White and Red Lesions of the Oral Mucosa Maryam Jessri, Hani Mawardi, Camile S. Farah, and Sook-Bin Woo Abstract There are several conditions that can present as white or red macular, papular, and/or plaque- like lesions of the oral mucosa. Based on etiol- ogy, red and white lesions of the oral cavity can be divided into developmental, reactive, infec- tious, immune-mediated/autoimmune, and potentially malignant and malignant conditions. Whiteness of the oral mucosa can be caused by changes in the epithelium such as keratinization of normally nonkeratinized mucosa (such as the buccal mucosa), increased keratinization of nor- mally keratinized mucosa, abnormal keratiniza- tion of the epithelium, thickening of the epithelium, and epithelial edema. Fibrosis and/or reduced vascularity of the underlying mucosa may also lead to whiteness which tends to appear deep without discernible surface alterations. Some of the more common causes of redness (erythema) of the oral mucosa include reduced keratinization of the oral epi- thelium, epithelial atrophy, erosion or inflam- mation, and vascular dilatation or proliferation. Generally, the prevalence of red and white oral lesions increases with age. Based on diagnostic and inclusion criteria and characteristics of the population, prevalence of oral mucosal lesions has been reported in 2–84% of the population (Do et al. 2014). A large proportion of red and white lesions are benign. However, the most common premalignant condition in the oral cav- ity is a white plaque (leukoplakia), and this must be managed expeditiously and appropriately. Many conditions can be accurately diagnosed with careful history taking and clinical exami- nation. However, a biopsy is often necessary for a definitive diagnosis. This chapter discusses the clinical features of these white and red lesions, how to distinguish between them, and how to manage them. M. Jessri Division of Oral Medicine and Dentistry, Brigham and Women’ s Hospital, Boston, MA, USA Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA School of Dentistry and Oral Health Centre of Western Australia, University of Western Australia, Perth, WA, Australia e-mail: maryam.jessri@gmail.com; mjessri@partners.org H. Mawardi Faculty of Dentistry, King Abdulaziz university, Jeddah, Saudi Arabia Division of Oral Medicine and Dentistry, Brigham and Women’ s Hospital, Boston, MA, USA e-mail: hmawardi@kau.edu.sa C.S. Farah (*) School of Dentistry and Oral Health Centre of Western Australia, University of Western Australia, Perth, WA, Australia e-mail: camile.farah@uwa.edu.au S.-B. Woo Division of Oral Medicine and Dentistry, Brigham and Women’ s Hospital, Boston, MA, USA Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA e-mail: swoo@rics.bwh.harvard.edu; swoo@partners.org # Springer International Publishing AG 2017 C.S. Farah et al. (eds.), Contemporary Oral Medicine, DOI 10.1007/978-3-319-28100-1_16-1 1