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Prevention of oral squamous carcinoma 1 Indidence, survival • About 36,000 American patient will be diagnosed with oral or pharyngeal cancer this year • It will cause over 8,000 deaths, killing roughly 1 person per hour • Of the newly diagnosed individuals, only half will be alive in 5 years • This is a number which has not significantly improved in decades Mortality of oral cancer in Hungary (1948-99) 3 Mortality of OSCC in Mid-Eastern Europe (1992-1995) Besides the metastasis, 5 Mortality • The death rate for oral cancer is higher than that of cervical cancer, Hodgkins disease, cancer of the brain, liver, testes, kidney, or skin cancer (malignant melanoma • Together with cancer of the larynx, for which the risk factors are the same, the numbers of diagnosed cases are over 350,000 to 400,000 new cases being found each year worldwide Mortality of OSCC • The death rate associated with this OSCC is especially high because this disease is routinely discovered late in its development • Often it is discovered when the cancer has metastasized to another location, especially to the lymph nodes of the neck • Prognosis at this stage of discovery is significantly worse than when it is diagnosed localized in the oral cavity • at these later stages, the primary tumor has had time to invade deep into local structures besides the metastasis oral cancer • Oral squamous cell cancer persist and grew on the head and neck above the level of the clavicle untill the most advanced phases of the disease • Left untreated, oral cancers allways lead to death of the patient within 1,5-2 years, due to local invasion to the surrounding tissues, and metastases on the neck, rarely to the bones and lungs) • The most common causes of death are marasmus, erosion bleeding from the great vessels (e.g. int. or external carotid artery,) • Inability of eating, drinking due to pharyngeal masses necessitates arteficial nutrition via surgical or percutaneous gastrostomy, • Tumorous upper airway obstruction necessitates tracheostomy 8 Factors determining survival • Oral cancer is particularly dangerous because it has a high risk of producing second primary tumors ( at a different site of oral cavity) • Patients who survive a first encounter with the disease, have up to a 20 times higher risk of developing a second cancer! • This heightened risk factor can last for 5 to 10 years after the first occurrence • There are several types of oral cancers, but 90% are squamous cell carcinomas Factors of etiology Smoking Drinking Alcohol Poor oral hygiene Viruses Poor fitting prosthesis Etiology • The human papilloma virus, particularly versions 16 and 18, a sexually transmitted infection between partners, • possible association with the increasing incidence of young non-smoking oral cancer patients • This virus is the causative agent in more than 90% of all cervical (gynecological) cancers Demographics • For decades OSCC has been a cancer which affected 6 men for every woman • That ratio has now become 2 men to each woman Demographics • Age is a risk factor for oral cancer, as most of the time it occurs in those over the age of 40 • The age of diagnosed patients may indicate a time component in the biochemical or biophysical processes of aging cells that allows malignant transformation, or perhaps, immune system competence diminishes with age 13 Risk factors • the accumulative damage from other factors, such as tobacco use, and alcohol consumption are responsible • Alcohol and smoking have a synergistic effect in the carcinogenesis in the oral cavity • It may take several decades of smoking to precipitate the development of a cancer • ( cca. 95% of oral cancer patients have been smoking for 3-4 decades ) Risk factors • Tobacco- 75% of all dx tobacco users • Alcohol- heavy usage • Alcohol + Tobacco- Those who both smoke and drink, have a 15 times greater risk of developing oral cancer than others – Considered both chemical and lifestyle factors • Ultraviolet radiation- lip and skin cancers – Have decreased over the years due to use of sunblocks and education • Radiation exposure ( enviromental and industrial /due to profession/ ) Risk factors • Biologic Factors – Viral and fungal infection – HPV is a common, sexually transmitted virus, e.g about 40 million individuals are infected in USA • 1% of those infected, have the HPV16 strain which is a causative agent in cervical cancer, and now is linked to oral cancer as well Risk factors • Risk factors exert their carcinogenic effects on the entire oral cavity, paryngeal , upper aerodigestive system mucosa ( so called fieldcancerization !) • Bronchial, laryngeal, esophageal cancer !!! 17 Signs and symptoms • In its early stages, it can go unnoticed • It can be painless, and little in the way of physical changes may be obvious • dentists or doctors can see or feel the precursor tissue changes, or the actual cancer while it is still very small, or in its earliest stages symptoms • White or red patch in the oral cavity • Small indurated ulcer • Many benign tissue changes that occur normally in your mouth, and some things as simple as a bite on the inside of your cheek may mimic the look of a dangerous tissue change. • It is important : any sore or discolored areain the oral cavity , which does not heal within 14 days, should be looked at by an oral and maxillofacial surgeon !! Signs and symptoms • Lump or mass in the mouth or felt in neck • Pain or difficulty in swallowing, speaking or chewing • Wart like lesion • Common areas – Lip – Tongue – Floor of mouth Progression of OSCC • • • • • Hyperkeratosis Dysplasia Erythroplakia Carcinoma in situ Invasive carcinoma Hyperkeratosis • Excessively thickened layer of the stratum corneum composed of orthokeratin (hyperorthokeratosis) or parakeratin (hyperparakeratosis). • Clinical features: – – – – – – – mucosal lesion anywhere in the oral cavity appears lighter in color than the normal color flat or raised may be rough duration may be weeks to months cannot be wiped off usually adult occurance 22 Hyperkeratosis • Etiology – chronic irritant • Thickened keratin layer • Organized connective tissue layer • Possible to have inflammatory reaction in connective tissue due to irritation • Normal maturation of epithelial cells • No evidence of dysplasia Hyperkeratosis • Main Pathologic Process – benign hyperkeratosis • Treatment – removing cause of lesion – may be excised • Prognosis – good Dysplasia • A pre-malignant change in epithelium characterized by a combination of individual cell and architectural alterations • Clinical features – white leukoplakic lesion of the oral mucosa – duration varies from months to years • • • • • Differential diagnosis: hyperkeratosis squamous cell carcinoma epthelial dysplasia lichen planus Displasia Histology • • • • • • basal cell proliferation pleomorphism (cell variation) mitotic activity, hyperchromatic nuclei dyskeratosis (abnormal keratosis) premalignant (cellular change in the epithelium and noinvasion into the connective tissue) Dysplasia - treatment • Removal of the cause • biopsy the lesion to determine severity of dysplasia • PROGNOSIS: • may regress to normal in early stages • usually considered to be premalignant Erythroplakia • Chronic red oral mucosal patch usually not attributed to traumatic, vascular or inflammatory causes but frequently caused by epithelial dysplasia, ca in situ, or squamous cell carcinoma. • asymptomatic red macule or patch on a on a mucosal surface • floor of mouth, tongue and palate • multiple lesions may be present Erythroplakia • typical oral lesion is less than 1.5 cm. • well-demarcated from the surrounding pink mucosa • surface is typically a smooth, soft, velvety texture and regular in coloration • predominantly a disease of older males • a lack of keratin production in the epithelium • thin atrophic epithelium covering the underlying microvasculature • underlying connective tissue often demonstrates chronic inflammation along with increase in size and number of vascular structures Differential diagnosis • atrophic candidiasis • erythroplakia • focal inflammed mucosa Erythroplakia • Treatment: • biopsy to determine the exact nature of the lesion • Prognosis – depends on the specific histopathologic diagnosis Carcinoma in Situ • White, red, or red/white patch on lining mucosa; may also appear as a small (<1.0 cm) soft ulcer. Carcinoma In Situ- Histology • Anaplasia with or without hyperkeratosis; no invasion • Anaplasia= cells lack differentiation Oral squamous cell cancer • Malignant neoplasm of stratified squamous epithelium that is capable of locally destructive growth and distant metastasis • possible sites – – – – – – • • • • • • lower lip tongue floor of the mouth soft palate gingival / alveolar ridge buccal mucosa more common in adult males early presentation of leukoplakias and erythroplakias painless ulcer, tumorous mass, or verrucous (papillary growth) painless ulcer, tumorous mass, or verrucous (papillary growth) occasionally loosening or loss of teeth possible paresthesia of the teeth and lower lip Differential diagnosis • • • • • squamous cell carcinoma primary syphilis tuberculosis deep fungal infection traumatic ulcerated granuloma Histological features • • • • • • • increased mitotic activity well differentiated keratin pearls (abnormal keratinization) hyperchromatic nuclei pleomorphism epithelium islands connective tissue stroma with chronic inflammation (histiocytes, lymphocytes, etc.) OSCC • Treatment: surgical excision, radiation therapy or both • Prognosis: left untreated, metastasis via the lymphatic vessels most often to the lungs and liver complex oncological treatment • • • • Reduce risk factors Regular Screening Early detection Appropriate treatment ( surgical, radiotherapy, chemotherapy, psychological,surgical and dental rehabilitation) Prevention • Thorough examination of the oral cavity and head and neck region is essential part of all dental and medical examination! • Alcohol consumption and smoking should be cleared among anamnestic data • Meticulous inspection and palpation of the oral cavity, face and the neck requires: » Proper lighting » Dental mouth mirror » Gauze squares » Gloves » 5 minutes Prevention • Avoiding risk factors and increasing protective factors may help prevent cancer. • The following risk factors may increase the risk of oral cancer: – Tobacco use – Alcohol use – Sun exposure – HPV infection • Majority of OSCC cases can be prevented by avoiding the risk factors • Quitting smoking (reduces the risk of oral cancer by one-half (50%) within 5 years. Within 10 years of quitting, the risk of oral cancer is the same as for a person who never used tobacco) Prevention • The protective factors may decrease the risk of oral cancer: • Dietary factors – Chemoprevention • Cancer prevention clinical trials are used to study ways to prevent cancer. • New ways to prevent oral cancer are being studied in clinical trials. • Education of self-examination of the risk patients • Regular check-ups for risk patients Chemoprevention Use of drugs, vitamins or other agents to prevent or delay the growth of cancer The purpose of some cancer prevention clinical trials is to find out whether actions people take can prevent cancer. These may include eating fruits and vegetables, exercising, quitting smoking, or taking certain medicines, vitamins, minerals, or food supplements Erlotinib Prevention of Oral Cancer (EPOC) Secondary Primary Tumor Prevention With EGFR, OSI-774, and Cyclooxygenase-2 Phase I/II Study of Chemoprevention With EGFR and COX-2 Inhibitor Clinical Evaluation of Bioadhesive Gels for Oral Cancer Chemoprevention Lyophilized Black Raspberries in Preventing Oral Cancer in High-Risk Patients Previously Diagnosed With Stage I-IV or In Situ Head and Neck Cancer Bowman-Birk Inhibitor Concentrate in Preventing Cancer in Patients With Oral Leukoplakia Vandetanib in Preventing Head and Neck Cancer in Patients With Precancerous Head and Neck Lesions Phase I Chemoprevention Trial With Green Tea Polyphenon E and Erlotinib in Patients With Premalignant Lesions of the Head and Neck A Randomized Study of Sulindac in Oral Premalignant Lesions