Oral manifestations of sexually transmitted diseases/ dental courses

INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

 Nomenclature
 STDs and Dentistry
 STDs and Causative Agents
 Vertical Transmission of STIs
 Oral manifestations and treatment of sexually
transmitted diseases.
 Dental & Medical Considerations
 Conclusion

Definition: STD
Sexually transmitted diseases are a group of
infections transmitted through sexual contact.
Synonym:
Sexually transmitted infections (STIs)

 The term “Venereal disease” was initially limited to
Gonorrhea, Syphilis, Chancroid, Lymphogranuloma
venereum, and Granuloma inguinale but at present it is
considered as a narrow and pejorative term.
 This “ Venereal diseases" (VDs) largely has been superseded
in the past 50 years by “Sexually transmitted diseases"
(STDs), and more recently by “Sexually transmitted
infections" (STIs).

Some STDs are incurable -----all are preventable.
Dental health care workers can be important components of STD
control because:
 STDs are transmitted by intimate interpersonal contact that can
result in oral manifestations.
 They can be transmitted by direct contact with lesions, blood,
or saliva.
 A single STD is accompanied by additional STDs in about 10%
of cases and STD-associated genital ulceration increases the
risk for human immunodeficiency virus (HIV) infection.
 STDs exhibit antimicrobial resistance, and proper treatment is
essential.

 Acquired immunodeficiency syndrome (AIDS) Human immunodeficiency virus
 Amebiasis Entamoeba histolytica
 Bacterial vaginosis Bacteroides spp, Mobilunais spp
 Chancroid Haemophilus ducreyi
 Condyloma acuminatum (genital warts) Human papillomavirus infection
(HPV-6, HPV-11)
 Cytomegalovirus infection Cytomegalovirus
 Enterobiasis Enterobius vermicularis
 Epididymitis, mucopurulent cervicitis,
lymphogranuloma venereum,
nongonococcal urethritis,
pelvic inflammatory disease, Reiter's syndrome. Chlamydia trachomatis
 Epididymitis, gonorrhea,
mucopurulent cervicitis, pelvic inflammatory ds Neisseria gonorrhoeae

 Genital herpes Herpes simplex viruses (HSV-1, HSV-2)
 Giardiasis Giardia lamblia
 Granuloma inguinale
(donovanosis) Calymmatobacterium granulomatis
 Hepatitis B Hepatitis B virus
 Molluscum contagiosum Poxvirus
 Nongonococcal urethritis,
nonspecific vaginitis Trichomoniasis vaginalis
 Nongonococcal urethritis Ureaplasma urealyticum
 Pediculosis Pediculus pubis
 Salmonellosis Salmonella spp
 Shigellosis Shigella spp
 Streptococcal infection Streptococcal group B spp
 Syphilis Treponema pallidum
 Vulvovaginal candidiasis Candida spp, Torulopsis spp

 This refers to transmission of infections from an infected
mother to her progeny and the mother usually acquires it
through close interpersonal contact.
Transmission may occur:
 ANTE-PARTUM- (transplacently, e. g. syphilis, HIV) or
 INTRA-PARTUM- (during the passage through birth canal, e.g.
gonorrhoea, herpes, Chlamydia) or
 Rarely POST-PARTUM- (breast milk).

 Syphilis
 Gonorrhoea
 Chancroid
 Donovanosis
 Lymphogranuloma Venereum
 Herpes Simplex
 Condyloma acuminatum
 Hepatitis B
 HIV

 Syphilis is caused by Treponema pallidum.
 It produces skin and mucous membrane lesions in the acute
phase, and bone, visceral, cardiovascular, and neurologic
disease in the chronic phase.
 Humans are the only known natural hosts for syphilis.
 The primary site of syphilitic infection is the genitalia,
although primary lesions also occur extragenitally.

 Treponema pallidum- slender, fragile anaerobic spirochete.
 It is transmitted predominandy sexually, including by oral-
genital and rectal-genital contact with contaminated sores.
 Transmission also can occur via nonsexual means such as
kissing, blood transfusion, or accidental inoculation with a
contaminated needle.
 Indirect transmission by fomites is possible but uncommon -
organism survives for only a short time outside the body.

 T. pallidum does not invade completely intact skin;
 It can invade intact mucosal epithelium and gain entry via
minute abrasions or hair follicles.
 The risk of transmission occurs during the Primary,
Secondary, and Early latent stages of disease, but not in
late syphilis. Overall, patients are most infectious during
the first 2 years of the disease.

 The chancre, a solitary firm, round, painless, granulomatous lesion.
 The genitalia, oral cavity (lips, tongue), fingers, nipples, and anus are
common sites for chancres.
 Occurs within 2 to 3 weeks (range, 10 to 90 days) after exposure.
 Patients are infectious even before it appears.
 Associated regional lymph nodes are enlarged, painless, hard.
 Usually subsides in 3 to 6 weeks without treatment, leaving variable
scarring in the form :if a healed papule.
 If adequate treatment is not provided, the infection progresses to secondary
syphilis.

 The symptoms and signs of secondary syphilis include fever, arthralgia and
malaise, generalized lymphadenopathy, and patchy hair loss and develop in
80% of patients.
 The manifestations appear 6 to 8 weeks after initial exposure.
 Generalized eruptions of the skin and mucous membranes. The papules of
the rash are well demarcated and reddish brown and have a predilection for
the palms and soles; they are typically not itchy.
 Oral manifestations of secondary syphilis include pharyngitis, papular
lesions, erythematous or grayish white erosions (mucous patches) irregular
linear erosions, and, rarely, parotid gland enlargement.
 The lesions of skin and mucous membranes are highly infectious.
 Without treatment, secondary syphilis ultimately resolves; however,
infection progresses to latent or late stages.

 Patients are seroreactive but are asymptomatic and show no clinical
evidence of disease.
Latent syphilis is divided:
 Early latent syphilis (acquired the disease within the preceding year)
 Late latent syphilis (longer than 1 year).
During the first 4 years of latent syphilis, patients may have mucocutaneous
relapses and are considered infectious.
After 4 years, relapses do not occur, and patients are considered non
infectious (except for blood transfusions and pregnant women).
The latent stage may last for many years or for the remainder of the person's
life.In some untreated patients - progression to tertiary syphilis occurs.

 The tertiary (late) stage occurs in 10% to 40% of untreated persons, generally
several years after disease onset.
 It is the destructive stage of the disease.
 Patients are noninfectious.
 Any organ of the body (mucocutaneous, osseous, visceral, or neural) may become
involved.
 Signs and symptoms of this stage do not occur until years after the initial infection.
 The gumma, which is the classic localized lesion of tertiary syphilis, may involve the
skin, mucous membranes, bone, nervous tissue, and/or viscera.
 It is believed to be the end result of a hypersensitivity reaction and is basically an
inflammatory granulomatous lesion with a central zone of necrosis.
 It is not infectious.

 The oral lesions of tertiary syphilis consists of:
 Diffuse interstitial glossitis and the gumma.
 Interstitial glossitis should be considered a premalignant condition.
The tongue may appear lobulated and fissured with atrophic papillae,
resulting in a bald and wrinkled surface.
Leukoplakia frequently is present.
 The oral gumma is a rare lesion that most commonly involves the tongue
and palate.
 It appears as a firm tissue mass with central necrosis. Palatal gummas
may perforate into the nasal cavity or maxillary sinus.

 All other manifestations - vascular in nature and result from an
obliterative endarteritis.
 Cardiovascular syphilis is most commonly seen as an aneurysm
of the ascending aorta.
 Neurosyphilis can result in a meningitis-like syndrome i.e.
 Argyll Robertson pupils (which react to accommodation but not
to light), altered tendon reflexes, general paresis, tabes dor-
salis (degeneration of dorsal columns of the spinal cord and
sensory nerve trunks), difficulty in coordinating muscle
movements, or insanity.

 Syphilis or its sequelae occur in newborn if the mother is infected while
carrying the child.
 The disease is transmitted to the fetus in utero, usually after the 16 th
week, because before this time, the placenta prevents transmission of
bacteria.
The sequelae of early infection include:
• Osteochondritis,
• Periostitis (frontal bossing of Parrot),
• Rhinitis,
• Rash,
• Ectodermal changes.

Syphilis contracted during late pregnancy may involve:
• Bones,
• Teeth
• Eyes,
• Cranial nerves,
• Viscera,
• Skin, and
• Mucous membranes.
A classic triad of congenital syphilis known as Hutchinson's triad includes
interstitial keratitis of the cornea, eighth nerve deafness, and dental
abnormalities (i.e., Hutchinson's incisors and mulberry molars).

 These are the residua of the past inflammatory processes due
to congenital syphilis and hence may be seen in untreated and
treated patients for the rest of their lives. Some popular
stigmata include Hucthinson’s teeth (peg shaped incisors),
mulberry molars, depressed bridge of the nose, frontal bossing
and rhagades.

 Penicillin is the drug of choice for the treatment of syphilis.
 Hence, antibiotics other than penicillin can be used only in
individuals with proved penicillin hypersensitivity.
The antibiotics include :
 Erythromycin or tetracycline 500 mg QDS for 15 days or
 Doxycycline 100 mg BD for 14 days.
 Cephalosporins e.g. Ceftriaxone 1 gm IM OD for 10-14 days or
 Cephalexin 500 mg q.i.d orally for 2 weeks can also be used
but may cause cross-sensitivity to penicillin.

 This is also called therapeutic shock and is due to sudden
release of treponemal antigens, from killed treponemes, as
a result of institution of therapy.
 Fever, headache, body ache, joint pains, hypotension,
vomiting may accompany exacerbation or appearance of
new mucocutaneous lesions.
 The reaction begins within hours of penicillin injection and
lasts 12-24 hours.

 All patients treated for syphilis need an extended follow up to
ensure that there is no relapse. This is all the more important
in HIV positive cases.
 Follow up includes a clinical check-up and a VDRL test
performed every 3 monthly for 2 years.
 VDRL titre falls to ¼ of original in successfully treated
individuals.
 The test may take several months or even years to become
negative.
 In patients with late syphilis it may never become negative.

 Neisseria gonorrhoeae.
 It produces symptoms in men
 Infections in women often do not produce recognizable
symptoms until complications have occurred.
 Because gonococcal infections among women often are
asymptomatic, screening of women who are at high risk for
STDs is essential.
 Patients infected with N. gonorrhoeae are often coinfected with
Chlamydia trachomatis.

 N. gonorrhoeae a gram-negative intracellular diplococcus.
 N. gonorrhoeae is an aerobic microbe that replicates easily in
warm, moist areas and preferentially requires high humidity
and specific temperature and pH for optimum growth.
 It is a fragile bacterium that is readily killed by drying, so it is
not easily transmitted by fomites.
 It develops resistance to antibiotics rather easily, and many
strains have become resistant to penicillin and tetracycline, as
well as to other antibiotics.

 N. gonorrhea displays differential invasiveness.
 Columnar epiielium (as found in the mucosal lining of die uredira and
cervix) and transitional epidielium (as in the oropharynx and rectum)
are highly susceptible to infection.
 Stratified squamous epidielium (skin and mucosal lining of die oral
cavity) is generally resistant to infection.
 Gonococcemia, although infrequent (1% to 2% of cases), may occur
and results in dissemination of die disease to distant body sites.
 Gonococcemia can lead to widespread dissemination and may result
in a variety of disorders, including migratory arthritis, skin and mucous
membrane lesions, endocarditis, meningitis, PID, and
pericarditis.Epididymitis is another complication of infection that can
lead to infertility.

 Within the oral cavity, the pharynx is most commonly affected.
 It usually is seen as an asymptomatic infection with diffuse,
nonspecific inflammation or as a mild sore throat.
 The likelihood of transmission of pharyngeal gonorrhea to the
genitalia seems much less than that of genital-genital
transmission.
 Of significance, however, is the fact that N. gonorrhoeae has
been cultured from the expectorated saliva of two thirds of
patients with oropharyngeal gonorrhea.

 Gonococcal stomatitis or oral gonorrhea appears to be
uncommon; case reports in the literature are limited.
 Acute ulceration,
 Diffuse erythema,
 Necrosis of the inter-dental papillae,
 Lingual edema,
 Edematous tissues that bleed easily,
 Vesiculations, &
 Pseudomembrane that is non-adherent and leaves a bleeding
surface on removal.
 Lesions may be solitary or widely disseminated.

 Symptoms include a burning or itching sensation, dryness,
increased salivation, bad taste, fetid breath, fever, and
submandibular lymph-adenopathy.
 The lesions of oral gonorrhea may closely resemble the
lesions of erythema multiforme, bullous or erosive lichen
planus, or herpetic gingivostomatitis.
 Acute temporomandibular joint arthritis may be caused by
disseminated gonococcal infection from a genital site.

 Diagnosis of N. gonorrhoeae infection can be made
presumptively on the basis of a finding of Gram-negative
diplococci within polymorphonuclear leukocytes in a smear of
urine or of purulent discharge.
 However, culture is the gold standard for the diagnosis of N.
gonorrhoeae.
 Nucleic acid amplification testing (NAAT) is highly sensitive and
specific for the organism and can be used to simultaneously
test for C. trachomatis.
 In suspected cases of oropharyngeal gonorrhea, because
other species of Neisseria are normal inhabitants of the oral
cavity, a smear and Gram stain are not as helpful. Therefore,
culturing with selective media or use of NAAT is necessary.


 Oral Cefixime 400 mg in a single dose, or
 Injectable Ceftriaxone 125 mg (intramuscularly [IM]) in a single
dose), or
 Asingle oral dose of a Quinolone (ciprofloxacin [Cipro] 500 mg,
or ofloxacin [Floxin] 400 mg or levofloxacin [Levaquin] 250 mg)
plus coverage against the common coinfecting organism
Chlamydia trachomatis with azithromycin 1 g given orally in a
single dose, or doxycycline 100 mg orally two times a day for 7
days.

For patients who cannot take ceftriaxone,
 Spectinomycin (2 g IM) is a recommended alternative.
 The clinician should be aware that gonococcal pharyngitis is
more difficult to eradicate than infections at urogenital and
anorectal sites.
 Few antigonococcal regimens can reliably cure such infections
more than 90% of the time, and IM cefixime is recommended.

 Genital herpes is a recurrent, incurable viral disease of the
genitalia that is caused by one of two closely related types of
herpes simplex virus (HSV)—type 1 and type 2.
 HSV -eight human herpesviruses that includes cytomegalovirus,
Epstein-Barr virus, varicella-zoster virus, human herpes virus type
6 (HHV-6), human herpes virus type 7 (HHV-7), and Kaposi's
sarcoma-associated herpes virus (HHV-8).
 HSV-1 -most herpetic infections that occur above the waist,
(herpetic gingivostomatitis, herpes labialis).
 HSV-2 - most herpes infections that occur below the waist, such as
in or around the genitalia (genital herpes).

 Infection arises from intimate contact with a lesion or infective
fluid (e.g., saliva).
 Epithelial cells are invaded, and viral replication occurs.
 Characteristic cellular changes include ballooning
degeneration, intra-nuclear inclusion bodies, and the formation
of multinucleated giant cells.
 With cellular destruction come inflammation and increasing
.edema, which result in formation of a papule that progresses
to a fluid-filled vesicle.
 These vesicles rupture, leaving an ulcerated or crusted surface.

 Lymphadenopathy and viremia are prominent features.
 In normal individuals, the infection is contained by usual host
defenses and runs its course within 10 to 20 days.
 However, spread to other epidermal sites (e.g., herpetic
whitlow [infection of the fingers], keratoconjunctivitis [eyes])
and in neonates during childbirth has been documented.
 In rare cases, infants and immunosuppressed persons can
develop systemic (meningitis) and widespread infection that
may result in significant morbidity and death.

 During the epithelial infection, progeny enter the ends of local
peripheral neurons and migrate up the axon the regional
ganglion (HSV-1 primarily in the trigeminal and HSV-2 primarily
in the sacral), where they reside. After stimulation such as
trauma, sunlight, menses, or intercourse, the virus reactivates,
migrates down the axon, and produces recurrent infection with
lesions similar to the primary, but less severe in nature and
more localized.

 Most (about 60%) new cases of HSV-2 infection are asvmptomatic; newly
acquired cases are asymptomatic more frequently in men than in women.
 After an incubation period of 2 to 7 days, lesions (i.e., papules, vesicles,
ulcers, crusts, and fissures) of primary genital herpes may appear.
 Lesions in moist areas tend to ulcerate early, are painful, and may cause
dysuria.
 Lesions on exposed dry areas tend to remain pustular or vesicular and then
crust over.
 Painful regional lymphadenopathy accompanies infection, along with
headache, malaise, myalgia, and symptoms of fever.
 These subside in about 2 weeks, and healing occurs in 3 to 5 weeks.

Cytologic examination of a smear taken from the base of a herpetic lesion
reveals typical features, including ballooning degeneration of cells,
intranuclear inclusion bodies, and multinucleated (fused) giant cells.
 However, cytology is nonspecific and less sensitive than viral culture.
 Diagnosis is best established by swabbing an infected secretion or ulcer
and isolating the virus by cell culture.
 The virus is identified by staining the infected cells for HSV antigen with the
use of immunofluorescence or immunoperoxidase.
 Alternatively, NAAT may be usedand is particularly useful when neurologic
symptoms develop and cerebrospinal fluid is sampled.
 Serologic detection of antibodies to HSV-1 glycoprotein G1 or HSV-2
glycoprotein G2 aids in diagnosis and management (e.g., counseling the
patient about the potential for recurrence).

Management of patients with a first clinical episode of genital herpes includes :
 Antiviral therapy and counseling regarding the natural history of genital herpes,
sexual and perinatal transmission, and ways to reduce transmission.
 Acyclovir (Zovirax), famciclovir (Famvir), or valacyclovir (Valtrex) are nucleoside
analog drugs that act as DNA chain terminators during virus replication in infected
cells.
 Topical acyclovir therapy is substantially less effective than systemic drug
administration, and its use is not recommended for genital herpes.
 Use of systemic antiviral drugs can shorten the duration, frequency, and symptoms
of outbreaks and can reduce the frequency of asymptomatic shedding and the risk
of transmission.
 However, antiviral agents do not eliminate the virus from the latent state, nor do
they affect subsequent risk, frequency, or severity of recurrence.
 Antiviral drugs are most effective when given preventatively at least 1 day within the
appearance of symptoms, whether for primary or recurrent disease.

DEFINITION
 Although not classically defined as an STD, the transmission of infectious
mononucleosis occurs through intimate personal contact.
 Infectious mononucleosis is an infection that is caused, in at least 90% of
cases, by the Epstein-Barr virus (EBV), a lymphotropic herpes virus.
 Other viruses may also produce features of acute infectious mononucleosis.
Infectious mononucleosis produces the classic clinical triad of fever,
pharyngitis, and lymphadenopathy.
 Transmission of the virus occurs primarily by way of the oropharyngeal route
during close personal contact (i.e., intimate kissing).
 Children, adolescents, and young adults are most commonly affected.

 EBV is a lymphotropic herpesvirus that is transmitted primarily
through exposure to oropharyngeal secretions.
 Infrequently, it is transmitted through shared infected drinks,
eating utensils, or infected blood products. Incubation time is
30 to 50 days.
 A prodromal period .of 3 to 5 days precedes the clinical phase,
which lasts 7 to 20 days.
 During the prodromal phase, the virus infects oropharyngeal
epithelial cells and spreads to B lymphocytes in the tonsillar
crypts. Infected B lymphocytes circulate through the RE system,
triggering a marked lyphocytic response.

 In normal blood smears, large reactive lymphocytes represent about 1% to 2% of
cells whereas in infectious mononucleosis, they constitute 10% to 40% of circulating
white blood cells.
 Reactive lymphocytes are not EBV-infected B lymphocytes but are T-lymphocytes that
react to the infection. The combination of reactive lymphocytes, the cytokines
they produce, and the B-cell-produced (heterophile) antibodies directed against EBV
antigens contributes to the clinical manifestation of the acute infection.
 Hepato-splenomegaly develops in about 40% to 50% of patients, splenic rupture
occurs in 0.1% to 0.2% of all cases, and death is a rare outcome.
 After the acute infection, the virus remains latent in B lymphocytes for the life of the
host.
 As effective transforming agents, EBV-associated lymphomas and carcinomas are
common.

 Infectious mononucleosis usually is asymptomatic when
found in children; however, when young adults are affected,
about 50% are mildly symptomatic.
 Fever,
 sore throat,
 Tonsillar enlargement, and Lymphadenopathy

Additional features include:
 malaise,
 fatigue, an absolute lymphocytosis (>10% reactive lymphocytes),
and
 a positive heterophil antibody test.
 About a third of patients develop palatal petechiae during the
first week of the illness, and about 30% of patients experience an
exudative pharyngitis.
 Generalized skin rash and petechiae of the lips are seen in about
10% of cases. Also, the liver and spleen can enlarge and become
tender.
 Symptoms tend to dissipate within 3 weeks of onset.

 The diagnosis of infectious mononucleosis is made on the
basis of symptoms and a laboratory profile characterized by :
 peripheral lymphocytosis (e.g., 50% lymphocytes [primarily T
lymphocytes]) and at least 10% atypical lymphocytes .
 along with a positive heterophile antibody test.
Heterophile antibodies are immunoglobulin (Ig)M antibodies that
bind (agglutinate) to erythrocytes from nonhuman species such
as sheep and horses.

 Although a number of antiviral drugs can inhibit EBV replication in culture,
no drug is licensed for use in the clinical treatment of EBV infection.
 The lack of efficacy of antivirals results from the fact that mononucleosis is
largely due to the immune response.
 As such, treatment of patients with infectious mononucleosis remains
symptomatic and consists of:
 bed rest, fluids, acetaminophen or nonsteroidal anti-inflammatory agents
for pain control, and gargling and irrigation with saline solution or lido-caine
to relieve symptoms of pharyngitis and stomatitis.
 Vigorous activity is to be avoided to reduce die risk of splenic rupture.

 In some patients with severe toxic exudative pharyngotonsillitis, pharyngeal
edema and upper airway obstruction, or seizures, a short course of predni
sone may be given.
 About 20% of patients with symptomatic infectious mononucleosis have
concurrent beta-hemolytic streptococcal pharyngotonsillitis and should be
treated with penicillin V, if they are not allergic to penicillin.
 Ampicillin should be avoided because at least 90% of patients develop a
hypersensitivity skin rash when treated with this drug.

 DEFINITION
 Human papillomaviruses (HPVs) are small, double-stranded,
nonenveloped DNA viruses that infect and replicate in
epithelial cells.
 More than 100 genotypes of HPV have been identified, and
more than 30 types are known to be sexually transmitted and
to affect the ano-genital epithelium.
 Each HPV subtype exhibits preferential anatomic sites of
infection and a propensity for altering epithelial growth and
replication.
 The spectrum of disease that is induced is dependent on the
type of HPV infection, location, and immune response.

 Subtypes of HPV have been classified as "high-risk" or "low-
risk" types.
 Low-risk HPVs (HPV-6, -11) produce benign proliferative lesions
of mucocutaneous structures.
 High-risk HPV types (HPV-16, -18, -31,-33, -35, -45) are strongly
associated with dysplasia and carcinoma of the uterine and
anal tract and other mucosal sites.

 Condyloma acuminatum 6, 11
 Epithelial dysplasia, carcinoma in
situ, squamous cell carcinoma 2, 16, 18
 Focal epithelial hyperplasia(Heck's disease) 13,32
 Lichen planus 11, 16
 Oral bowenoid papulosis 6, 11, 16
 Squamous papilloma 6, 11
 Verruca plana 3, 10
 Verruca vulgaris 2,4,6, 11, 16
 Verrucous carcinoma 2,6, 11, 16, 18

 Genital HPV can be transmitted by direct contact during sexual
intercourse or passage of a fetus through an infected birth
canal, or by autoinoculation. Genital lesions usually appear
after an incubation period of HPV in epithelium for 3 weeks to 8
months.
 The most common manifestation of HPV replication is the
venereal wart (or condyloma acuminatum).
 HPV types 6 and 11 are the subtypes most frequently
associated with condyloma acuminatum.
 HPV types 2 and 6 also have been identified in condylomata
but are not considered the primary etiologic agents.

 HPV is transmitted through intimate or sexual contact.
 The virus replicates in the nuclei of epithelial cells and increases the
turnover of infected cells, or it remains episomally in a latent state.
 Benign types such as HPV-6 and -11 have a strong tendency to
induce epithelial hyperplasia such as condylomata and a spreading
infection.
 HPV-16 and -18 have a propensity to induce dysplasia and malignant
transformation.
 HPV types 31, 33, 35, 39, 45, 51, 52, 54, 56, and 58 convey
intermediate to high risk for inducing carcinoma.
 Cofactors such as smoking contribute to the progression to cancer.

 Most individuals infected with HPV are asymptomatic, and the
infection clears on its own.
 Visible genital warts caused by HPV-6 or -11 are typically
diagnosed as condyloma acuminatum.
 These growths are seen in sexually active individuals in warm,
moist, intertriginous areas such as the anogenital skin and
mouth, where friction and microabrasion allow entrance of the
pathogen.

 Condylomata appear as small, soft, exophytic papillomatous
growths .
 The surface is cauliflower-like or broccoli-like; the base is
sessile.
 The borders are raised and rounded.
 The color varies from pink to dusky gray.
 Lesions often are multiple and recurrent and can coalesce to
form large, pebbly warts.
 Most condylomata are asymptomatic; however, patients may
report itching, irritation, pain, or bleeding as a result of
manipulation or trauma.

 During pregnancy, condylomata may enlarge as the result of
increased vascularity.
 Condylomata can occur on the vagina, anus, mouth , pharynx, or
larynx, and may appear weeks or months after the onset of infection.
 HPV types 16, 18, 31, 33, and 35 have an infrequent association
with genital warts and a more common association with dysplasia
and carcinoma of the cervix.
 These high-risk HPV types also contribute to the development of
squamous intraepithelial neoplasia (Bowen's disease) of the
genitalia.

 HPV does not grow in cell culture, and serologic tests are not routinely
performed, in part because 90% of infected persons become serologically
HPV negative within 2 years.
 Therefore, lesions of condyloma acuminatum should be biopsied and
examined microscopically, if the clinical diagnosis is uncertain.
 Its microscopic appearance consists of a sessile base, with raised epithelial
borders, a thick spinous spinosum layer (acanthosis), and hyperkeratosis.
Identification of HPV within the lesion confirms the diagnosis.
 This is generally achieved with the use of commercial in situ hybridization
kits that use RNA probes to detect viral DNA specific to HPV genotypes.
 Viral sub-typing may be important for determining risk of carcinogenesis
when cervical tissue and an abnormal Papanicolaou smear are involved

A major advance occurred in 2006 with the introduction of the
HPV vaccine (Gardasil).
 This vaccine is 95% to 100% effective in preventing infection
with HPV types 6, 11, 16, and 18.
 It has been approved for use in girls and women aged 9 to 26
years and is administered in a 3-shot regimen over a 6-month
period.
 They have not been shown to eliminate or cure HPV and do not
work against all HPV types.

 HPV-induced genital warts can be completely removed with
chemicals, antiviral drugs, or surgery.
 The best response is attained with small warts that have been
present for less than 1 year.
 The CDC"' recommends podofilox 0.5% (Condylox) be the
medication of first choice.
 It causes necrosis by arresting cells in mitosis.
 Alternatively, the patient may apply imiquimod (Aldara) 5%
cream at bedtime, 3 times per week for up to 16 weeks.
 Imiquimod is an immune response modifier drug.
 Most warts dissipate within 8 weeks.

 Other available therapies include surgery (excision, cryotherapy,
laser), weekly topical therapy with podophyllum 10% to 25% in
tincture of benzoin, and trichloroacetic acid 80% to 90% or bichlo-
roacetic acid.
 Topical and intralesional therapy with 5-fluorouracil, an
antimetabolite, has resulted in a greater than 60% response rate,"
and cidofovir is an antiviral that yields an effective response.
 Intralesional interferon is an option, but it is rarely recommended
because of cost and adverse effects.
 Recurrences are common despite the use of first-line therapies (in
about 10% to 25% of cases, generally within 3 months), even
when the entire lesion, including the base, is removed.

 Hepatitis is the inflammation of the liver that may result from
infectious or other causes.
 Hepatitis –B is caused by DNA hepadnavirus with main route of
transmission being parental and sexual contact.

Hepatitits viruses replicate in hepatocytes and ultimately damage
the host cells- causing ballooning degeneration and necrosis of the
liver cells and jaundice becomes clinically apparent and the
consequences could either be recovery, persistent infection,
Chronic hepatitis, cirrhosis, hepato-cellular carcinoma and death.

 Abnormal bleeding is asociated with hepatitis and significant
liver damage. This may result from abnormal synthesis of blood
clotting factors, abnormal polymerisation of fibrin stabilization,
excessive fibrinolysis, or thrombocytopenia associated with
splenomegaly that accompanies chronic liver disease.
 Chronic hepatitis increases the risk of hepato-cellular
carcinoma and oral metastasis primarily present as
hemorrhagic expanding masses located in the premolr and
ramus regions of the mandible.

 HIV virus is a retrovirus that replicates in host cells through the step of reverse transcription in
which DNA copies of the virus are made from RNA dependent DNA polymerase. This viral DNA
then incorporates into host cell nucleus and manufactures viral proteins necessary for
replication.

 The human immunodeficiency virus has a peculiar affinity for
CD4 receptors. Hence, all CD4 receptor-bearing cells are
selectively infected and the virus uses the cellular machinery of
these cells to continuously replicate within the body.
 Once, it has completely used up the cell machinery for its own
replication, the cell dies releasing hundreds of virions that are
ready to infect new cells.
 There is a reversal of CD4/CD8 ratio leading to exhaustion of
immune system.
 Loss of this effector arm of immunity leads to variety of
infections and malignancies.

 Consult whenever possible with patient’s physician to establish
current status; if severe thrombocytopenia is present
(<50,000), platelet replacement may be needed before
surgical procedures are performed.
 Determine whether prophylactic antibiotics are needed to
protect patients with severe immune neutropenia (<500
cells/mm3) from postoperative infection.
 Render only more immediately needed treatment for patients
with advanced AIDS.
 In most cases, provide dental procedures in accordance with
the patients with AIDS of the relative risks involved and how
they can be minimized.

 Gonorrhea—Little threat of transmission to dentist; oral lesions are possible
 Syphilis—Untreated primary and secondary lesions infectious; biood also is
potentially infectious
 Genital herpes—Little threat of transmission to dentist; oral lesions
(possible from autoinoculation) are infectious.
 HPV Infection- Little threat of transmission to dentist; oral lesions are
possible.
 Persons with sexually transmitted disease are at risk for HIV infection.
 AIDS- Dentists should always use standard precautions and prevent high
risk exposure. High risk exposure includes exposure to large volume of
infected fluid, deep penetrating injury with sharp device covered with visible
blood from the infected patient, and needle stick injury during injection of
the infected patient.

 STDs are incurable but all are preventable.
 Proper preventive measures should be
instituted so that in-adverdent transfer of
infectious agents to the dental professionals
and henceforth to the other patients in the
clinics are prevented.

 Thankyou!

 Dr. Uday Khopkar: Skin Diseases and sexually
transmitted infections with an update on HIV
infection,fifth edition 2004, pg 262.
 James W. Little, Donal A.Falace, Craig S.Miller, Nelson
L. Rhodus: Dental Management of the Medically
Compromised patients, seventh edition, pg 193.
 Perspective – Oral Manifestations Volume 13 Issue
5 December 2005/January 2006;
http://www.iasusa.org/pub/topics/2005/issu
e5/143.pdf

 Burket’s Oral medicine diagnosis and treatment,
ninth edition.
 Oral and Maxillofacial Pathology, Second
edition, Brad W. Neville, pg 213.

Oral manifestations of sexually transmitted diseases/ dental courses

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