Introduction
Oral mucosa is composed of specialized stratified epithelium derived from the ectoderm. The tongue originates from the endoderm. The oral cavity is divided into the vestibule and oral cavity proper.[1,2]
Dermatological conditions involving the oral cavity present as ulcers, swellings, erythema, pigmentation, blisters, and white patches. Oral mucosal lesions (OML) are recognized based on their site, size, color, distribution, and symptoms.[3] Clinical examination is difficult due to anatomical and functional peculiarities. Diagnosing and treating oral cavity lesions is challenging due to similarity in symptoms and appearances. Confirmation of diagnosis requires histopathology and occasionally immunohistochemistry. An OML is defined as any abnormal change affecting the oral mucosal surface[3] resulting from local pathology or secondary to systemic diseases, including those of skin.[3]
This study aims to understand the etiology and clinical features of OML. This study duration was one and a half years.
Materials and Methods
A descriptive study of 369 cases with OML of all age groups and both sexes was carried out over a period of 18 months. Institutional Ethics Committee approval was taken. Patients with only lip lesions were excluded. Informed written consent for biopsy and photographs was taken. A complete history and detailed examination was recorded in pre-designed proforma.
Results
Three hundred and sixty-nine patients were enrolled in the study. Males constituted 61.78% of the cases. Details of patients including presenting symptoms and habits are mentioned in [Table 1].
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Table 1: Table showing patient details
The various disease groups with oral involvement are mentioned in [Table 2]. The largest disease group was that of papulosquamous diseases, such as oral lichen planus (LP) [Figure 1a and b] and psoriasis vulgaris (PV) (geographic tongue), in which oral LP constituted largest group of patients.
Table 2: Etiology of oral cavity lesions
Figure 1: (a) Nail involvement with oral lichen planus, (b) Reticular variant of oral lichen planus, (c) Xeroderma pigmentosum – squamous cell carcinoma of tongue and right cheek, (d) Pseudomembranous candidiasis, (e) Oral erosions in a patient of pemphigus vulgaris
Malignancies, such as squamous cell carcinoma (SCC) [Figure 1c] and verrucous carcinoma, were seen in 20.33% of patients.
Oral candidiasis [Figure 1d], herpetic gingivostomatitis, measles, and hand foot mouth disease were the common infectious conditions causing OML (11.92%).
Vesiculobullous diseases, such as pemphigus vulgaris (PV) [Figure 1e], mucous membrane pemphigoid (MMP), paraneoplastic pemphigus, and linear IgA pemphigus, accounted for 10.29% of cases.
Miscellaneous conditions included Behcet’s disease (BD) [Figure 2a and b], blue rubber bleb nevus syndrome [Figure 2c and d], mucocele [Figure 2e], fibroma [Figure 2f], Hecks’s disease [Figure 3a], hemangiolymphoma [Figure 3b], Melkersson–Rosenthal syndrome [Figure 3c and d], rhinoscleroma [Figure 3e], etc., have been mentioned in [Table 2].
Figure 2: Behcet’s disease – (a) Major aphthae on the tongue, (b) Two ulcers over the shaft of penis; Blue rubber bleb nevus syndrome – (c) Hemangioma on the tongue, (d) Hemangiomas on the feet, (e) Mucocele - mucosal aspect of lower lip, (f) Fibroma- right buccal mucosa
Figure 3: (a) Heck’s disease- right buccal mucosa, (b) Hemangiolymphoma of tongue; Melkersson Rosenthal syndrome – (c) Hard palate, (d) Upper lip, (e) Rhinoscleroma - granulomatous growth over palate, (f) Oral leucoplakia over ventral aspect of tongue, (g) Oral submucous fibrosis (OSMF) - left buccal mucosa, (h) Toxic epidermal necrolysis
Aphthous stomatitis was seen in 8.94% of cases.
Premalignant lesions, such as oral leukoplakia [Figure 3f], oral submucous fibrosis (OSMF) [Figure 3g], smoker’s palate was seen in 7.05%.
Drug reactions, such as fixed drug reaction, toxic epidermal necrolysis (TEN) [Figure 3h] and Stevens–Johnson syndrome (SJS) were seen in 1.89% cases.
OML with genodermatoses was seen in two cases (0.54%), one case each of congenital ichthyosiform erythroderma and xeroderma pigmentosum (SCC) [Figure 1c].
Diseases with oral lesions per se and those with cutaneous involvement are shown in Tables 3 and 4.
Table 3: Diseases with both oral and cutaneous manifestations
Table 4: Diseases with only oral manifestations
A total of 209 (56.64%) cases gave consent for histopathology, out of which 186 cases (88.99%) showed clinico-histopathological correlation (CHC). Out of 72 cases of oral LP [Figure 4a], 65 (90.27%), 14 (82.35%) out of 17 cases of oral pemphigus [Figure 4b], 16 (100%) out of 16 cases of PV showed CHC. CHC was seen in five (83.33%) out of six cases of leukoplakia, all 73 cases (100%) of oral SCC [Figure 4c] and one case each of BD, mucocele [Figure 4d], hemangioma of the tongue [Figure 4e], OSMF [Figure 4f], squamous papilloma, verrucous carcinoma, linear IgA pemphigus, Heck’s disease, fibroma [Figure 4g], paraneoplastic pemphigus, rhinoscleroma [Figure 4h], MMP, and TEN demonstrated CHC.
Figure 4: (a) H and E stain, 10X, oral lichen planus, (b) H and E stain, 10X, oral pemphigus, (c) H and E stain, 10X, oral squamous cell carcinoma, (d) H and E stain, 10X, mucocele, (e) H and E stain, 10X, hemangioma, (f) H and E stain, 10X, oral submucous fibrosis, (g) H and E stain, 10X, fibroma, (h) H and E stain, 10X, rhinoscleroma
Discussion
In our study, the maximum number of cases with oral lesions were seen in the age group of 31-50 years, whereas, a study by Roy et al.[4] showed the maximum incidence between 10 and 30 years.
In our study, the M: F ratio was 1.62:1. In a study done by Roy et al.,[4] M: F ratio was 2:3. Patients with only oral lesions comprised 82.11% of patients, in which, oral LP was the commonest condition (24.42%), followed by oral SCC (23.76%), aphthous stomatitis (10.89%), oral candidiasis (10.56%) and oral pemphigus (5.61%). In a study conducted by Roy et al.,[4] aphthous ulcers constituted the major bulk of patients (28.57%). Patients with both oral and cutaneous lesions comprised 17.89% of patients which included PV (28.79%), oral LP (9.09%), BD (9.09%) and SLE (7.57%) vis-a-vis the study conducted by Roy et al.,[4] wherein 26.60% patients had PV, followed by SLE (17.02%), DLE (13.83%), and LP (12.77%).
Seventy five cases (20.33%) were diagnosed with oral carcinomas. SCC was diagnosed in 73 cases (97.33%). M: F ratio was 2.57:1 with a male preponderance (72%). Common sites involved were buccal mucosa (33.3%) and lateral aspect of tongue (28%). A total of 48% patients were tobacco chewers, smokers or alcoholics. Histopathological changes seen were anaplastic squamous cells arranged in sheet and cord-like pattern, individual tumor cells showed pleomorphism, high N: C ratio with hyperchromatism, prominent nucleoli, areas of necrosis and at places keratin pearls. Histological grading of the tumors revealed 81.43%, 18.57%, and 0% of the tumors being, well differentiated (WD), moderately differentiated (MD) and poorly differentiated (PD) oral SCC, respectively. In a study conducted by Leite et al.,[5] 60.82% cases were males with M: F ratio 1.5:1. Border of the tongue, ventrum of tongue and buccal mucosa were involved respectively in 26.71%, 18.8% and 7.39% of cases. Histologically, 54.6% were WD, 37.1% were MD and 10.52% were PD in her study. In a study conducted by Abdulla et al.,[6] the tongue (29.07%) and buccal mucosa (27.9%) were commonly involved sites. Rai et al.[7] reported 50.77% were WD, 29.33% were MD, and 20% were PD.
Oral LP constituted 21.96% of the total cases. Oral lesions alone were seen in 20.87% patients, whereas, 1.09% had both oral and cutaneous manifestations. A total of 41 cases (50.61%) were in the age group of 31 to 50 years and 45 cases (55.55%) were males. Reticular type of LP was seen in 52 patients (64.19%), erosive type in 15 patients (18.51%), atrophic type in six patients (7.40%), plaque type in three patients (3.70%) and bullous lesions in one patient (1.23%). In a study conducted by Roy et al.,[4] erosive type was seen in eight patients (66.67%), and reticular type in four patients (33.33%). Silverman et al.[8] documented erosive LP in 22% and reticular LP in 7% of patients. Juan Seoane et al.[9] also reported reticular LP to be common. CHC in our study was observed in 90.27% patients. The histopathological changes seen were hyperparakeratosis, mild acanthosis, hydropic degeneration of the basal layer, lymphocyctic infiltration in the subepithelial layer. The same was observed in 52.2%, 92.31%, and 50% of cases in studies conducted by Bukhari et al.,[10] Bandyopadhyay et al.,[11] and Van der Meij et al.[12], respectively.
Pemphigus was diagnosed in 35 cases (9.49%). M: F ratio was 1: 2.13. Fifteen cases were in 31 to 50 years of age group. Buccal mucosa was involved in 42.8% of PV cases. CHC was seen in 30 (85.71%) with histopathological changes such as acantholysis in the lower spinous layers, basal layer cells are attached to the basement membrane and suprabasal cleft is seen at the tips of epithelial rete ridges. Shamim et al.[13] reported M: F ratio as 1:1.73. Buccal mucosa was involved in 90.14% of cases with 100% CHC. Iamaroon et al.[14] reported M: F ratio as 1:2, buccal mucosa was affected in 61.11% of cases and 100% CHC was seen.
Thirty two cases of oral candidiasis (8.67% of total cases) were included. Tobacco chewing and smoking was observed in 25% and 12.5% of patients, respectively. Dorsum of tongue (75%) and buccal mucosa were commonly involved. Acute pseudomembranous type was seen in 18 cases. Meira et al.[15] reported involvement of palate in 52.9% and tongue in 43.4% patients. Roy et al.[4] reported oral candidiasis in 16.07%.
Oral leukoplakia constituted 14 cases (3.80%). Dorey et al.[16] reported a slight male predilection, especially in the age of 50–70 years. Roy et al.[4] reported four patients (7.14%) of leukoplakia. Eight patients (57.14%) were above 50 years of age. All the patients were addicted to smoking and tobacco. Buccal mucosa and tongue were involved in 71.48%. Silverman et al.[8] reported involvement of buccal mucosa in 91% of cases. Six patients were biopsied out of which five showed CHC with squamous epithelial hyperplasia with hyperkeratosis.
Nine cases of OSMF (2.44% of total cases) were included. Six patients (66.67%) were males. Most common presentations were decreased mouth opening and burning. All of them had history of smoking and chewing tobacco. Buccal mucosa and palate were commonly affected. Pindborg et al.[17] found buccal mucosa, lips and palate commonly involved. Roy et al.[4] reported OSMF in 10.71% of patients.
Mucocele was diagnosed in eight (2.16%) cases. The common site involved was lower lip. Four cases were biopsied and showed hyperplastic parakeratinized stratified squamous epithelium, small cystic spaces containing mucin and mucus-filled cells with few sebaceous cells arranged in group. Roy et al.[4] reported the incidence of mucocele as 3.57%.
Drug reactions causing OML were seen in seven cases (1.89%). Three cases (0.81%) were of fixed drug eruption (FDE) caused by ciprofloxacin and diclofenac, three cases (0.81%) of SJS caused by carbamazepine (two cases) and ciprofloxacin (one case) and one case (0.27%) of TEN caused by carbamazepine which also showed CHC with changes such as subepidermal bullae with widespread epidermal necrosis and subsequent separation or loss of the entire epidermis. In studies conducted by Roy et al.,[4] FDE, SJS, TEN were seen in 7.14%, 8.51%, and 4.26% of patients, respectively. Babu RA et al.[18] reported TEN and SJS in 4.61% and 18.46% of patients, respectively.
BD was diagnosed in six cases (1.64%). All presented with painful ulcers over tongue, lips and buccal mucosa. Biopsy revealed ulceration of epidermis, leucocytoclastic vasculitis, endothelial swelling with perivascular neutrophillic and lymphocytic inflammatory infiltrate; consistent with a study conducted by Chun SI et al.[19]
SLE was diagnosed in five cases. Lips and buccal mucosa were commonly involved. Burge SM et al.[20] on SLE reported that 48 were females with lips and palate being the commonest site. Roy et al.[4] reported palate to be the commonest site.
DLE was diagnosed in two cases with erosive plaques on the hard palate and lips. Roy et al.[4] and Burge SM et al.[20] reported lips and buccal mucosa to be the commonest site in DLE respectively.
Fordyce spots was diagnosed in two cases (0.54%), with asymptomatic papules over upper lip. Roy et al.[4] reported the same in 3.57% of cases.
Heck’s disease, Melkersson–Rosenthal syndrome, squamous papilloma, hemangioma of the tongue, caviar tongue, Fibroma were some of the miscellaneous cases in this study.
Conclusion
In our study, lesions of oral LP were most common followed by those of oral SCC. Several rare conditions may be missed if not sought for diligently. Our study emphasizes the need to correctly diagnose oral lesions on the basis of detailed clinical examination and histopathology. It is prudent to discuss such cases with maxillofacial and ENT surgeons. Several conditions may be missed out by other specialists. Indeed, there is a need to demystify the diverse clinical presentations and management of oral lesions.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
1. Pocock G, Richards CD. Human Physiology: The Basis of Medicine Oxford Core Texts. 4th ed. Oxford University Press; Oxford, United Kingdom; 2013. 586
2. Kumar GS, Bhaskar SN. Orban's Oral Histology and Embryology. 14th ed. Elsevier; India; 2015; 194–239
3. Berkovitz B, Holl G, Moxham B. Oral Anatomy, Histology and Embryology. 4th ed. Mosby/Elsevier; Edinburgh; 2015. 223–51
4. Roy S, Varshney S. Oral dermatological conditions:A clinical study. Indian J Otolaryngol Head Neck Surg 2013;65:97–101
5. Leite AA, Leonel ACLDS, Castro JFL, Carvalho EJA, Vargas PA, Kowalski LP, et al. Oral
squamous cell carcinoma:A clinicopathological study on 194 cases in northeastern Brazil. A cross-sectional retrospective study. Sao Paulo Med J 2018;136:165–9
6. Abdulla R, Adyanthaya S, Kini P, Mohanty V, D'Souza N, Subbannayya Y. Clinicopathological analysis of oral
squamous cell carcinoma among the younger age group in coastal Karnataka, India:A retrospective study. J Oral Maxillofac Pathol 2018;22:180–7
7. Rai HC, Ahmed J. Clinicopathological correlation study of oral
squamous cell carcinoma in a local Indian population. Asian Pac J Cancer Prev 2016;17:1251–4
8. Silverman S Jr, Gorsky M, Lozada-Nur F, Giannotti K. A prospective study of findings and management in 214 patients with oral lichen planus. Oral Surg Oral Med Oral Pathol 1991;72:665–70
9. Seoane J, Romero MA, Varela-Centelles P, Diz-Dios P, Garcia-Pola MJ. Oral lichen planus:A clinical and morphometric study of oral lesions in relation to clinical presentation. Braz Dent J 2004;15:9–12
10. Bukhari SS, Gupta V, Dogra DR, Goswami KC, Ahmed A, Rather MI. Clinicohistopathological correlation of oral lesions. Int J Contemp Med Res 2017;4:1398–401
11. Bandyopadhyay A, Behura SS, Nishat R, Dash KC, Bhuyan L, Ramachandra S. Clinicopathological profile and malignant transformation in oral lichen planus:A retrospective study. J Int Soc Prevent Communit Dent 2017;7:116–24
12. van der Meij EH, van der Waal I. Lack of clinicopathologic correlation in the diagnosis of oral lichen planus based on the presently available diagnostic criteria and suggestions for modifications. J Oral Pathol Med 2003;32:507–12
13. Shamim T, Varghese VI, Shameena PM, Sudha S. Pemphigus vulgaris in oral cavity:clinical analysis of 71 cases. Med Oral Patol Oral Cir Bucal 2008;13:E622–6
14. Iamaroon A, Boonyawong P, Klanrit P, Prasongtunskul S, Thongprasom K. Characterization of oral pemphigus vulgaris in Thai patients. J Oral Sci 2006;48:43–6
15. Meira HC, De Oliveira BM, Pereira IF, Naves MD, Mesquita RA, Santos VR. Oral candidiasis:A retrospective study of 276 Brazilian patients. Oral Maxillofac Pathol 2017;21:351–5
16. Dorey JL, Blasberg B, Conklin RJ, Carmichael RP. Oral leukoplakia. Current concepts in diagnosis, management, and malignant potential. Int J Dermatol 1984;23:638–42
17. Pindborg JJ, Bhonsle RB, Murti PR, Gupta PC, Daftary DK, Mehta FS. Incidence and early forms of oral submucous fibrosis. Oral Surg Oral Med Oral Pathol 1980;50:40–4
18. Babu RA, Chandrashekar P, Kumar KK, Reddy GS, Chandra KL, Rao V, et al. A study on oral mucosal lesions in 3500 patients with dermatological diseases in South India. Ann Med Health Sci Res 2014;4 (Suppl 2):S84–93
19. Chun SI, Su WP, Lee S. Histopathologic study of cutaneous lesions in Behçet's syndrome. J Dermatol 1990;17:333–41
20. Burge SM, Frith PA, Juniper RP, Wojnarowska F. Mucosal involvement in systemic and chronic cutaneous lupus erythematosus. Br J Dermatol 1989;121:727–41
