitis, retinal vasculitis, iridocyclitis and optic atrophy.

 Pathogenesis
The exact cause is not known. However, several pathogenic factors have been
suggested:
1. Genetic predisposition.
2. Streptococcus anguis: Has been found in a high concentration in the oral
flora of patients with BehÇet’s syndrome.
3. Immunologic mechanisms: e.g. the presence of circulating antibodies
against mucous membranes as well as increased levels of circulating
immune complexes.

 Diagnosis
International Study Group Criteria for diagnosis of BehÇet’s syndrome:
(1) Recurrent oral ulceration: At least 3 times/year.
(2) Plus 2 of the following criteria:
- Recurrent genital ulceration.
- Eye lesions (Uveitis, cells in the vitreous or retinal vasculitis).
- Skin lesions (Eythema nodosum like lesions, papulopustular lesions or
acneiorm nodules).
- Positive pathergy test (Read after 24-48 hours).

Pathergy test:
- A sterile pustule surrounded by erythema appears within 24-48hours at
the site of needle puncture.
- It is positive in 40-90% of patients.

 Course and prognosis

- The disease is characterized by remissions and exacerbations. Remissions may
last for weeks, moths or years.
- The disease may lead to blindness if there is eye affection, particularly
posterior uveitis.
- CNS involvement is associated with high mortality rate.

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Dentist's Manual Of Dermatology & Venereology Wael Hosam , M.D.

Treatment of BehÇet's syndrome

1. Tetracycline mouth wash: is the drug of choice for oral ulcers.
2. Topical steroid in a gel base: may be also useful for oral ulcers.
3. Intralesional injection of corticosteroids: e.g. Triamicinolone acetonide 5-
10mg/ml may be justified in severe oral ulcers.
4. Dapsone: 100mg/day can be efective in persistent oral and cutaneous
manifestations.
5. Cyclosporine A: 5mg/kg/day is quite efective
6. Benzathin penicillin combined with oral colchicine 0.6mg 3 times/day is
effective in treatment of mucocutaneous manifestations.

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