Mucositis

Mucositis is a form of mucosal barrier injury, characterized clinically by oral erythema, ulceration, and pain (Figure 10.1). It is a common complication of therapeutic procedures involving chemotherapy, radiotherapy, or both, and in patients receiving bone marrow transplants, which are damaging to the epithelial cells (Scully et al., 2003). Published evidence points toward the activated innate immune responses with reactive oxygen species (ROS)–mediated inflammatory cascade and dysbiotic relationship of oral microflora playing the central role in pathogenesis oral mucositis (Chen et al., 2020). Commonly, the oral manifestation of cancer therapy is a generalized stomatitis whose association with the primary underlying infection is more obvious (for further details, see “Oral mucosal bacterial infections” later in this chapter). Secondary bacterial infections may also arise in bite wounds, and in viral stomatitis and aphthous ulcerations, and lead to streptococcal bacteremia in any area of the mouth, such as the tongue, buccal mucosa, floor of the mouth, palate, and gingiva.

In addition, there is increased occurrence of opportunistic pathogens such as aerobic Gram‐negative bacilli (AGNB), including enterics (Escherichia coli, Enterobacter spp.) and pseudomonads, as well as yeasts (Candida spp.), in mucositic lesions. If xerostomia prevails, oral health can be seriously compromised (Sonis, 2007). Xerostomia can lead to decreased clearance of oral microorganisms, along with decreased pH, resulting in increased colonization by lactobacilli, Candida albicans, and other opportunistic microorganisms, such as Staphylococcus aureus, enterococci, and enteric rods (Pajukoski et al., 2001). The simple ways to help alleviate and prevent the symptoms of xerostomia include drinking water to hydrate tissues and cleanse the mouth just as saliva does; using oral mouthwashes, gels, sprays, and artificial saliva; use of oral care products specifically formulated for dry mouth (containing no detergents, with a mild taste and containing antimicrobial proteins); sugarless chewing gum and hard candies; as well as some commercially available lozenges and sprays. Vitamin C tablets have also been recommended to stimulate salivary flow as it acts as a reducing agent, breaking disulfide bonds between cysteine residues in proteins, leading to a decrease in saliva viscosity. Alcohol, caffeine, and smoking should be avoided as they can further irritate and dry out the mucosa (Ristevska et al., 2015).

Recurrent aphthous stomatitis

Otherwise known as canker sore, this is the most common nontraumatic type of oral ulcer (Figure 10.2). The sore is often mistaken for a virus infection (herpes simplex), and is differentiated by appearance only in the nonkeratinized mucosa, such as the labial mucosa, buccal mucosa, ventral tongue, and vestibule (Ship et al., 2000). Based on their clinical appearance, aphthous ulcers can be classified as minor (<1 cm in diameter), major (>1 cm diameter), and herpetiform, in which multiple minute ulcers might coalesce to form plaques (Woo and Sonis, 1996). Most aphthae are of the minor variety and heal within 10 days. Factors predisposing to this condition include stress, poor nutrition, infection, hormonal fluctuation, and trauma (McCullough et al., 2007). The disease is usually self–limiting, and nutritional supplementation, alleviation of stress, and warm saline rinses have been found to help in its management. Orthodontic attachments are considered to be one among the main reasons for triggering its appearance. AlDahash et al. (2020) reported that more than half of the orthodontic patients (out of 196 patients in the study) developed oral ulcers, which mainly develop due to trauma. If the ulcers appear following orthodontic bonding, the irritating attachment can be either covered with orthodontic wax or removed to prevent further irritation aggravating the process. The patient should be well instructed in what to do in such instances before leaving the office. It is suggested that primary care practitioners should be educated to provide adequate supportive management for oral ulceration caused by orthodontic fixed appliances.

Burning mouth syndrome

Scala et al. (2003) defined burning mouth syndrome as a chronic pain syndrome that mainly affects middle‐aged/older women with hormonal changes or psychological disorders. This disorder reduces the quality of life, especially with large psychological implications. Although the etiology of the syndrome remains unclear, the presence of salivary gland dysfunction or systemic diseases, such as diabetes, makes a patient prone to it. In addition, patients with chronic pulmonary diseases, asthma, and rheumatic fever can develop epithelial atrophia, glossitis, xerostomia, and burning mouth syndrome. All these symptoms are due to superimposing fungal and bacterial infections that follow adverse reactions to immunosuppressive medications and reduced salivary flow. Chemotherapeutic agents also have the potential to induce changes in the oral epithelium, leading to superinfection (Lopez‐Jornet et al., 2010).

Reducing the chronic pain is still a quest. In a recent network meta‐analysis, four pain‐relieving strategies were investigated: photobiomodulation therapy, alpha‐lipoic acid, phytotherapics, and anxiolytics/antidepressants (Alvarenga‐Brant et al., 2023). Only the anxiolytic clonazepam seemed to relieve pain. Pain‐relief measures such as cold beverages, ice chips, and avoidance of irritants such as tobacco, spicy or acidic foods, and alcohol are considered home remedies for burning mouth syndrome.

Staphylococcus aureus

Staph. aureus is a relevant pathogen in symptomatic oral mucosal lesions. Until then, if isolated, it was considered to be a part of a transient microbial flora that seems to increase with advanced age. This bacterium is frequently isolated from infections of the facial skin and lips (Faergemann and Dahlèn, 2009). Angular cheilitis is commonly secondarily infected by Staph. aureus (Figure 10.3), with a particular predilection in young individuals and those with dry skin. If a healthy individual harbors high numbers of salivary Staph. aureus (>100,000 colony‐forming units/mL) over an extended period, they are considered to be healthy carriers (Dahlèn, 2009). Infected medical and dental professionals pose a risk of transmitting the pathogen to other individuals visiting them. A serious concern in this regard is the infection caused by methicillin‐resistant Staph. aureus. Treatment of infection with Staph. aureus typically includes penicillinase‐stable penicillins, such as cloxacillin, dicloxacillin, or flucloxacillin, because of the risk of developing resistant strains (Dahlèn, 2009).

Enterococci

Enterococci, particularly Enterococcus faecalis, are commonly involved in oral mucosal infections. These infections occur sporadically in the oral mucosa and around the teeth in healthy individuals, but enterococci are a typical opportunist in immunocompromised patients, often in combination with other opportunists such as enterics and yeasts (Dahlén, 2009).

Enterococci were known as streptococci for a long time, and were classified as Lancefield group D. However, owing to their survival in harsh environments (temperature, dryness, salts, dyes, antiseptics, and antibiotics), they were classified as a new genus, which normally resides in a significant part of the upper intestine and is resistant to bile salts. It is spread to the oral cavity by vomiting and fecal contamination. Enterococci are commonly used in food processing, for instance in cheese, and their spread through food cannot be excluded (Templer et al., 2008). It is resistant to penicillin V and clindamycin, and broad‐spectrum penicillins such as ampicillin and amoxicillin remain the drugs of choice (Dahlén et al., 2009).

Enterococci are of particular interest to dentists due to their persistence even after treatment of endodontically involved teeth. Studies have elucidated the presence of Enterococcus faecalis in root‐filled teeth with persistent lesions, and confirmed its ability to invade dentinal tubules and to survive for a prolonged period under adverse conditions such as starvation, high pH of calcium hydroxide medication, and adhesion of E. faecalis to collagen (Ørstavik and Haapasalo, 1990; Evans et al, 2002). A study has confirmed that demineralization and apical resorption at root cementum play a significant role in penetration of E. faecalis into root cementum. The severity of infection is directly proportional to the depth of penetration of E. faecalis into root cementum (Halkai et al., 2014).

AGNB, including E. coli, Enterobacter spp., Klebsiella spp., Proteus spp., and more, are typically involved in human opportunistic infections, including oral mucosal infections. AGNB are part of the normal resident intestinal flora, frequent participants in nosocomial infections, and cause the classic opportunistic infections affecting the oral cavity. Transmission of these bacteria to the oral cavity can occur through poor personal hygiene, or through food and drinking water. They are frequently associated with periodontitis and peri‐implantitis. They rapidly become drug resistant, and the drug to be used should be selected only after a susceptibility test, although the choices are more or less exhausted. Quinolones (ciprofloxacin, norfloxacin) are the drugs of choice for the infections with AGNB, but should be prescribed only under proper medical supervision. Empirically, it has been observed that it is difficult to harm the bacteria and to heal the infection as long as the patient is in a compromised state (Dahlèn et al., 2009).

Acute necrotizing ulcerative gingivitis

Acute necrotizing ulcerative gingivitis (ANUG) is an infectious disease of the gingiva (Figure 10.4) caused by a mixed flora consisting of spirochetes, fusobacteria, Prevotella intermedia, Veillonella spp., and streptococci (Rivera‐Hidalgo and Stanford, 1999; Dufty et al., 2017). This disease often results in gingival bleeding, ulceration, and episodes of severe pain. Factors predisposing to the condition include stress, smoking, malnutrition, and poor oral hygiene (Horning and Cohen, 1995). ANUG is common in patients with human immunodeficiency virus (HIV) infection and in undernourished children (Aaron and DeBlois, 2022). If it is associated with rapid alveolar bone loss, it is categorized as necrotizing ulcerative periodontitis, in which severe deep, aching pain is a characteristic feature (Murayama et al., 1994).

The treatment of this condition is directed toward debridement of affected soft tissues and teeth, along with antibiotic therapy (Rivera‐Hidalgo and Stanford, 1999). A referral to a competent periodontist, if an orthodontist encounters such a condition, can be of great value in its management.

Acute pharyngitis

Acute pharyngitis, otherwise known as a sore throat, can have either viral or bacterial etiology. The most common bacterium involved is Streptococcus pyogenes (beta‐hemolytic streptococci or group A streptococci [GAS]; Peterson and Thomson, 1999). During the acute phase of the disease, these microorganisms can be detected in the saliva. It is among the 20 most common diseases that occur without any age, sex, or racial predilection. The exotoxins produced in this infection by the beta‐hemolytic streptococci act as superantigens that upregulate the T lymphocytes, prompting the release of proinflammatory cytotoxins, and have synergistic effects along with the lipopolysaccharides of the extracellular matrix. The superantigens then evade the pharyngeal immune response, resulting in proliferation of Strep. pyogenes. The most common symptoms of acute pharyngitis are sore throat, odynophagia, headache, nausea, vomiting, and abdominal pain. On physical examination, the patient may have fever, tonsillopharyngeal erythema, exudates, beefy red swollen uvula, anterior cervical tender lymph nodes, petechiae on the palate, and scarlatiniform rash. The gold standard diagnostic test for acute pharyngitis is throat culture, but unfortunately this test takes 24–48 hours to be completed (Buensalido and Nepomuceno, 2022). Instead, rapid antigen detection tests (RADTs) with commercial kits or nucleic acid amplification (via polymerase chain reaction, PCR) for group A Streptococcus (GAS) are available, but these are relatively expensive. Samples for throat culture or RADTs should be obtained from the posterior pharynx or the tonsils. Imaging studies have no role in the diagnosis of this disease.

Oral penicillin V, 1.2M IU orally (PO) every 12 hours for 8–10 days, is the drug of choice for this disease. Amoxicillin remains a better alternative, but tetracyclines or sulfamethoxazole should not be used due to the high resistance rate. In the case of penicillin allergy, cephalosporins, which contain a beta‐lactam ring, can be used with caution. In rare cases, the pharyngitis spreads to adjacent areas, forming abscesses requiring surgical drainage. Surgery is an option, especially if the history reveals recurrent tonsillitis (Brook, 2009). The patient should be allowed to eat a normal diet and drink warm liquids that provide symptomatic relief (Buensalido and Nepomuceno, 2022). An otorhinolaryngologist should be consulted for local suppurative complications such as peritonsillar abscess and mastoiditis. An infectious disease expert should be consulted for patients with immunocompromising conditions, or when HIV infection is suspected.

A rare but often underdiagnosed form of an oropharyngeal infection is the Lemierre syndrome, an infection caused by Fusobacterium necrophorum (Karkos et al., 2009), which occurs in adolescents and young adults as a complication of tonsillitis (“sore throat”), especially in recurrent forms (Klug et al., 2009). It is life‐threatening if neglected and is characterized by acute venous thrombosis of the vena jugularis interna and septic emboli to the lungs (Pleming et al., 2022). It should be treated aggressively with antibiotics (metronidazole) and/or surgery (Ridgway et al., 2010).

Peritonsillar abscess

Peritonsillar abscess (PTA) is a localized accumulation of pus in the peritonsillar tissues, which forms as a result of suppurative tonsillitis (Figure 10.5). The peritonsillar space is bounded by the tonsillar pillars antero‐posteriorly, the piriform fossa inferiorly, and the hard palate superiorly. The area can be infected with both aerobic (S. pyogenes) and anaerobic (Prevotella and Peptostreptococcus spp.) bacteria. The infection begins superficially, progresses into deep tissues, and has no age, sex, or racial predilection. The symptoms include sore throat, dysphagia, and change in the voice, headache, malaise, fever, neck pain, otalgia, and odynophagia. Physical examination reveals mild to moderate discomfort, fever, tachycardia, dehydration, drooling of saliva, trismus, cervical lymphadenitis, asymmetrical tonsillar hypertrophy, inferior and medial displacement of a tonsil, contralateral deviation of the uvula, and erythema and exudates from the tonsils. Complete blood count (CBC) and electrolytes, heterophile antibody test (to rule out suspicion of infectious mononucleosis), pus culture sensitivity from needle aspirate of the abscess, and C‐reactive protein blood culture might be required in patients presenting with features of sepsis (Gupta and McDowell, 2022). Patients are often managed in the outpatient department, unless they show signs of airway obstruction, sepsis, toxicity, or other complications. Along with incision and drainage, analgesics, and throat wash, antibiotics are typically prescribed for complete resolution of PTA. A combination therapy of penicillin and metronidazole is generally preferred. Clindamycin is a good choice in people with penicillin allergy. Consultation with an otorhinolaryngologist should be sought whenever a PTA is recognized, before, during, or after the onset of orthodontic treatment, for proper management of these patients. Help from an anesthetist might sometimes be required if the patient develops difficulty in maintaining airway patency (Flores et al., 2022).

Suppurative parotitis/sialadenitis

Acute suppurative parotitis (ASP) is an infectious process of the parotid gland, usually seen in elderly people who are dehydrated, malnourished, or recovering from surgery (Raad et al., 1990). Although the infection is usually confined to the parotid capsule, it can occasionally spread to cervical fascial planes. Immunosuppression states such as diabetes, alcoholism, HIV infection, autoimmune disorders (e.g. Sjögren syndrome), poor oral hygiene, decreased salivary flow, postsurgical dehydration, sialolithiasis, tumors, or foreign bodies in the duct can increase the risk for ASP. The most common clinical manifestation of ASP is an indurated, erythematous, warm swelling of the cheek. The patient will also have mild fever along with pain. Intraorally, the orifice of Stensen’s duct will be red, and pus may be expelled while palpating it (Brook, 2009). In rare instances, facial nerve dysfunction may be the end result (Noorizan et al., 2009). Diagnosis can be established by a thorough clinical examination, along with CBC and chemistry, and culture and sensitivity. Radiological evaluation should include computed tomographic (CT) scanning with an intravenous contrast medium, ultrasound scanning for detection of abscesses, and also sialography.

Traditionally, the main causative agent of ASP is thought to be Staph. aureus. However, Brook et al. (1991) isolated strict anaerobes such as Peptostreptococcus spp. and Gram‐negative anaerobic rods from ASP lesions. The key treatment for ASP is rehydration and supportive treatment, which should include intravenous (IV) fluids, nutritional support, a warm compress, sialogogs, good oral hygiene, and antibiotic therapy. The drugs of choice in ASP are penicillin, first‐generation cephalosporins, or clindamycin; however, more important is the selection of the drug in relation to the causative agent. Intraductal injections of antibiotics usually lead to improvement in the condition. If there is lack of improvement after 3–5 days of antibiotic treatment, and if there is facial nerve involvement or involvement of adjacent vital structures, surgical opinion must be sought; usually incision and drainage via a standard parotidectomy incision will be the preferred treatment. Proper follow‐up, repeated clinical examinations, fine needle biopsy, and imaging should be performed on a regular basis to ensure the absence of any neoplastic changes in the gland (Brook, 2009).

Rhinitis and sinusitis

Rhinitis implies a heterogeneous group of nasal disorders, characterized by sneezing, nasal itching, rhinorrhea, and nasal congestion, which can be allergic, nonallergic, infectious, occupational, or hormonal in nature. Dykewicz and Hamilos (2010) suggested that in 44–87% of patients with rhinitis, the condition is either allergic or nonallergic in nature. Common allergens causing the problem include proteins and glycoproteins in airborne dust, mite fecal particles, cockroach residues, animal dander, molds, and pollens. Within minutes of inhalation, these allergens are recognized by immunoglobulin (Ig)E antibody bound to mast cells and basophils, causing degranulation and release of preformed mediators, such as histamine and tryptase, and inflammatory mediators, such as leukotrienes and prostaglandin D2. These mediators cause plasma extravasation from blood vessels, with consequent edema, pooling of blood in cavernous sinusoids, and occlusion of nasal passages. These developments are accompanied by active secretion of mucus from glandular and goblet cells, and release of histamine, which manifests as itching, rhinorrhea, and sneezing. In late stages a prominent nasal congestion develops (Rosenwasser, 2007). Rhinitis is often accompanied by nonnasal symptoms, such as allergic conjunctivitis, and it is frequently associated with allergic asthma, pathophysiologically and epidemiologically.

Diagnosis should include evaluation of all specific symptoms and the pattern of occurrence of the symptoms (infrequent/intermittent, seasonal and perennial) along with identification of predisposing factors, previous responses to medication, and coexisting diseases. A handheld otoscope or head lamp with nasal speculum permits viewing of the anterior third of the nasal airway, including the anterior tip of the inferior turbinates. Determination of specific antibody involvement can be made through skin testing, which has high sensitivity, and at the same time is simple, easy, and can be rapidly performed (Wallace et al., 2008). The main treatment for rhinitis is directed toward avoidance of the inciting factors, such as allergens and irritants. A multitude of drugs are available for the management of this disease, including antihistamines, corticosteroids, oral and nasal decongestants, and leukotriene receptor antagonists. For the orthodontist, making a referral to an otorhinolaryngologist is an important step in managing the condition. The specialist will determine an individualized treatment approach for each patient, based on their responses, preferences, and the cost‐effectiveness of the treatment options (Dykewicz and Hamilos, 2010).

Sinusitis or rhinosinusitis is defined as inflammation of the nose and the paranasal sinuses, and is usually infectious in nature (Meltzer et al., 2004). Typically, from a microbiological point of view sinusitis follows a characteristic pattern, starting as a viral infection, followed by superinfection with facultative bacteria after a couple of days, and after one week showing anaerobes as the predominant organisms (Brook, 2009). Acute rhinosinusitis is diagnosed when there is purulent nasal drainage of up to four weeks, accompanied by nasal obstruction, facial pain, pressure, fullness, or both. The pain is usually described as being dull, or felt as pressure in the upper cheeks, between the eyes, or in the forehead. The most common bacteria isolated from sites of acute rhinosinusitis are H. influenzae, Strept. pneumoniae, Moraxella catarrhalis, and sometimes Staph. aureus. Disturbances in the sense of smell, which occur in sinusitis, can be either partial (hyposmia) or complete (anosmia), and are usually associated with mucosal thickening or opacification in the anterior ethmoid sinuses, which can be seen as hyperdense areas in an orthopantomograph and CT images (Dykewicz and Hamilos, 2010; Figure 10.6). An initial period of watchful waiting without initiation of antibiotics is the best treatment for acute rhinosinusitis.

An important aspect of the diagnosis of sinusitis is to differentiate between bacterial and viral causes, as only bacterial infections respond to antibiotic therapy. Clinical signs suggestive of bacterial infection include symptoms that last for more than seven days. Patients with more severe forms of the disease can be treated with antibiotics, and if this approach is decided on, amoxicillin is the drug of choice. If the patient is allergic to penicillin, a combination of trimethoprim and sulfamethoxazole (not used in Scandinavian countries) or macrolide antibiotics can be considered. Intranasal decongestants can be prescribed, but for no more than three days, to avoid rebound decongestions (Brook, 2010). In contrast to acute rhinosinusitis, chronic rhinosinusitis (CRS) is defined as an inflammatory condition involving the paranasal sinuses and nasal passages over a minimum duration of 8–12 weeks, despite attempts at medical management (Meltzer et al., 2004). Superimposed bacterial infections further complicate the process. The four major symptoms of CRS are anterior, posterior, or mucopurulent drainage; nasal obstruction or blockage; facial pain, pressure, or fullness; and decreased sense of smell (Meltzer et al., 2004). The bacteria can also form a biofilm over the sinus epithelium. Sequestration of bacteria within biofilms allows the bacteria to resist antibiotic treatment and persist as a low‐grade infection within the sinus mucosa. Topical corticosteroid nasal sprays are preferred for all forms of CRS, along with antihistamines for underlying allergic causes, and antibiotics (penicillin V, amoxicillin, or cloxacillin) are prescribed when nasal purulence is present (Dykewicz and Hamilos, 2010). Functional endoscopic sinus surgery (FESS) is the management of choice of chronic refractory rhinosinusitis.

Epiglottitis

Epiglottitis, or inflammation of the epiglottis, is a medical emergency, as it can lead to airway obstruction and death. It follows oral infection with H. influenzae (Peterson and Thomson, 1999). This microorganism is abundant in the oral mucosal surfaces and in dental plaque. However, certain capsulated strains are considerably more virulent and are thought to be a major pathogen in the respiratory tract, causing otitis, sinusitis, and pharyngitis. Other agents such as Streptococcus pyogenes, S. pneumoniae, and S. aureus have been implicated. In immunocompromised patients, Pseudomonas aeruginosa and Candida have been named. The signs of epiglottitis, often referred to as the four Ds, include dysphagia, dystonia, drooling, and distress, and it is often associated with fever (38 °C/100.4 °F or higher) as well.

An oropharyngeal exam is usually not performed to evaluate a suspected case of epiglottitis because manipulation of the oral cavity may lead to disaster, such as respiratory arrest. This diagnosis is primarily one of clinical suspicion. A lateral neck radiograph will show swelling of the epiglottis, also referred to as the “thumb sign.” A flexible fiberoptic laryngoscopy can theoretically be performed (which will show cherry‐red and swollen epiglottis and arytenoids; Jenkins and Saunders, 2009), but only in a very controlled setting such as the operating room due to the risk of inducing laryngospasm. This is almost never done. If clinical suspicion for acute epiglottitis exists, the patient should be taken urgently to the operating room for airway examination under the most optimal conditions possible. Ultrasonography has been mentioned as another way to evaluate these patients, revealing an “alphabet P sign” in a longitudinal view. A CBC with differential, a blood culture, and an epiglottal culture should only be obtained in patients with a secured endotracheal tube. CT scan of the neck is rarely needed and can precipitate disaster. The chest x‐ray may reveal concomitant pneumonia in 10–15% of patients (Guerra and Waseem, 2021).

This condition requires immediate medical attention, with urgent endotracheal intubation, to protect the airway. This procedure should be performed by a competent anesthetist, with the help of a respiratory therapist and otorhinolaryngologist (D’Agostino, 2010). In addition, the patient should be given antibiotics, such as ceftriaxone or chloramphenicol, either alone or in combination with penicillin or ampicillin, for streptococcal coverage.

Actinomycosis

Actinomycosis is a chronic disease characterized by the formation of abscesses, fibrosis, and draining sinuses (Figure 10.7). The causative agent is the non‐spore‐forming anaerobic or microaerophilic bacterial species of the genus Actinomyces (most commonly A. israelii), which are normal inhabitants of cervicofacial, thoracic, and abdominal areas (Rivera‐Hidalgo and Stanford, 1999). A similar infection, nocardiosis, is caused by the related facultative Nocardia spp. Cervicofacial actinomycosis is the most common form of the disease (Laskaris, 1996). Actinomyces get access to the host tissues when there is an interruption in the mucosal barrier, caused by procedures such as tooth extraction and endodontic infection and treatment. Following this initial superficial invasion, the infection spreads deep into the tissues and a hard, slow‐growing, relatively tender swelling may form with multiple drainage areas or sinus tracts. The discharge from these tracts typically contains the visible yellowish colonies of the microorganisms and are termed “sulfur granules.” If left untreated, osteomyelitis with extensive bone destruction will result (Feder, 1990; Brook, 2008).

Diagnosis can be confirmed by isolation of Actinomyces species from clinical specimens. Indirect immunofluorescence can also be utilized for this purpose (Gohean et al., 1990). The gold standard test for diagnosis is tissue biopsy culture with anaerobic pus cultures. Swabs from the infected sites should be avoided. Cultures can be falsely negative; Gram stain may demonstrate the presence of branched, beaded, Gram‐positive filamentous rods with sulfur granules, which helps in making a preliminary diagnosis (Sharma and Hashmi, 2022). Actinomyces species are susceptible to several antibiotics such as penicillins, tetracyclines, erythromycin, clindamycin, and ciprofloxacin. Antibiotics need to be given at high doses for long periods (2–6 weeks) for a complete cure. Surgery might be required in some cases to aspirate or surgically drain the abscesses (Brook, 2008). Consultation with an oral medicine specialist and with an otorhinolaryngologist will be of great help in managing these patients.

Gonorrhea

Gonorrhea is the most frequently encountered sexually transmitted disease, caused by Neisseria gonorrhea, a nonmotile spherical oval coccus. The organism is aerobic, Gram negative, and cannot penetrate an intact stratified squamous epithelium, such as that of the skin and oral mucous membrane (Rivera‐Hidalgo and Stanford, 1999). However, it can directly invade the urethra, cervix, pharynx, and conjunctiva, because of the presence of columnar and transitional epithelium in these areas. From these sites, infection may spread readily along mucosal surfaces, or systemically, resulting in disseminated disease (Guinta and Fiumara, 1986). Humans are the only known hosts for N. gonorrhea, and the organism has been cultured from saliva of infected individuals. There is oral, pharyngeal, and tonsillar involvement in 20% of patients with gonorrhea. The tonsils are red and swollen, with grayish exudates. Lesions in the oral mucosa may appear fiery red and edematous, and occasionally there may be painful ulcerations. Diagnosis is established by culture and identification of N. gonorrhoeae (Laskaris, 1996; Bruce and Rogers, 2004). Sugar fermentation tests aid in species differentiation, and fluorescent antibody techniques have been used for rapid identification of gonococci. Penicillin is the drug of choice for this infection, and in drug‐resistant patients ceftriaxone and ciprofloxacin have been used successfully (Chue, 1975).

Tuberculosis

Tuberculosis is a chronic infectious disease and spreads almost exclusively via droplets from a person with active disease. Tuberculosis is still among the most life‐threatening infectious diseases in humans and one‐third of the world’s population comes into contact with the disease at some stage in their life (Kakisi et al., 2010). It commonly affects the lungs, but can occur in any part of the body, and is characterized by formation of granulomas with caseation necrosis caused by cell‐mediated response. Primary tuberculosis is seen in patients who have had no previous exposure to the disease and initially is predominantly subclinical. Secondary tuberculosis is seen in previously sensitized patients (Phalen et al., 1996). Oral lesions are rare (0.1–5%; Kakisi et al., 2010), but if they occur they appear as chronic, painless, irregular ulcers, with a vegetative surface covered by grayish or yellow exudates. The dorsal surface of the tongue is a common site of secondary tuberculous infection, followed by the palate, gingiva, buccal mucosa, and lips (Hale and Tucker, 2008). The Mantoux reaction following the injection of a dose of purified protein derivative (PPD) is the traditional screening test for exposure to tuberculosis. Diagnosis is reached based on the medical history, identification of acid‐fast mycobacteria in clinical specimens, a positive delayed hypersensitivity skin reaction to PPD, and chest radiograph findings, which include infiltrates or consolidations and/or cavities in the upper lungs with or without mediastinal or hilar lymphadenopathy (Ellner et al., 1988). A chest x‐ray is indicated to rule out or rule in the presence of active disease in all screening test–positive cases. Other diagnostic evaluation methods include acid‐fast staining–Ziehl‐Neelsen, culture, and the new generation of nuclear amplification and gene‐based tests, which enable identification of the bacteria or bacteria particles making use of DNA‐based molecular techniques.

Combination therapy is always indicated, and monotherapy should never be used for tuberculosis. A four‐drug regimen (usually including isoniazid, rifampicin, ethambutol, and pyrazinamide) for two or six months, along with vitamin B6 to prevent neural damage (neuropathies) caused by isoniazid, is the first‐line treatment for tuberculosis (Adigun and Singh, 2022).

If a patient has tuberculosis, all orthodontic procedures should be carried out under strict medical or pulmonologist supervision, in order to prevent the spread of the disease as well as its aggravation.

Leprosy

Leprosy, otherwise known as Hansen disease, is a chronic disease and is characterized by damage to the nerves and skin, resulting in deformities and disability. M. leprae is a Gram‐positive, acid‐fast, nonspore‐forming, nonmotile, pleomorphic bacillus, which causes four types of leprosy: indeterminate, tuberculoid, borderline, and lepromatous (Rivera‐Hidalgo and Stanford, 1999). Oral lesions have been demonstrated in tuberculoid, borderline, and lepromatous leprosy. The lesions present as nodules/lepromas that progress to necrosis and ulcerations. The ulcers may heal with scarring or progress to produce further tissue destruction. Lepromas are filled with M. leprae, and might occur in the palate, dorsum of the tongue, uvula, and lips. When left untreated, these lesions can cause extensive destruction of the oral tissues (Ghosh et al., 2009). The diagnosis is based on clinical signs such as anesthetic skin lesions and enlarged peripheral nerves, and laboratory techniques such as histopathological analysis using skin biopsies and PCR to detect M. leprae and M. lepromatosis DNA in tissue.

General treatment of leprosy usually involves multiple‐drug therapy (MDT) to ensure no microbial resistance. The treatment depends on the type of disease – for tuberculoid disease dapsone (100 mg daily) with rifampicin (600 mg daily) for 12 months; and for lepromatous disease dapsone, rifampicin, and clofazimine (50 mg daily) for 24 months (Bhandari et al., 2021).

Syphilis

Syphilis caused by the spirochete Treponema pallidum is a venereal disease, with a decreasing prevalence rate. Syphilis can be either congenital (when the fetus becomes infected in utero) or acquired (contracted by sexual contact, direct inoculation, or transfusion with fresh human blood). Early congenital syphilis may manifest itself as papulosquamous lesions of the skin and the oral mucous membranes. The lesions at the commissures of the lips, angle of the nose, and eyes heal with radiating scars called rhagades (Rivera‐Hidalgo and Stanford, 1999). Oral manifestations of late congenital syphilis include Hutchinson’s triad of deafness, interstitial keratitis, and malformed incisors, along with other dental anomalies such as hypoplastic molars with poorly developed cusps, called mulberry molars.

Acquired syphilis has three classic phases. Primary syphilis is characterized by chancre, a centrally ulcerated granulomatous lesion with a raised, indurated border; the lesion is painless and resolves within 2–8 weeks. Secondary syphilis is the systemic or disseminated phase and may occur 2–12 weeks after contact. Signs and symptoms consist of fever, headache, malaise, a symmetrical rash, and mucous patches in the oral cavity. The oral lesions appear as grayish‐white, glistening patches on the soft palate, tongue, and buccal mucosa, but rarely on the gingiva. After this the patient enters a latent stage and 30–40% of untreated patients develop tertiary syphilis, which includes multiorgan involvement. Gumma is the characteristic lesion in this phase and is seen in the hard palate. This phase is not infectious (Little, 2005).

Clinical examination and serological tests aid in the diagnosis of syphilis. Dark field microscopy can sometimes be useful when serological test results are negative but there is a high index of suspicion (Seigel, 1996