Mr. C is a 62-year-old Hispanic male who presents to the dental clinic for a routine evaluation. During the oral exam, a white patch on his left lateral tongue was noted. According to Mr. C, the white patch has been there for 6 months. It was diagnosed as candidiasis by his primary care provider, and he was prescribed nystatin oral preparation without much improvement. Recently, the white patch has grown in size and has become increasingly irritated.
It is estimated that 49,670 new cases of oral cavity and oropharynx cancer will be diagnosed in the United States in 2017.1 More than 90% of oral cancers are oral squamous cell carcinoma (OSCC).2 OSCC often presents as a nonhealing mouth wound (see Oral squamous cell carcinoma). According to the National Cancer Institute, approximately 1.1% of all individuals in the United States will be diagnosed with oral cancer at some time in their lives.3 The most effective approach to reduce morbidity and mortality from oral cancer is early detection and immediate treatment.
OSCC can have a deceptively benign clinical appearance. It may present as a white patch (leukoplakia), red patch (erythroplakia), or mixed red and white lesions (erythroleukoplakia). Upon discovering white, red, or mixed oral lesions, a biopsy must be performed to rule out dysplasias (oral precancer) and OSCC.4 When these suspicious lesions are examined under the microscope, most are usually benign epithelial hyperplasias and hyperkeratoses. A small percentage of oral lesions exhibit cellular atypism, which requires further evaluation.4
If discovered early, prior to local or distant metastasis, the 5-year survival for OSCC is 83% as opposed to 38% when discovered after metastasis has occurred.3 Therefore, it is imperative to focus on early detection of OSCC to improve patients' overall prognosis and survival. The patient with potentially malignant oral lesions may seek initial care from either dental or primary care providers, so both should be aware of the clinical presentation of potentially malignant oral lesions. Appropriate collaboration of care is required to ensure appropriate and timely workup.
It is essential that primary care providers and dental professionals include oral cancer screening in their routine exams. In a survey of medical clinicians, only 20% performed oral exams, and 80% could not correctly identify early OSCC on presentation.5 Screening for OSCC risk factors and performing routine extraoral and intraoral exams is recommended.6
The leading risk factors implicated in oral cancer are tobacco and alcohol use, which increase an individual's risk for developing cancer by a factor of 15 or more.6,7 Approximately 75% of oral cancer cases in the United States may be attributed to tobacco and alcohol use.6 These substances may initiate the multistep carcinogenic process that leads to OSCC. There does appear to be a direct relationship between tobacco use and oral cancer. Although alcohol is considered a risk factor for oral cancer, it is difficult to identify alcohol as an independent risk factor for oral cancer because most individuals with oral cancer who use alcohol have other risk factors such as tobacco use.8
Betel nut and products derived from the areca nut, such as betel quid, cause oral mucosa changes that may lead to development of OSCC. Roughly 700 million individuals worldwide consume the addictive substance betel nut in a variety of forms.9 Discontinuing betel nut and betel quid use significantly reduces the risk of developing OSCC.9
Chronic inflammatory conditions, such as those seen in patients with oral lichen planus and tobacco users, are etiologic factors in oral cancer. Prolonged exposure to inflammatory cytokines is thought to induce carcinogenesis via constitutive activation of oncogenes.10 Leukoplakia is the most common potentially malignant oral disorder (see Leukoplakia).4
Leukoplakia is a benign reactive process that represents hyperplasia of the squamous epithelium.11 Presence of lichen planus manifests as white spots in the mouth and throat and may vary from lacelike white patches to painful erosions. Lichen planus affects middle-aged individuals and may increase the risk of developing OSCC (see Lichen planus).12
General risk factors for developing OSCC include male gender, older age, and UV light exposure (individuals exposed to prolonged sunlight have an increased risk).6
Immune system suppression is also a causative agent in the development of OSCC. Immunosuppressive medications, including rejection medication regimens for organ transplant patients or immunosuppressive therapies used to treat certain autoimmune diseases, increase a patient's risk of developing OSCC.6
There is an established strong relationship between high-risk human papillomavirus (HPV) and OSCC.2 In the past decade, the incidence of HPV-related oral cancer has increased and non-HPV related OSCC has stabilized.13 The percentage of high-risk HPV-positive oropharyngeal cancers has increased from 20% to 95% over the past 20 years.6 There are more than 200 subtypes of HPVs, but the high-risk HPV subtypes are 16 and 18.14
HPV 16 and 18 cause OSCC of the posterior oropharynx, tonsils, and base of the tongue.15 Vaccination for types 6, 11, 16, and 18 is available, as well as vaccination for nine types of HPV (6, 11, 16, 18, 31, 33, 45, 52, and 58) with the HPV 9-valent vaccine. It is expected that this will reduce the spread of HPV infection and ultimately reduce the carcinogenic potential of HPV in the oral cavity.13
It is vital to ascertain a detailed history when evaluating a patient's oral health. The primary care provider should review social, familial, and medical histories, including history of irradiation to the head and neck, familial history of head and neck cancer, or a personal history of cancer. When reviewing systems (head, ears, eyes, nose, and throat), the clinician should include the oral cavity.16
When asking about tobacco use, the type of tobacco product, amount used daily, and duration of use should be noted. This also applies to alcohol consumption. It is important to ask about betel nut, betel quid, and other related product usage. Additionally, it should be determined if the patient has received or been offered the HPV vaccination.
The primary care provider should perform thorough extraoral and intraoral exams on all patients during complete annual evaluations, especially for patients with oral complaints, head and neck complaints, and oral cancer risk factors. The extraoral exam begins with inspection of the face, neck, lips, and nasolabial folds. The next step is to palpate the masseter muscles externally at the angle of the mandible, the temporal muscles during clenching and relaxation of the jaw, and the pterygoid muscles internally between the tonsillar pillars at the mandible.
While palpating the temporomandibular joint for clicking, crepitus, trismus, or tenderness, ask the patient to demonstrate the threefold range of motion: opening and closing, protrusion and retraction, and lateral motion. For the neck exam, palpate the lymph nodes to assess for size, shape, delimitation, mobility, consistency, and tenderness. The lymph nodes should be palpated in sequence: preauricular, posterior auricular, occipital, tonsillar, submandibular, submental, superficial cervical, posterior cervical, and deep cervical chain.17
For the intraoral exam, visual inspection as well as palpation of the buccal mucosa, gingiva, floor of the mouth, tongue, and hard and soft palates should be conducted.18 High-risk sites of OSCC include the lateral and ventral tongue and the floor of the mouth.6 While wearing gloves, have the patient protrude the tongue; grasp the tip of the tongue with gauze and gently pull it to each side, inspecting each side and palpating the mucosal surface. Run a gloved finger along the remainder of the oral mucosa, palpating for tenderness or induration.
The gold standard for diagnosing OSCC is tissue biopsy followed by microscopic exam.19 Biopsy should be performed by either an oral surgeon or oral pathologist. Also available are noninvasive methods for screening of OSCC, which include an oral brush test, toluidine blue, and a saliva-based oral cancer test.20 It is important to note these are screening methods only. Any case with atypical findings must be followed by tissue biopsy to rule out OSCC.
Survival rate and treatment
Prognosis of OSCC is based on tumor-node-metastasis (TNM) staging: the size of the primary tumor (T), lymph node involvement (N), and evidence of distant metastases (M).21 The 5-year survival rate for localized OSCC is 83%; 63% for patients with regional disease; and 38% for patients with distant disease.3 Treatment of oral cancer is dependent on the TNM stage.22 Early stage OSCC is treated by surgical excision with or without neck dissection. Advanced stages may require postsurgical radiation therapy or chemoradiotherapy.23
Clinical case continued
Mr. C has a social history of smoking 40 packs annually and consuming three to four alcoholic beverages daily. He works for a roofing company, which requires him to work outside 5 to 6 days a week. His medical history is significant for dyslipidemia and hypertension, for which he is taking atorvastatin and losartan daily. His family history is noncontributory, and he has never been vaccinated for HPV.
Mr. C explains that he saw his primary care provider twice for the irritating white plaques on his tongue. He was diagnosed with candidiasis and was prescribed nystatin oral suspension during the first visit. When the lesion did not resolve, he was prescribed nystatin lozenges. The lesion remained, and he stopped following up.
Mr. C went to the dental clinic for comprehensive care, which was his first dental visit in 3 years. The dentist noted poor oral hygiene, multiple restorations that required repair, moderate gingivitis, and several caries. Leukoplakia with irregular borders measuring approximately 0.7 mm was also noted in the left posterior lateral tongue. There was no lymphadenopathy palpable on extraoral exam.
Mr. C was immediately referred to the division of oral pathology for a biopsy. The microscopic exam revealed well-differentiated squamous cell carcinoma. Following additional clinical and imaging studies, the tumor was assigned TNM Stage III (T2 N1 M0). Mr. C received surgical excision with radical neck dissection followed by radiation therapy.
It is recommended that all oral lesions not responding to a prescribed treatment plan be biopsied after 2 weeks of therapy.19Mr. C could have been referred for a biopsy when he did not respond to the antifungal medications, which would have allowed for earlier intervention and treatment of OSCC.
Applying an interprofessional oral health approach to caring for patients is essential for improving patient outcomes, as patients often seek healthcare at multiple points of service. The Institute of Medicine has called for the redesign of healthcare education to be aligned with the need for increased collaboration within healthcare systems.24 This requires health profession educators to redesign curriculum and incorporate interprofessional collaboration opportunities for students.
The World Health Organization defines interprofessional education as a collaborative effort through which students from two or more professions learn together.24 Core Competencies for Interprofessional Collaborative Practice were developed, outlining knowledge, skills, and attitudes required for interprofessionalism by the Interprofessional Education Collaborative.25
For more than a year, the dental and nursing schools at Columbia University have been partnering faculty, students, and resources to improve the outcomes of their patients. A dental/NP collaboration has been established to provide students from both programs the opportunity to collaborate in a clinical learning environment. Research shows that interprofessional education allows for active learning, engages students during formative training, and encourages collaboration between professions.25
The Columbia University interprofessional collaboration requires dental and graduate nursing students to work as a team; the students maintain respective professional roles and responsibilities to provide safe quality care. They evaluate and treat patients together in a clinical setting, collaborating on clinical decision-making while supervised by faculty from both the schools of dentistry and nursing.
Dental care utilization has declined in the United States, regardless of dental benefit status and income level.26 Thus, primary care providers must be able to recognize common oral manifestations of disease and collaborate with dental professionals.27
Diagnosis of oral pathologies by nondentist providers can be done safely with proper training.28 Because many patients do not receive routine oral care from dental providers, primary care providers must have competence in assessing, identifying, and collaborating care of extraoral and intraoral diseases.
1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017. CA Cancer J Clin
2. Sritippho T, Chotjumlong P, Iamaroon A. Roles of human papillomaviruses and p16 in oral cancer
. Asian Pac J Cancer Prev
3. National Cancer Institute. SEER Stat Fact Sheets: Oral Cavity and Pharynx Cancer
. Bethesda, MD: National Cancer Institute; 2012.
4. Farah CS, Woo SB, Zain RB, Sklavounou A, McCullough M, Lingen M. Oral cancer
and oral potentially malignant disorders. Int J Dent
5. Morgan R, Tsang J, Harrington N, Fook L. Survey of hospital doctors' attitudes and knowledge of oral conditions in older patients. Postgrad Med J
6. Moyer V. Screening for oral cancer
: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med
7. Muwonge R, Ramadas K, Sankila R, et al Role of tobacco smoking, chewing and alcohol drinking in the risk of oral cancer
in Trivandrum, India: a nested case-control design using incident cancer cases. Oral Oncol
8. The Oral Cancer
Foundation, Risk factors. 2016. http://oralcancerfoundation.org/understanding/risk-factors.
9. Sharan RN, Mehrotra R, Choudhury Y, Asotra K. Association of betel nut with carcinogenesis: revisit with a clinical perspective. PLoS One
10. Mignogna MD, Fedele S, Lo Russo L, Lo Muzio L, Bucci E. Immune activation and chronic inflammation as the cause of malignancy in oral lichen planus: is there any evidence. Oral Oncol
11. Gillenwater AM, Vigneswaran N, Fatani H, Saintigny P, El-Naggar AK. Proliferative verrucous leukoplakia
(PVL): a review of an elusive pathologic entity! Adv Anat Pathol
12. Reamy BV, Derby R, Bunt CW. Common tongue conditions in primary care. Am Fam Physician
13. Pringle GA. The role of human papillomavirus in oral disease. Dent Clin North Am
14. Doorbar J. Model systems of human papillomavirus-associated disease. J Pathol
15. Cleveland JL, Junger ML, Saraiya M, Markowitz LE, Dunne EF, Epstein JB. The connection between human papillomavirus and oropharyngeal squamous cell carcinomas in the United States: implications for dentistry. J Am Dent Assoc
16. Haber J, Hartnett E, Allen K, et al Putting the mouth back in the head: HEENT to HEENOT. Am J Public Health
17. Bickley L. Bates' Guide to Physical Examination
. 11th ed. Philadelphia, PA: Wolters Kluwer; 2013.
18. Olson C, Burda B, Beil T, Whitlock E. Screening for Oral Cancer: A Targeted Evidence Update for the U.S. Preventive Services Task Force
. Publication number 13-05186-EF-1. Rockville, MD: Agency for Health Care Research and Quality; 2013.
19. Guze K, Pawluk HC, Short M, et al Pilot study: Raman spectroscopy in differentiating premalignant and malignant oral lesions from normal mucosa and benign lesions in humans. Head Neck
20. Omar E. Current concepts and future of noninvasive procedures for diagnosing oral squamous cell carcinoma
—a systematic review. Head Face Med
21. Amin MB, Edge S, Greene F, et al AJCC Cancer Staging Manual
. 8th ed. New York, NY: Springer; 2016.
22. Sathish N, Wang X, Yuan Y. Human papillomavirus (HPV)-associated oral cancers and treatment strategies. J Dent Res
. 2014;93(7 suppl):29S–36S.
23. Budach W, Bölke E, Kammers K, et al Induction chemotherapy followed by concurrent radio-chemotherapy versus concurrent radio-chemotherapy alone as treatment of locally advanced squamous cell carcinoma of the head and neck (HNSCC): a meta-analysis of randomized trials. Radiother Oncol
24. Kahaleh AA, Danielson J, Franson KL, Nuffer WA, Umland EM. An interprofessional education panel on development, implementation, and assessment strategies. Am J Pharm Educ
25. Bentley R, Engelhardt JA, Watzak B. Collaborating to implement interprofessional educational competencies through an international immersion experience. Nurse Educ
26. Wall T, Nasseh K, Vujicic M. Most important barriers to dental care are financial, not supply related. American Dental Association. 2014. http://www.ada.org
27. Sutherland SE, Moline KA. The ARCTIC workshop: an interprofessional education activity in an academic health sciences center. J Dent Educ
28. van der Waal I, de Bree R, Brakenhoff R, Coebergh JW. Early diagnosis in primary oral cancer
: is it possible. Med Oral Patol Oral Cir Bucal