Candidate Information
Theme: History
Patient demographics:
Name | Angela Oxwith |
Age/DOB | 15/03/1982 |
Gender | Female |
Employment | n/a |
Pertinent Social History | None |
Pertinent Medical History | Ulcers |
Pertinent Dental History | None |
Scenario
You have been asked to review this patient with concerns about a lump in their palate.
Listen to the patient’s history and explain management options available.
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In the realm of clinical dentistry, practitioners regularly confront an array of diverse oral lesions. These oral lesions emanate from a multitude of underlying causes encompassing infective, idiopathic, inflammatory, reactive, and neoplastic origins. To navigate this diagnostic landscape effectively, a clinician must meticulously acquire a comprehensive clinical history from the patient. Furthermore, the clinician must possess a sophisticated understanding of the nuanced signs and symptoms associated with these oral lesions. This includes an adept assessment of factors such as the precise localisation within the oral mucosa, the dimensions of the lesion, its chromatic attributes, and its distinctive morphological characteristics. This meticulous approach is imperative to ensure an accurate and precise diagnosis in the multifaceted domain of oral pathology.
Recurrent Aphthous Stomatitis (RAS):
Epidemiology and Risk Factors
Recurrent Aphthous Stomatitis (RAS) stands as the most prevalent ulcerative oral condition, affecting roughly 20% of the general population. However, its prevalence demonstrates significant variability, ranging from 5% to 50%, contingent upon demographic factors, including personal and occupational stressors. The incidence of RAS in children is profoundly influenced by familial history. Offspring of parents with RAS exhibit a remarkable 90% likelihood of developing the condition, in stark contrast to the 20% probability observed among children of unaffected parents. RAS incidence tends to peak during the second decade of life, diminishing in frequency in later stages.
Aetiology and Risk Factors
While the precise aetiology of RAS remains elusive, several putative factors have been postulated as potential contributors. Trauma is recognised as a causative agent, with RAS patients often presenting ulcerations at trauma-prone sites, commonly associated with activities such as toothbrushing, dental interventions, or inadvertent biting of the oral mucosa. Dysregulated salivary composition, xerostomia, and heightened stress levels have also been correlated with an increased susceptibility to RAS.
Notably, RAS should not be misconstrued as a consequence of microbial infections, as extensive research has dispelled any causal association between RAS and pathogens such as HSV, Helicobacter pylori, and EBV.
Furthermore, RAS has exhibited an association with nutritional deficiencies, including low levels of iron, zinc, folate, and vitamins B1, B2, B6, and B12, which are identified in up to 20% of individuals with RAS. It is crucial to dispel the misconception that tobacco use exacerbates RAS; in fact, the incidence of RAS is lower among smokers compared to non-smokers, potentially attributed to tobacco’s tendency to enhance the keratinization of oral mucosa, rendering it less susceptible to ulceration.
RAS is frequently associated with underlying medical disorders, including nutritional deficiencies, anaemia, Behcet’s syndrome, HIV, cyclic neutropenia, and MAGIC syndrome, among others. Behcet’s syndrome, in particular, is characterised by RAS-like ulcerations, which may involve major and herpetiform ulcers. Similarly, HIV-positive patients may manifest RAS in approximately 5%-15% of cases, with immunocompromised individuals exhibiting a higher predisposition to RAS.
Clinical Features and Classification
RAS encompasses three primary clinical subtypes: Minor RAS, Major RAS, and Herpetiform RAS, each distinguished by distinct morphological and distributional characteristics. Minor RAS presents as round or oval lesions, accompanied by an erythematous halo and a grey-white pseudomembrane. Major RAS exhibits similar features but tends to manifest larger, more extensive ulcerations. In contrast, Herpetiform RAS presents as small, deep multiple ulcers that often coalesce into irregular margins.
Treatment
The treatment of RAS is contingent upon the severity of the condition and the resultant symptoms experienced by the patient. Drug therapy is generally considered for individuals presenting with severe pain, eating difficulties, or frequent RAS episodes. Palliative measures involve protective emollients (e.g. Zilactin or Orabase) and topical agents/anaesthetics (e.g. lidocaine or benzocaine) to alleviate minor ulcer-related discomfort. Tetracycline mouth rinses and NSAIDs may also reduce pain and expedite healing. Topical corticosteroid therapy typically proves effective; however, severe cases of Major RAS may necessitate systemic corticosteroids like prednisone. In severe instances, referral to an oral medicine specialist may be warranted.
Herpes Simplex Virus Infections (HSV) in-depth:
Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are globally widespread pathogens capable of infecting various anatomical sites within the human body, including the oral cavity. In the United States, seroprevalence data indicates that approximately 40% of individuals under the age of 20 exhibit detectable antibodies against HSV-1, a proportion that escalates to 65% in individuals aged 70 and older. This prevalence underscores the significance of understanding HSV and its clinical manifestations.
Clinical Presentation
HSV infections are clinically diverse, encompassing primary herpetic stomatitis and secondary (recurrent) herpes labialis. Primary infections predominantly occur during childhood, wherein individuals may either contract the virus asymptomatically or exhibit a viral prodrome characterised by fever, headache, and cervical lymphadenopathy. This prodrome is succeeded by the emergence of vesicular lesions within the gingival area, a condition termed primary herpetic gingivostomatitis. These vesicular lesions can manifest on the gingiva, lip borders, or the perioral skin region, occurring either as solitary vesicles or clusters (refer to Figures 3 and 4). These vesicles are susceptible to rupture, leading to crusting or ulceration. Primary episodes typically resolve spontaneously within a span of 10 to 14 days, following which the virus establishes dormancy within the trigeminal nerve ganglion.
Secondary herpes labialis, on the other hand, denotes recurrent herpes, presenting as a localised eruption of vesicles, often seen at the vermilion border of the lips. Notably, HSV can shed into oral saliva in approximately 10% of individuals. Various triggers, including ultraviolet (UV) light exposure, trauma, psychological stress, fatigue, or menstruation, may reactivate the virus during later stages, provoking episodic outbreaks of shorter duration.
Treatment Strategies
Diagnosing herpetic mouth lesions primarily relies on clinical assessment, with confirmation attainable through polymerase chain reaction (PCR) swabs. Given the self-resolving nature of most mild cases, supportive care is typically adequate, encompassing measures such as maintaining sufficient fluid intake and administering analgesic antipyretics, such as paracetamol.
However, in specific patient groups, such as neonates, pregnant women, and immunocompromised individuals, systemic antiviral medications like valaciclovir or famciclovir assume a pivotal role, especially when administered promptly in the initial stages of the disease.
Recurrences stemming from viral reactivation, termed “cold sores,” often present milder symptoms. Patients are most contagious within the first 24 hours of lesion appearance. While most cases resolve spontaneously, larger lesions may benefit from topical acyclovir cream or famciclovir. For individuals experiencing severe recurrences or those with chronic lesions due to immunocompromised states, prophylactic antiviral therapy on a daily basis may be warranted.
Oral squamous cell carcinoma (OSCC):
Oral squamous cell carcinoma (OSCC) stands as the predominant malignancy within the oral cavity, constituting more than 90% of all oral cancer cases. This condition primarily afflicts individuals aged 40 and older, with a notable male predilection, occurring approximately twice as frequently as in females. While OSCC can manifest anywhere within the oral cavity, it most commonly arises on the lateral borders of the tongue, followed by the gingiva, alveolar mucosa, the floor of the mouth, and the ventral surface of the tongue. In regions where the habitual consumption of areca nut and tobacco is prevalent, such as certain Southeast Asian countries, OSCC often manifests on the buccal mucosa.
Risk Factors
The risk factors associated with the development of OSCC encompass alcohol use, tobacco use, betel quid, areca nut chewing, and human papillomavirus (HPV) infection. Tobacco consumption, in particular, releases pro-carcinogenic agents that contribute to cancer development, demonstrating a dose-risk relationship. Alcohol consumption also serves as a risk factor, generating cytotoxic agents during metabolism, in addition to fostering nutritional deficiencies, compromised immune responses, and local mucosal effects. Supplementary risk factors include solar radiation exposure, immunosuppression conditions (e.g. transplant patients, HIV/AIDS), and specific HPV strains, notably HPV 16 and 18. Solar radiation predominantly affects the lower lip due to heightened sun exposure.
Clinical Features
Early-stage OSCC often presents as a painless and asymptomatic condition, leading to delayed diagnosis in a significant proportion of cases, with more than half being diagnosed at an advanced stage. OSCC exhibits diverse clinical presentations, ranging from non-healing oral ulcers, palpable lumps or swellings, to dental symptoms like ill-fitting prostheses. Additional features may include erythroplakia, leukoplakia, pain or numbness, ulcers with fissures, raised exophytic margins, and non-healing extraction sockets. Two pivotal malignant features to observe are induration (increased tissue density) and fixation (lack of tissue mobility). Any suspicious oral lesion persisting beyond a three-week timeframe warrants further investigation and expedited referral to a specialist.
Treatment
The management of OSCC primarily revolves around surgical excision, with the approach tailored to tumour characteristics, including site, location, size, depth, and bone involvement. Metastatic cases of OSCC frequently involve cervical lymph nodes, necessitating lymph node resection as a crucial aspect of management. Radiotherapy and/or chemotherapy may be employed in cases of locally advanced squamous cell carcinoma. Despite advancements in medical treatment options, the 5-year survival rate for oral cancer hovers around 50%.
Oral Candidosis:
Oral candidosis refers to the proliferation of commensal yeast, primarily Candida albicans, within the oral cavity. This condition is often categorised as an opportunistic infection, as alterations in the oral microflora create favourable conditions for Candida overgrowth.
Risk Factors
Common predisposing factors for oral candidosis include recent use of broad-spectrum antibiotics, wearing dentures, inhalation of corticosteroids without mouth rinsing, smoking, diabetes, and immunosuppression (e.g. AIDS, haematological malignancies, chemotherapy). Additionally, xerostomia, or dry mouth, is a significant contributor to oral candidosis.
Clinical Features and Treatment
Oral candidosis can be classified into four categories: pseudomembranous, erythematous, hyperplastic, and denture-induced stomatitis. Diagnosis is primarily based on clinical appearance, but an oral swab or smear can be useful for confirmation. First-line treatment involves topical antifungal agents such as nystatin liquid, amphotericin lozenges, or miconazole gel. Refractory cases necessitate investigation for underlying causes, potentially involving fluconazole or ketoconazole.
Oral Lichen Planus (OLP):
OLP is a chronic inflammatory condition affecting the oral mucosa, associated with cell-mediated immunological dysfunction. It has a prevalence of 1–2% and primarily affects adults, with a male-to-female ratio of 1:2.
Clinical Features
OLP typically manifests on the gingiva, tongue, and buccal mucosa, with less frequent occurrences on the lip’s vermillion border and labial mucosa. Palate and floor of the mouth lesions are rare. Symptoms, experienced by about two-thirds of affected individuals, include mucosal roughness, burning sensation, irritation, xerostomia, bleeding, and dysgeusia. Gingival involvement can resemble desquamative gingivitis.
OLP carries the potential for malignant transformation into squamous cell carcinoma, categorising it as a potentially malignant disorder by the World Health Organization. Regular monitoring is required, with reported malignant transformation rates ranging from 0% to 5.8%. Diagnosis relies on clinical findings and biopsy, recommended for both confirming the diagnosis and ruling out dysplastic changes.
Premalignant Disorders:
Oral potentially malignant disorders encompass lesions or conditions in the oral cavity that may lead to malignancy. These disorders include leukoplakia, erythroplakia, oral submucous fibrosis, actinic cheilitis, and OLP. Timely identification and intervention are essential to prevent the progression to oral squamous cell carcinoma.
Leukoplakia is characterised by white mucosal plaques of unknown origin, potentially increasing malignancy risk. It should be differentiated from other benign conditions. Smokers face a significantly elevated risk, with a 1% annual malignant transformation rate. Leukoplakia presents in two main types: homogenous and non-homogenous.
Erythroplakia refers to red patches within the oral mucosa that lack identifiable clinical characteristics. These lesions warrant close attention due to their high potential for malignancy.
What is the approximate prevalence of Recurrent Aphthous Stomatitis (RAS) in the general population?
Which demographic factor significantly influences the incidence of RAS in children?
Trauma is recognised as a causative agent for RAS. Which of the following activities is commonly associated with trauma-induced RAS?
Which of the following factors has NOT been associated with an increased susceptibility to RAS?
What is the classification of RAS characterised by small, deep multiple ulcers that often coalesce into irregular margins?
What is the recommended treatment for alleviating minor ulcer-related discomfort in RAS patients?
In cases of severe Major RAS, which treatment option may be necessary, especially when topical therapies are ineffective?
Which underlying medical disorder is characterised by RAS-like ulcerations and may involve major and herpetiform ulcers?
What is the estimated incidence of RAS in immunocompromised patients, such as those with HIV?
Which clinical condition refers to recurrent herpes that presents as localised vesicles at the vermilion border of the lips?
What is the estimated percentage of individuals who may have oral HSV shedding?
In which anatomical site does the herpes simplex virus establish dormancy after a primary infection?
What are the common triggers for reactivation of herpes simplex virus leading to episodic outbreaks?
Which diagnostic method is primarily employed to confirm herpetic mouth lesions?
What treatment strategy is generally recommended for mild cases of herpetic mouth lesions?
When might systemic antiviral medications like valaciclovir or famciclovir be especially useful in the treatment of herpetic mouth lesions?
What is the primary reason for administering daily prophylactic antivirals in individuals with herpetic mouth lesions?
What is the most common malignancy within the oral cavity, accounting for over 90% of all oral cancer cases?
Who is most commonly affected by OSCC in terms of age and gender?
Which region within the oral cavity is most frequently affected by OSCC?
What are the primary risk factors associated with the development of OSCC?
Which of the following is a common clinical presentation of early-stage OSCC?
What is the primary treatment approach for OSCC, tailored to tumour characteristics?
In cases of OSCC with metastasis, which anatomical site is often involved?
What is the approximate 5-year survival rate for oral cancer despite advances in treatment options? a