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    leukoplakia

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    leukoplakia

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    © All Rights Reserved
    Download as DOCX, PDF or read online from Scribd
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    16 views4 pages

    Burket's Oral

    Uploaded by

    wahyuekam
    leukoplakia

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF or read online from Scribd
    Flag for inappropriate content
    of 4
    ‘VY PREMALIGNANT LESIONS Oral Leukoplakia and Erythroplakia ‘ETIOLOGY AND PATHOGENESIS ‘The development of oril leukoplakia and erythroplakia as ‘premalignant lesions involves diferent genetic events This notion s supported by the fac that markers of genetic defects, are different expressed in different levkoplakias and ery throplakias.- Activation of oncogenes and deletion and. injuries suppressor genes anal genes responsible for DNA, repair will all contribute toa defective functioning ofthe geome that governs celldivision Following aseries of muta- tions, a malignant transformation may occur. For example, carcinogens sich as tobacco may induce hyperkratiization, with the potential to revert fallowing cessation, but at some ‘tags, mutations wall ead toan unrestreined protration ad cell division, Pipemioioey The prevalence of oil leukoplakia vaties among scientific studies. A comprehensive global review points at prevalence (0f 28%. Most oral ukoplakiasare seen in patierts over the age of 50 and infequenty encountered below the age of 30. In population studies, leukoplakias are more common in mca but alight majority for women was oundin reviews offered materials. 2 Oral erytheoplakia isnot as common as oa Keoki, and the prevalence his been estimated tobe inthe range of 0.02 10 0.190. The gender distribution is reported 10 be equal, and the prevalence his been estimated tobe in the range of 0.02 6 0.19658 The gender distribution is reported 10 be equal, (oral eakoplakis s defined as predominantly whit lesion of the oral mucosa that cannot be characterized as any other definable lesion. This disorder canbe further divided into a hhomogencous and a nonhomogeneous ype. The typical homogeneous leukoplakia is clinically characterized as a ‘whit, wel-demarcated plaque with an identical reaction pat- tern throughout the entire lesion (Figure 10). The surface texture an vary from 4 smooth thin surface toa leathery appesrance with surface fissures sometimes relerred to as “cracked mud.” The demarcation i usually very dissinet, ‘which is diferent from an ona lichen planus (OLP) lesion, ‘where the white components havea more difase ansiton 0 the normal oral mucost. Another difference between these two lesions is the lack of a peripheral erythematous zone in homogeneous orl leukoplakia. The ksionsare asymptomatic in most patents. ‘The noshomogencous type ofl lsuhoplakia may have white patches or plague intermixed with red tisae elements (Figure 11A). Due to the combined appearance of white and red ates, the nonhomogeneous oral leakoplikia has also bncen called erytheoleukeplakiaand speckled leukoplakia. The clinial manifestation ofthe white component may vary from ‘tinal manifestation of the white component may Vary irom FIGURE 10 A ronogeneseiapti ot FIGURE 11.4.4 seahorogenees Moll i heavy sack Th eh part th ison has ape aeperane. A The att il et tend ‘he olow-g vss for yeas and dvelpeda sqcamaus al carcinoma large white verrucousares tosmall nodular structures. Ifthe surface exture is homogeneous but contains verrucous pap ill (nodular) or exophytic components the eukoplakia is also regarded as nonhomogereous. Both homogeneous and. noahomogencous leskoplakias may be encountered in all sites ofthe oral mucesa. (Oral leukoplakia, where the white component is domi- nated by papillary projections, similar wo ora pupillomas ate referred to as verrucous or veruciform leukoplakies Oral leukoplakias wit this clinical appearance but with a more aggresive proliferation pattern and recurrence rate are desig nated as proliferative verrucous leukoplakia (PVL) (Figure 12) This lesion may starts homogeneous leukoplakia but. ‘overtime develop verrucousappeatance containing various degrees of dysphsia, PVL is usually encountered in older women, and the lower gingiva isa predilection site ® The malignant potential i ery high, and verrucous carcinoma oF squamous cell carcinoma may be present at the primary examination. As the common surface rection pattern is similar to what i seen in oral papillomas, the PVL has been suspected to havea viral etiology. although no such asscia- tion as been confirmed. ‘Oral leukoplakia may be found at all sites of dhe oral ‘mucosa. Nonsmokers have a higher percentage of leukopla- kias atthe border of the tongue compared with smokers + ‘The Moor ofthe mouth and the lateral borders ofthe torgue ate high-risksites for malignant tassformation (Figur 1B). These sits have abo bren found to havea higher frequency of loss of heterozygosity compared with low-risk sites.” However, the separation into high- and low-risk sites has recently been questioned. ‘Oral erythroplakis has not best! studied as intensively 4s oval leakoplaks.®* Erythroplakia is defined as a red lesion ‘of the oral mucosa that cannot be

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