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19.2.2.3 Management
Depending on the state of the tooth, deep scaling, periodontal surgery or extraction of the tooth are
suggested.
19.2.3 Necrotising Ulcerative Gingivitis (NUG) and Necrotising Ulcerative Periodontitis
Necrotising ulcerative gingivitis is also known as acute necrotising ulcerative gingivitis (ANUG)
and trench mouth. When NUG progresses, it involves periodontal tissues resulting in attachment loss. This disease is an acute, rapidly destructive, microbial disease of the gingiva and/or
periodontium in immunocompromised and malnourished individuals. It is also an opportunistic infection associated with organisms such as Bacteroides and Fusobacterium groups
(9,24, 25).
19.2.3.1 Clinical Features
These patients present with pain, halitosis, bleeding and ulceration resulting in punched- out
interdental papillae. This is characteristic of acute onset. These patients may also have fever,
malaise and lymphadenopathy. The diagnosis is mainly based on the clinical presentation
(Figure19.8).
19.2.3.2 Management
Treatment is given in two phases. Initially, ultrasonic superficial debridement is followed by antibiotics such as metronidazole with 0.12% chlorhexidine gluconate mouth rinse. This regimen is
followed by scaling, root planing and maintaining good oral hygiene. If NUG is not controlled at
this stage, it will progress to necrotising ulcerative periodontitis (NUP).
19.2.4 Syphilis, Tuberculosis andGonorrhea
Bacterial oral infections caused by Treponema pallidum, Mycobacterium tuberculosis and Neisseria
gonorrhoeae are varied and uncommon. Early and effective management is essential. Bacterial
infections are infrequent due to the protective role of the oral epithelium and the antibacterial
properties of saliva. Bacterial infections are more frequent in immunocompromised patients such
Figure19.8 Clinical photograph
showing punched- out interdental
papillae.
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as those receiving chemotherapy, organ transplantation, human immunodeficiency virus (HIV)/
acquired immune deficiency syndrome (AIDS) and corticosteroid use.
19.2.4.1 Syphilis
Syphilis is a sexually transmitted disease caused by Treponema pallidum, a spirochete transmitted
through direct contact with oral, genital or anal mucosae. Other routes of infection include blood
transfusion (rarely) and intrauterine maternal/fetal transmission(26, 27).
19.2.4.2 Aetiology andPathogenesis
Syphilis is caused by the spirochete, Treponema pallidum. The Treponema genus is a spiral- shaped
bacteria with a rich outer phospholipid membrane that belongs to the spirochetal order. The clinical
manifestations of the disease, particularly in the secondary and tertiary stages, are so variable that
the term ‘The great imitator’ has been applied. Syphilis is considered a sexually transmitted disease,
except for transplacental transmission from an infected mother. The ‘primary’ lesion occurs at the
site of inoculation on the genitals, anus, rectum, lips and mouth. This lesion, known as a ‘chancre’,
appears 10– 90days following exposure with an average of 20 days. Even without treatment, the
chancre will heal. About 25% of individuals will then develop ‘secondary’ syphilis with a wide variety of clinical signs and symptoms. Again, even without treatment, the lesions will clear, although
the period for resolution is highly variable. Some individuals will then enter a long ‘latent’ period
10– 30 years later when the manifestations of ‘tertiary’ syphilis develop. Tertiary syphilis, most commonly involving the cardiovascular and nervous stems, is rare today, at least in developed countries
because of the widespread use of antibiotics, both in treating syphilis and given for other infections.
The mechanism of tissue injury by T. pallidum and effective immune response is not well
understood. Experimental studies in rabbits suggest that much of the tissue injury is due to the
ineffective reaction of the immune system, rather than the organism itself, producing chronic
inflammation and ischemic necrosis secondary to obliterative endarteritis. Although the primary and secondary lesions appear to be cleared by an immune response, chronic infection
results in delayed hypersensitivity reaction and granulomatous response, leading to the formation of ‘gummas’. Systemic elimination of T. pallidum does not occur, leading to a period of
‘Latency’. When immune surveillance becomes ineffective, the manifestations of ‘tertiary’
syphilis may develop.
Syphilis is a much more aggressive disease when associated with AIDS. In this circumstance,
primary and secondary syphilis may occur simultaneously as well as multiple chancres. Progression
to tertiary syphilis is rapid, especially with neurologic involvement. Treatment requires higher
doses of penicillin, and relapse may occur following treatment(28– 31).
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19.2.4.3 Clinical Features
Signs and symptoms of syphilis are multiple and depend on the stage of the disease. Primary
syphilis is characterised by a painless ulcer, known as a chancre, at the site of contact. This nonpainful ulceration appears on the lips and occasionally elsewhere in the oral cavity, lasting three
to eight weeks. Secondary syphilis, following the primary infection, usually manifests with systemic symptoms and multiple oral lesions. These painless lesions can occur anywhere in the oral
cavity as patches, split papules and condylomata lata. After this stage, the patients manifest no
symptoms entering into latent syphilis lasting for weeks to years. Tertiary syphilis follows the
latent phase, affecting multiple organs. Gummas are the active sites of tertiary infection in the palate leading to perforation and are histologically characterised by granulomatous inflammation.
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19.2.4.4 Management
A definitive diagnosis of syphilis generally requires at least one positive nontreponemal assay
(Venereal Disease Research Laboratory [VDRL] and Rapid Plasma Reagin [RPR]) and a positive
treponemal test (Fluorescent Treponemal Antibody Absorption Test [FTA- ABS] and Treponema
pallidum particle agglutination assay [TP- PA]). Primary and secondary syphilis are treated with a
single dose of intramuscular long- acting benzathine penicillin G, while tertiary syphilis is treated
with intramuscular benzathine penicillin G once weekly for three to four weeks. Patients allergic
to penicillin are treated with tetracycline, doxycycline or ceftriaxone(26).
19.2.4.5 Tuberculosis
Tuberculosis is a granulomatous disease caused by the aerobic acid- fast bacillus, Mycobacterium
tuberculosis. Oral tuberculosis may follow primary lung infections in immunosuppressed
patients.
19.2.4.6 Aetiology andPathogenesis
Tuberculosis is caused by Mycobacterium tuberculosis, an ‘acid- fast’ organism, so named
because it resists discolouration when stained with the dye carbolfuchsin due to the lipid- rich
membrane of the bacteria. This same membrane also renders the organism relatively resistant
to disinfectants and antibiotics. Infection is transmitted via person- to- person through infected
sputum, often produced by coughing. Following aspiration of infected droplets, the organisms
lodge in the pulmonary alveoli, where their presence elicits an innate immune response dominated by macrophages. The bacteria may be destroyed if the inoculum is small and the individual’s immune system is competent. M. tuberculosis, because of its lipid- rich membrane,
tends to resist degradation in the phagolysosome of the macrophage and may replicate within
the macrophage and be released into surrounding tissue. The adaptive immune response also
plays a role in destroying organisms via sensitised T cells. If, however, M. tuberculosis is not
killed during the initial immune responses, a granulomatous inflammatory reaction, dominated by activated macrophages, results in an attempt to wall off the offending organisms, thus
forming a ‘tuberculous granuloma’ with a soft, necrotic centre. The microorganisms may persist for years within this granuloma, only becoming proliferative when the immune system
weakens, AIDS being the best example. These granulomas may expand and rupture into bronchi, thus producing highly infective sputum.
19.2.4.7 Clinical Features
Oral tuberculosis is rare. Oral tuberculous lesions almost always arise from mycobacteria colonising small areas of oral mucosal disruption, secondarily infected by contaminated sputum(32– 34),
although primary oral lesions have rarely been reported. It presents ulcerations usually on the
posterior dorsum of the tongue, though it can occur anywhere on the oral mucosa. These persistent ulcers are painful and may be associated with enlarged painful cervical lymph nodes. The
infected patients may present with fever, night sweats, chronic cough and haemoptysis. A biopsy
of the ulcer will reveal a necrotising granulomatous inflammatory reaction unless the individual is
immunosuppressed. A positive culture of the organisms is confirmatory(26).
19.2.4.8 Treatment
The patients should be referred to an infectious disease clinic for treatment with a combination of
isoniazid, rifampin, pyrazinamide and ethambutol. The treatment should be continued until the
sputum is negative for the organisms.
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19.2.4.9 Gonorrhea
Gonorrhea, a sexually transmitted disease, is caused by a gram- negative coccobacterium, Neisseria
gonorrhoeae. Primary lesions usually involve the reproductive organs but may occur in the oral
cavity, oropharyngeal mucosa and rectum.
19.2.4.10 Aetiology andPathogenesis
Neisseria gonorrhoeae, a highly infectious, gram- negative obligate diplococcus is the cause of gonorrhoea. The bacteria are mainly transmitted through genital, orogenital and anogenital sexual contact, although genito- ocular transmission (gonococcal conjunctivitis) during childbirth is possible.
The bacteria preferentially infect mucosal epithelia of the male and female urethra, endometrium, fallopian tubes, epididymis, anorectal mucosa, nasopharynx and conjunctiva. As untreated
infection progresses, adjacent structures and even distant sites, such as joints, may be involved.
Infected tissue injury appears to occur primarily as a consequence of the immune response with
an outpouring of neutrophils resulting in cellular destruction, pus and sometimes abscess formation which may eventuate in scar tissue formation, especially in the fallopian tubes. Although
there is a robust innate immune response, the adaptive immune response is less so. Although there
may be some suppression of the bacteria, immunity develops only rarely, if at all. Therefore,
repeated infections are frequent.
The bacteria attach to and gain entrance to the epithelial cells primarily through the expression
of Type IV pili and opacity protein (OPA) interaction. The ability to attach to spermatozoa is a critical feature facilitating infection due to the high bacterial load contained in the ejaculate.
The role of nasopharyngeal infection has become an area of increasing interest because of the
development of nucleic acid testing, which is more sensitive than culture in documenting an
infected individual. Since nasopharyngeal testing is currently infrequent, it is proposed that many
asymptomatic infections go untreated and yet are a source of transmission through orogenital sex.
It has been reported that oropharyngeal gonorrhoea is more treatment- resistant than genital infection. Due to increasing antibiotic resistance, only one class of antibiotics, cephalosporins, is now
recommended for treatment(35– 41).
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19.2.4.11 Clinical Features
Males are more frequently affected. Oropharyngeal lesions are usually asymptomatic but can
result in a persistently sore throat with ulcerations and flu- like symptoms. Nuclei acid amplification will assist in confirming infection(27, 28).
19.2.4.12 Management
Centres for Disease Control and Prevention (CDC) recommends a single dose of 500 mg of intramuscular ceftriaxone.
19.2.5 Oral andMaxillofacial Viral Infections
Oral viral infections include herpes simplex, herpes zoster and the coxsackie group of viruses.
Primary herpes simplex and coxsackie viral lesions affect children, while herpes zoster infection
affects older patients.
19.2.5.1 Herpes Virus Infections
The Herpes viruses are DNA viruses with eight subtypes causing oral cavity lesions. These include
Herpes simplex virus 1 and 2 (HSV- 1 and HSV- 2), Varicella- zoster virus (VZV), cytomegalovirus
(CMV), human herpes virus- 8 (HHV- 8 or Kaposi sarcoma- associated herpesvirus) and Epstein– Barr
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virus (HHV- 4). HSV and VZV cause disease in the young, while CMV causes oral ulcerations.
HHV- 8 causes Kaposi sarcoma in the immunocompromised. Epstein– Barr virus causes hairy leu-
koplakia in immunocompromised(42– 44).
19.2.6 Pathogenesis of HSV and VZV Infections
19.2.6.1 Herpes Viruses
The three alpha herpes viruses, HSV- 1, HSV- 2 and VZV, share some common features, both
pathogenetically and clinically, but differ in other aspects. All three are neurotropic viruses,
establishing latent residency usually in the neuronal nuclei of the dorsal root ganglia, although
other ganglia may also be infected. HSV- 1/HSV- 2 are transmitted through infected saliva, active
oral lesions and genital/orogenital sex. Although HSV- 1 has traditionally been associated with
orolabial infection and HSV- 2with genital infection, more recent studies have demonstrated that
crossover between sites is not that unusual, especially HSV- 1- producing genital lesions. Following
HSV infection of skin/mucosal epithelial cells leading to a symptomatic vesicular rash with
grouped blisters, the virus migrates along the sensory nerve fibres to establish latency in neuronal
nuclei. The cellular and humoral immune systems will control epithelial infection but will not
eliminate the latent infection. Although the mechanism for HSV latency is complex, one crucial
factor is the cellular internalisation of CD1d (a human gene), which is usually expressed on the
surface of the antigen- presenting cells. This lack of external expression inhibits an immune T- cell
response. The latent virus also downregulates viral gene expression. Since neurons do not divide,
active viral transcription is minimised.
VZV infection is transmitted through infected respiratory tract secretions or direct/indirect
contact with vesicular skin lesions. The initial infection, varicella, is better known as ‘chickenpox’. After establishing epithelial infection, the virus migrates preferentially to the trigeminal
and lumbosacral ganglia, although other sites may also be involved where it enters a latent
state. The mechanisms maintaining latency are not well understood, although the cellular
immune response is essential in keeping the virus in check. Under various cellular/physiological stress conditions, VZV undergoes replication and migrates along 1– 3 dermatome regions to
produce a symptomatic, vesicular rash, which may be associated with nerve pain. Disseminated
infection may be seen with immunosuppression. The development of the VZV vaccine in 1995
dramatically changed the course of the initial infection in children, significantly reducing
morbidity/mortality. To what extent the latent state exists after vaccination or to what extent it
might be expressed is unclear, although the incidence of shingles in children is significantly
reduced if vaccinated(45– 51).
19.2.6.2 Herpes Simplex Infections
HSV- 1 occurs in children, usually as a subclinical infection. Only 1% of the children manifest clinical symptoms resulting in primary herpetic gingivostomatitis. The most common form of transmission is direct contact with oral secretions. Research has shown that viral shedding may occur
without clinical lesions.
19.2.6.3 Clinical Features of HSV
Children present with fever, malaise and cervical lymphadenopathy of two to three days duration.
Oral lesions appear as painful ulcerations and vesicles with gingivostomatitis (Figure 19.9).
Associated bleeding of the gingiva may be noted.
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Figure19.9 Primary herpetic
gingivostomatitis presenting as
erythema and pain in the gingiva.
19.2.6.4 Management of Primary HSV
The diagnosis is usually based on clinical appearance. Treatment of fever is managed with antipyretics
such as acetaminophen. Aspirin is avoided in children. The lesions heal entirely in about 10days
in patients with normal immune status. Immunosuppressed individuals may be treated with
antivirals such as acyclovir or valacyclovir.
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19.2.6.5 Secondary Herpetic Stomatitis andHerpes Labialis
Recurrence in the form of secondary herpetic stomatitis/herpes labialis is due to the reactivation
of the dormant virus in the trigeminal ganglion. The predisposing factors include changes in
ambient temperature, immunosuppression, uncontrolled diabetes, stress and following dental
treatment(45– 51).
19.2.6.6 Clinical Features
Oral lesions occur on the keratinised mucosa of the lips, gingivae and hard palate, initially as
grouped vesicles with prodromal symptoms of tingling and pain. The blisters will rupture resulting
in grouped ulcerations (Figure19.10). Herpes labialis shows similar vesicles on the lips (Figure19.11
Figure19.10 Secondary herpes
presenting as grouped ulceration on
the palate.
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Figure19.11 Herpes labialis
presenting as grouped vesicles on the
left lip.
Figure19.12 Herpes labialis
presenting as a bulla and swelling on
the left lip.
and Figure 19.12). When the vesicles and ulcerations are weeping, they are highly infectious.
Reactivation lesions occur at the same sites in the oral cavity. The diagnosis is established based on
clinical features.
19.2.6.7 Management
Most patients usually need no treatment, but if they are immunosuppressed, they require systemic
acyclovir therapy. Topical antiviral therapy, such as penciclovir or acyclovir, used during the
prodromal period, may be helpful. It is important to note that treatment with acyclovir, either for
primary or secondary herpetic lesions, should be initiated within three days of the onset of symptoms.
19.2.7 Herpes Zoster (Varicella Zoster) Infections
Chickenpox is the primary infection caused by the VZV occurring in children as a rule. The patients
may present with systemic signs of infection, fever, malaise and lymphadenopathy. The cutaneous
lesions are vesiculopapular with pruritus. Oral lesions can occur on the palate and tonsillar pillar.
19.2.7.1 Varicella Zoster (Shingles)
Varicella Zoster, or shingles, occurs mainly in older patients with a history of chicken pox, presenting with lesions on the facial, thoracic or lumbar dermatomes. The oral findings seen in shingles
are, characteristically, painful vesicles and bullae rupturing over time, causing ulceration
(Figure19.13). The prodromal features in the oral cavity resemble odontalgia. The unilateral
distribution of vesicles, bullae and ulcerations helps diagnose shingles(45– 47).
t.me/Dr_Mouayyad_AlbtousH
Figure19.13 Shingles presenting as
unilateral painful ulceration on
the palate.
19.2.7.2 Management
Most healthy patients require only supportive care, while the immunosuppressed may need
acyclovir. Post- herpetic neuralgia and Ramsay- Hunt syndrome are complications of oral shingles.
19.2.7.3 Coxsackie Group ofVirus Infections
Coxsackieviruses are divided into A and B. Group A coxsackieviruses tend to infect the skin and
mucous membranes. Oral infections include herpangina and hand, foot and mouth disease
(HFMD). Both groups can cause non- specific febrile illnesses, rashes, upper respiratory tract infections and aseptic meningitis.
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19.2.7.4 Herpangina
Herpangina is an enterovirus infection that infects the gastrointestinal tract. Herpangina clinically
manifests as an acute febrile illness with small ulcerative or vesicular lesions in the posterior oropharynx. Infection is highly infectious. Herpangina is seen mainly in children up to 10 years of age but may
affect all ages, from infants to young adults. Herpangina is a self- limiting infection.
19.2.7.5 Aetiology andPathogenesis
The implicated etiological agents of herpangina include coxsackie A16 virus, coxsackie B virus and
enterovirus 71 virus serotypes. Infection typically spreads via the faecal– oral route or respiratory
droplets(52).
19.2.7.6 Clinical Features
Symptoms include sudden fever, sore throat, headache, loss of appetite and often neck pain. Within
two to four days, greyish lumps of 1– 2 mm in diameter form and develop into vesicles surrounded
by redness. Over the next 24 hours, these become shallow ulcers of 3– 5 mm in diameter and heal
in one to seven days. These lesions most often appear on the tonsillar pillars and the soft palate,
tonsils, uvula (Figure19.14) or tongue(52).
19.2.7.7 Management
A diagnosis is made from clinical signs and symptoms. Treatment is usually supportive. The disease is self- limiting and usually runs its course in less than a week.
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Figure19.14 Herpangina. Shallow
ulcers on the soft palate in a patient
with herpangina. Sterenau/
Wikimedia Commons/CC BY- SA 4.0.
19.2.7.8 Hand, Foot andMouth Disease
HFMD is a common viral childhood disease. HFMD is a common infection caused by a group of
enteroviruses(53).
19.2.7.9 Aetiology andPathogenesis
Coxsackievirus A 16 and Enterovirus 71 are the most common etiological agents. HFMD is highly
contagious. Nasopharyngeal secretions, including saliva and nasal mucus, transmit infection.
19.2.7.10 Clinical Features
The illness usually begins with one or all of the following: fever, sore throat, loss of appetite and
lethargy. However, many children remain well in themselves despite the rash. Blisters on the tops
of the hands, feet and/or palms, and soles (Figure19.15a) usually appear one to two days following
the fever. Small painful vesicles and ulcers may develop in and/or around the lips and mouth
(Figure19.15b) and the throat. The incubation period is typically 3– 6days, and children remain
infectious until the blisters have ruptured and healed (usually 7– 10days).
19.2.7.11 Management
HFMD is usually diagnosed clinically. Lesions on the hands, feet and mouth are distributed
symmetrically. Specific treatment is not usually required for HFMD; the focus should be symptomatic care.
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(a) (b)
Figure19.15 (a) Hand foot and mouth disease. Rash on the hand and feet of a 36- year- old man.
KlatschmohnAcker/Wikimedia Commons/CC BY- SA 3.0. (b) Hand foot and mouth disease: Facial skin
and lip lesions in hand, foot and mouth virus disease in an 11- month- old male. MidgleyDJ/
Wikimedia Commons/CC BY- SA 3.0.
19.2.8 Human Papillomavirus (HPV) Infections
There are many genotypes of HPV implicated in benign and malignant lesions. Low- risk mucosal
HPV 6 and 11 cause papillomas and condylomas, while HPV 13 and 32 are associated with focal
epithelial hyperplasia (Heck disease). Genotypes 16 and 18 are responsible for some bases of the
tongue, tonsillar and oropharyngeal squamous carcinomas. Transmission of the virus occurs by
contact either sexually or non- sexually, auto- inoculation or salivary transfer(54).
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19.2.8.1 Pathogenesis of HPV Infections
Over 150 types of HPV have been identified, although far fewer(14) have been implicated in causing malignant neoplasia. HPV has been divided, for pathogenetic purposes, into ‘low- risk’ and
‘high- risk’ types. The most significant difference between low- and high- risk types is the ability of
the high- risk type to integrate their DNA into the host genome. Transmission is person– person
through micro- abrasions where the virus gains access to the basal keratinocytes and establishes
low- copy infection in these ‘stem’ cells. This protects the virus somewhat from the immune system’s response. The virus only begins replication when the basal cells begin differentiation and
maturation. The virus is shed in high copy as the squamous cells reach the surface of the mucosa
or skin.
The proliferative effect of HPV lies primarily in the protein products produced by the viral oncogenes E6 and E7. These proteins interact with the protein products of the tumor suppressor genes
p53 and retinoblastoma, respectively, to inhibit their function allowing unchecked cellular division
and mutations to occur. HPV infection is cleared or kept in check by the cellular immune system.
Defects in this system, such as those seen in AIDS, greatly enhance the oncogenic potential of
the virus.
High- risk HPV types are estimated to be the cause of 99% of cervical cancers (there is no evidence of significant genetic predisposition for cervical cancer), 90% of anal cancer, 65% vaginal
cancers, 50% vulvar cancers and 45– 90% oropharyngeal cancers. Although 14 HPV types are considered high- risk, 16 and 18 are the most important. Low- risk types are site- specific and cause
common skin warts, oral warts and laryngeal papillomatosis. Anogenital condyloma is usually
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