**2. Acute ulcerative lesions**

A short-lived oral ulcerative lesion which resolves in less than two weeks is considered as an acute oral ulcer and is commonly referred to as an "aphtha" [1, 2]. This word itself is attributed to Hippocrates which was used to describe disorders of the mouth in general back in his time (460–370 BC) [3]. In order to accurately diagnose and evaluate patients with acute ulcerative lesions, it is crucial that the physician is aware of the broad spectrum of possibilities that may cause these lesions. It is recommended to assess the history of the lesions first, meaning to question the patient regarding any periodic episodes, in order to exclude conditions which are characterized with recurrent oral ulcerations [2].

Clinically acute oral ulcers usually have an oval shape with an erythematous periphery due to the dilation of the blood vessels. Although commonly these are painful lesions, the pain is relatively weaker when the ulcer bed is layered with a yellowish fibro-membrane [2].

Most common acute oral ulcerations may be related to trauma (i.e., traumatic ulcers), chemotherapy (i.e. chemotherapy induced ulcers), necrotizing sialometaplasia, primary herpetic gingivostomatitis, herpes zoster infection, herpangina, hand-foot mouth disease, erythema multiforme, necrotizing ulcerative gingivitis, oral hypersensitivity reactions or plasma cell stomatitis [1, 6, 7].

*Traumatic ulcerations* are one of the most common oral ulcerative lesions [8]. If a traumatic ulceration is due to the mucosal irritation of natal or neonatal teeth at the ventral surface of the tongue, then it is called "Riga-Fede disease". Ulcerations due to thermal and electrical injuries most commonly occur in children and affect the lip and commissure areas. On the contrary, malformed or fractured teeth, ill-fitting dentures or overheated food are usually encountered in adults (**Figure 1**) [1, 9]. Traumatic ulcerations tend to heal within ten days once the etiologic factor is discarded [8].

#### **Figure 1.**

*Irritation fibroma of the right vestibular sulcus and an acute traumatic ulceration of the maxillary frenulum due to ill-fitting dentures.*

#### *Ulcerative Lesions of the Oral Cavity DOI: http://dx.doi.org/10.5772/intechopen.101215*

*Chemotherapy induced ulcers* are commonly observed in oral mucositis, which is one of the most frequent complications of chemotherapy in oncologic patients [10]. These erythematous and painful ulcerative lesions are due to the detrimental effects of chemotherapy on oral mucosal epithelial cells. Patients receiving chemotherapy for a malignancy have a 24.8–67% incidence rate for oral ulcerations [11]. This rate increases to almost 90% in patients with head and neck cancer, who receive both chemotherapy and radiotherapy for their oncologic condition. Cisplatin, 5-fluoruracil, docetaxel, paclitaxel, everolimus, tenserolimus, ridaforolimus, cetuximab, panitunumab, erlotinib, gefinitib, afatinib, lapatinib and dacomitinib are among the most common chemotherapeutic agents associated with chemotherapy induced oral ulcers [12–15]. The risk to develop mucositis rises when a patient receives both chemotherapy and radiotherapy. The incidence and the severity of oral ulcerative lesions vary in patients with different agents and therapeutic regimen [15]. Besides the overall clinical manifestations such as mucosal congestion, edema, and severe pain, co-infection may affect these patients' oral intake and disturb the smooth progress of chemotherapy. Co-infection may progress into a more severe systemic infection and cumulatively threaten the lives of the patients [11]. Treatments using granulocyte colony-stimulating factor, keratinocyte growth factor, honey intake or low-level laser therapy have been proposed as preventive measures for chemotherapy induced ulcers however a consensus regarding the most effective preventive option is still not established [10]. Among these preventive options, the only drug approved both by Food and Drug Agency (FDA) and European Medical Agency (EMA) is palifermin, and it is a keratinocyte growth factor. It is advised to administer to patients undergoing high doses chemotherapy and radiotherapy prior to their oncologic treatment. Once oral ulcerations develop, it is important to prevent serious nutritional deficiencies due to inadequate food intake and consider parenteral nutrition options [15]. Current guidelines suggest morphine to provide analgesia for pain in these patients [16]. Moreover "magic" mouthwashes have also been formulated containing anesthetics, antacids and diphenhydramine. Formulations with steroids and anti-mycotics are also available [17].

*Necrotizing sialometaplasia* is a solitary benign condition due to an inflammatory reaction of salivary glands. The true etiology is still unknown however local infarction due to ischemia of the salivary tissue is blamed. Mostly these lesions occur on the posterior palate but may rarely observed on the lower lip, retromolar pad, sublingual region, tongue and the larynx. Clinically necrotizing sialometaplasia manifests as a crater like ulcer with indurated borders. Although it is a self-limiting condition, complete healing may take up to 7 weeks [1]. During this period, patients may aid supportive treatments focused on pain control. Necrotizing sialometaplasia may mimic salivary gland tumors, thus physicians should always question the evolution time since in most cases salivary gland tumors do not present such short evolution times like necrotizing sialometaplasia [18].

*Primary herpetic gingivostomatitis* is a viral condition due to Herpes Simplex Virus (HSV). It usually occurs in children younger than five years. Oral ulcerative lesions associated with primary herpetic gingivostomatitis develop as multiple pin-headed vesicles which rupture. These small lesions may merge and manifest as larger ulcerations. Systemic symptoms such as fever, nausea, anorexia, submandibular lymphadenopathy, halitosis and dysphagia are also noted [1]. Bed rest, fluids, soft diet and antipyretics are suggested for the systemic manifestations of primary herpetic gingivostomatitis. In order to reduce the spread of infection to other sites, patients must be discouraged from touching the ulcerative areas. Systemic antiviral therapies may be considered in severe cases or for immunocompromised patients [19].

*Herpes zoster infection* is a secondary viral condition due to Varicella Zoster Virus (VZV). Clinically it is a painful condition with vesicular eruptions both on the skin and the mucosa. Symptoms are unilateral with extreme pain along the course of the nerve [20]. The involvement of the trigeminal nerve is rare but painful, with clustered ulcers of less than 5 mm in diameter. Depending on the involvement of specific nerves, these ulcers may appear on the hard palate, buccal gingivae or tongue in a characteristic unilateral pattern. Antiviral medicine may be required to manage the herpes zoster infection whereas the oral ulcerations are self-limiting and usually heal within two weeks [1].

*Herpangina and hand-foot-mouth disease* are both self-limiting and mild viral conditions caused by coxsackievirus commonly affecting children. Herpangina clinically manifests with sore throat, fever, blisters and ulcers involving the palate, oropharynx and tonsillar pillars [1, 8]. Posterior involvement of the oral cavity may help alarm the physicians in diagnosing herpangina. Hand-foot-mouth disease differs from other lesions since it simultaneously involves the extremities and oral cavity [8]. Ulcerative lesions related to hand-foot-mouth disease usually involve the tongue, hard and soft palate, and the buccal mucosa. Both diseases are similarly managed targeting analgesia and fever control. Currently, there are no available medical treatments against coxsackievirus infections [1].

*Erythema multiforme* is an autoimmune mucocutaneous condition with varying etiologic factors. Although oral ulcerative lesions are not the only oral symptoms, several oral manifestations such as macules and bullae are observed in almost 70% of patients with erythema multiforme [1, 21]. Similar to viral infections, erythema multiforme also presents with generalized symptoms like fever, lymphadenopathy, headache, malaise, cough, and sore throat. Oral ulcerative lesions associated with erythema multiforme are usually large, multiple and confluent. Management depends on the severity of the condition. Mild forms usually heal within 10–20 days. Liquid diet is suggested, analgesics or antipyretics are prescribed, and local wound care is applied if necessary [1].

*Acute necrotizing ulcerative gingivitis* (ANUG) is a bacterial opportunistic infection. The most common etiological factors are *Fusobacterium* and *Prevotella* species [22]. It is a painful and destructive gingival condition that specifically affects the interdental gum tissue. Clinically three essential findings help physicians in an accurate diagnosis which are (a) halitosis, (b) rapid onset, and (c) ulceration and necrosis of the interdental papillae that look like punched out, crater-like lesions. ANUG is often associated with poor oral hygiene, low immune system, nutritional deficiency, smoking or psychological stress [23]. Proper ANUG treatment should focus on the management of the acute symptoms and the prevention of further tissue destruction. Debridement of superficial gingival plaques and calculi at the necrotic lesions along with a prescription for 0.12% chlorhexidine gluconate mouth rinse twice daily should be considered initially. Signs of systemic involvement are fever, malaise or lymphadenopathy [22]. Due to its anaerobic activity, the first drug choice is metronidazole 250 mg, three times daily; however, penicillin, tetracyclines, clindamycin, amoxicillin, and amoxicillin with clavulanate also show acceptable results and may be considered. On the contrary, topical antimicrobials are not recommended [23]. Simultaneous antifungal agents should be considered in immunosuppressed patients along with the antibiotic therapy. Once the acute phase is managed, scaling and root planning along with proper oral hygiene maintenance should be established. Management of any predisposing factors should not be disregarded. Additional periodontal surgical procedures such as gingivectomy or gingivoplasty may be considered on a case-by-case basis [22].

#### *Ulcerative Lesions of the Oral Cavity DOI: http://dx.doi.org/10.5772/intechopen.101215*

*Oral hypersensitivity reactions* may be associated with a range of allergens including food, medications, mouthwashes, gums, toothpastes, restorative or cosmetic materials. Clinically these reactions may manifest as mucosal ulcerations or lichenoid reactions (**Figure 2**). Ulcerations usually have irregular borders and a red halo. Other oral symptoms may include erythema and edema of the oral structures or white patches and plaques [24]. Itching of the oral and pharyngeal tissues may or may not be present [1]. Clinical data recording is crucial in these patients. In order to accurately identify the allergens, the patch test is considered the gold standard. It is recommended to order a patch test for all patients when a hypersensitivity reaction is suspected to spot the true etiological factor [25]. Once the etiology is revealed, elimination of this causative agent often results in the resolution of the symptoms usually within two weeks [24]. Patients may aid from topical corticosteroids either as an ointment or mouthwash during this period especially if they present with severe symptoms [26].

*Plasma cell stomatitis* or *plasma cell mucositis* is a rare benign condition. Although its true etiology is still debatable, several theories consider this entity also as a hypersensitivity reaction but with polyclonal plasma cell infiltration [27]. Clinically epithelial sloughing, desquamation and swelling may be observed besides ulcerations (**Figure 3**). It may affect anywhere on the oral mucosa but the gingivae is the most affected site [1]. Chewing gums, cinnamon, qat (a native plant in eastern Africa and Arabia), toothpaste or flavored mints have been suggested as possible etiologic factors but a specific causative agent is seldom identified [27–29]. Plasma cell

**Figure 3.** *Severe epithelial sloughing and erythema on a patient with plasma cell stomatitis.*

stomatitis is managed with corticosteroids, either topical, intralesional or systemic, with additional antimicrobial medications depending on the systemic symptoms of the patients. Although complete regression is rare, most patients experience disease stabilization. Plasma cell stomatitis is a rare condition however clinically it may easily be confused more common benign and neoplastic conditions of oral cavity.
