Verrucous leukoplakia.pptx

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1. Presented By- DR. Humaira hussain Guided by- Dr. Prashant jaju CASE PRESENTATION OF VERRUCOUS LEUKOPLAKIA

2. CONTENTS PERSONAL DETAILS CHIEF COMPLAINT HISTORY OF PRESENTING ILLNESS DENTAL/MEDICAL HISTORY PERSONAL HISTORY FAMILY HISTORY GENERAL PHYSICAL EXAMINATION EXTRAORAL EXAMINATION INTRAORAL EXAMINATION LOCAL EXAMINATION OF THE CONDITION PROVISIONAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS INVESTIGATIONS FINAL DIAGNOSIS TREATMENT PLAN

3. PERSONAL DATA: O.P.D. No: 34150/21 Name: Shanti Lal Age: 64 years Occupation: Farmer Date: 26/10/20 Address:Harniyakala Sawan , Tehseel Kala Peepal , Zila - Shajapur

4. CHIEF COMPLAINT Patient complaints of inability to chew food since 4 years

5. HISTORY OF PRESENT ILLNESS Patient was apparently alright 6 years ago. Then he developed dull aching pain after which his teeth loosened and gradually started falling. He lost all his teeth 4 years ago and since then he is not able to chew food DENTAL / MEDICAL HISTORY – Extraction of teeth in 2016 FAMILY HISTORY - No Relevant History PERSONAL HISTORY – Habit of chewing tobacco ( ghutka ) with slaked lime 3-4 times a day (4gm/day) since 30 years. Used to keep on tongue on left side

6. EDUCATION STATUS: Till class 7

7. GENERAL PHYSICAL EXAMINATION : Patient was conscious and well oriented to time, place and person. Built: Average Nutritional status: Well nourished Height & weight: Gait & posture: Speech: Pallor: No abnormality detected Icterus : Cyanosis: Clubbing: Oedema :

8. Vital signs: Temperature – Afebrile Pulse – 74 beats/minute Respiration – 18 breaths/minute Blood pressure – 130/90 mm Hg

9. Extra Oral Examination : Head Form: Facial form: Skin: Hair: Eyes: Ears: No abnormality detected Nose: Paranasal sinuses: Lymph nodes: TMJ: Bilaterally symmetrical with no clicking or popping sound heard

10. Salivary glands: Saliva: Muscles of mastication: Muscles of facial expression: No abnormality detected Thyroid gland: Trachea: Carotid artery: Others:

11. I NTRA-ORAL EXAMINATION Labial Mucosa – Vermillion Border of Lip – No abnormality detected Hard Palate – Buccal Mucosa – Grayish white homogenous patch seen on left buccal mucosa Tongue – Grayish white homogenous patch seen on left dorsal, ventral surfaces and lateral border of tongue Floor of the mouth – Palate – Uvula – No abnormality detected Vestibule – Gingiva –

12. HARD TISSUE EXAMINATION: Teeth present: Completely edentulous Teeth missing: 11,12,13,14,15,16,17,21,22,23,24,25,26,27,31,32,33,34,35,36,37,41,42,43,44,45,46,47

13. LOCAL EXAMINATION OF THE LESION SOFT TISSUE EXAMINATION INSPECTION – Well defined, homogenous, grayish white patch seen extending from tip of tongue till posterior 2/3 rd surface of tongue on left lateral border of about 5 cm anteroposteriorly and 1 cm mediolaterally (involving dorsal, lateral and ventral surfaces) in dimensions There is whitish warty growth of 1× 1cm in dimensions in middle third portion of ventral tongue on left side Well defined, homogenous, grayish white patch seen extending from left retro commissure till buccal mucosa adjacent to alveolar bone of 34 and 2 × 1 cm in dimensions

14. PALPATION - The white patches are non tender, non scrapable and have rubbery consistency The warty growth is also non tender, non- scrapable and is rubbery in consistency

15. PROVISIONAL DIAGNOSIS : Verrucous hyperplasia on left ventral surface of tongue Homogenous leukoplakia on dorsum of tongue

16. DIFFERENTIAL DIAGNOSIS Verrucous leukoplakia Verrucous Carcinoma Chronic hyperplastic candidiasis

17. INVESTIGATIONS BLOOD INVESTIGATIONS Complete blood picture Bleeding and clotting time BIOPSY Ex cisional biopsy of verrucous growth was done

18. Haemoglobin : 12.4 gm% WBC Count : 8200/ cmm Differential Count : Neutrophil :46.2% Lymphocytes : 47.4% Monocytes :6.4% RBC count : 4.47 mil./cu.mm RBC INDICES MCV – 99.3 MCH- 35.9 MCHC- 36 Platelet Count : 357000/ cumm Bleeding time : 1 min Clotting time : 3 min

19. TREATMENT PLAN Emergency Phase Capsule Lycopene 8 mg once a day for 15 days Topical retinoic acid 0.01% twice a day for 15 days Phase 1 – Quit the habit Preliminary impression taken Phase 3 – Removable prosthesis given Phase 4 – Patient recalled after 15 days

20. Histopathological findings : The H and E stained section on microscopic examination reveals hyperkeratotic filliform papilla Histopathological diagnosis : Normal Tongue tissue FINAL DIAGNOSIS Homogenous Leukoplakia with left dorso -lateral surface of tongue Verrucous leukoplakia on left lateral border of tongue

21. DISCUSSION White lesions are relatively frequent in the oral cavity with prevalence of approximately 24.8% Among them oral leukoplakia (OL) is quite prevalent (0.2-3.6%) In a retrospective study, Hansen  et al ., reported that 26 of the 30 lesions initially diagnosed as OL became oral carcinomas in patients followed for 1-20 years (average, 6.1 years). After this study, these lesions were named oral proliferative verrucous leukoplakia (OPVL) According to the latest World Health Organization nomenclature, OPVL conforms to the new terminology of “potentially malignant disorders” given that it is neither a delimited lesion nor a condition It is best-defined as a continuum of oral epithelial disease with hyperkeratosis at one end of a clinical and microscopic spectrum and verrucous carcinoma or squamous cell carcinoma at the other

22. Etiopathogenesis Many potential etiologies have been hypothesized, but little has been proved about the origin of this disease process The disease seems to be idiopathic Tobacco is frequently absent as a known risk factor as OPVL occurs both in smokers and non-smokers An association has been reported between human papillomavirus (HPV) and OPVL Between 0% and 89% of OPVL are reported to be HPV positive, especially for HPV types 16 and 18 Apparently, there is no unequivocal pathogenetic link between HPV and OPVL and it has also been reported in association with Epstein-Barr virus or candida infection Despite such extensive works, the etiology of OPVL is still as enigmatic as the disease itself

23. Clinical features Two of the largest studies of OPVL patients reported a predilection for this lesion in elderly women, with a ratio as high as 4:1 for women to men unlike other forms of OL. The mean age at the time of diagnosis is slightly over 60 years It has been shown that almost all lesions occur bilaterally, mainly affecting the lower alveolar ridge and buccal mucosa Clinically, it generally presents as a simple benign form, which tends to spread and become diffuse In time, OPVL develops exophytic , wart-like or erythroplakic areas that become oral carcinomas

24. Histopathological features The microscopic findings associated with OPVL are dependent on the stage of the disease and the adequacy of the biopsy Hansen  et al ., suggested histologic stages in the continuum of OPVL with intermediates Grade 0: Normal mucosa Grade 2: Hyperkeratosis (clinical leukoplakia ) Grade 4: Verrucous hyperplasia Grade 6: Verrucous carcinoma Grade 8: Papillary squamous cell carcinoma Grade 10: Less well-differentiated squamous cell carcinoma Batsakis  et al ., reduced the number of histologic stages to four with intermediates: Grade 0: Clinical flat leukoplakia without dysplasia Grade 2: Verrucous hyperplasia Grade 4: Verrucous carcinoma Grade 6: Conventional squamous cell carcinoma with intermediates

25. It is of interest that the early phase of these lesions usually exhibits an interface lymphocytic infiltrate that may have a pronounced lichenoid pattern characterized by basal vacuolar degeneration containing apoptotic cells and eosinophilic bodies, similar to types of oral lichenoid stomatitis such as lichen planus Therefore, OPVL has no single defining histopathologic feature Diagnosis Because of the lack of specific histological criteria, the diagnosis of OPVL is based on combined clinical and histopathologic evidence of progression In previously published series, diagnosis of OPVL was made according to Hansen's  et al ., definition There are few studies that apply a set of diagnostic criteria that are mentioned as follows

26. Ghazali   et al ., established the following criteria: The lesion starts as homogenous leukoplakia without evidence of dysplasia at the first visit With time, some areas of leukoplakia become verrucous The disease progresses to the development of multiple isolated or confluent lesions at the same or a different site With time, the disease progresses through the different histopathological stages reported by Hansen  et al .[ 2 ] The appearance of new lesions after treatment A follow-up period of no less than 1 year. Gandolfo  et al ., establish the following criteria: An initially innocuous lesion characterized by a homogenous plaque that progresses over time to an exophytic , diffuse, usually multifocal, lesion with a verrucous epithelial growth pattern Histopathologically , proliferative verrucous leukoplakia (PVL) changes gradually from a simple plaque of hyperkeratosis without dysplasia to verrucous hyperplasia, verrucous carcinoma or oral squamous cell carcinoma (OSCC).

27. Cerero-Lapiedra   et al ., established the following major and minor criteria: Major criteria A leukoplakia lesion with more than two different oral sites, which is most frequently found in the gingiva , alveolar processes and palate The existence of a verrucous area That the lesions have spread or engrossed during development of the disease That there has been a recurrence in a previously treated area Histopathologically , there can be from simple epithelial hyperkeratosis to verrucous hyperplasia, verrucous carcinoma or OSCC, whether  in situ  or infiltrating. Minor criteria An OL lesion that occupies at least 3 cm when adding all the affected areas That the patient be female That patient (male or female) be a non-smoker A disease evolution higher than 5 years

28. In order to make the diagnosis of PVL, it was suggested that one of the two following combinations of the criteria mentioned before were met. Three major criteria (being E among them) or Two major criteria (being E among them) + two minor criteria. Nevertheless, at present, there is no criterion that will allow for the early diagnosis of the disease Treatment Advise patients with OPVL to avoid other known factors associated with development of oral carcinoma, such as tobacco, alcohol and betel.

29. Medical care Owing to the progressive nature of OPVL, many forms of therapy used for the management of traditional leukoplakia have been disappointing. Carbon dioxide laser, radiation, topical bleomycin solution, oral retinoids , beta-carotene and systemic chemotherapy have all failed at achieving permanent cure. Methisoprinol is a synthetic agent capable of inhibiting viral ribonucleic acid synthesis and replication and of stimulating antiviral cell–mediated reactions that has been shown to have some clinical efficacy in HPV-induced lesions. Although improvements have been noted with some of these modalities, recurrence rates after cessation of therapy are high, often within months of discontinuation of treatment

30. Surgical care This lesion is resistant to the presently available treatment modalities; therefore, total excision with free surgical margins is critical combined with a lifelong follow-up Malignant transformation and recurrences OPVL is known for its aggressive pathology, given its multifocal involvement, high malignant transformation rates (60-100%), frequent recurrences (87-100%) and high mortality rates (30-50%) The gingiva and palate represented the areas with the highest frequency of these multiple malignant tumors Given the high tendency for (OSCCs) to appear in these patients, they should be checked for life at least once every 6 months

31. REFERENCES Issrani R, Prabhu N, Keluskar V. Oral proliferative verrucous leukoplakia : A case report with an update.  Contemp Clin Dent . 2013;4(2):258-262. doi:10.4103/0976-237X.114887