|Year : 2022 | Volume
| Issue : 4 | Page : 132-135
Assessment of the Relationship between Expression of p63 with Different Clinical Types of Oral Lichen Planus: A Retrospective Immunohistochemistry Study
Mustafa Mohammed Abdulhussain1, Karrar N Shareef2, Mohammed Al Zubidi3
1 Department of Oral Pathology, College of Dentistry, Mustansiriyah University, Baghdad, Iraq
2 College of Dentistry, Alkafeel University, Najaf, Iraq
3 College of Dentistry, Mustnsiriyiah University, Baghdad, Iraq
|Date of Submission||21-Jul-2022|
|Date of Decision||06-Oct-2022|
|Date of Acceptance||09-Oct-2022|
|Date of Web Publication||12-Dec-2022|
Mustafa Mohammed Abdulhussain
Department of Oral Pathology, College of Dentistry, Mustansiriyah University, Baghdad
Source of Support: None, Conflict of Interest: None
Introduction: We aimed to assess the expression of p63 among different clinical types of oral lichen planus. Methods: The current study includes 44 oral lichen planus cases from the oral pathology laboratory, oral diagnostic department, Baghdad University. P63-PRM114P used as primary monoclonal antibodies. The intensity of immunohistochemistry activity was calculated utilizing the following criteria: weak intensity: one positive cell, moderate intensity: two positive cells, and strong intensity: three or more positive cells (magnification 20×). Results: The mean age of participants was 52.82 ± 12. No significant relationship found between gender and expression of p63 (P = 0.65). The p63 expressed in all clinical types of oral lichen planus (OLP). Yet, expression of p63 was not significantly related to the clinical type of OLP (P = 0.98). Conclusion: We could not found relationship between expression of p63 among different clinical types of oral lichen planus. With respect to the limited sample size of this study, some larger scale studies among different populations are need to reach to a definitive conclusion regarding relationship between expression of p63 among different clinical types of oral lichen planus.
Keywords: Biomarkers, immunohistochemistry, oral lichen planus, p63
|How to cite this article:|
Abdulhussain MM, Shareef KN, Zubidi MA. Assessment of the Relationship between Expression of p63 with Different Clinical Types of Oral Lichen Planus: A Retrospective Immunohistochemistry Study. Dent Hypotheses 2022;13:132-5
|How to cite this URL:|
Abdulhussain MM, Shareef KN, Zubidi MA. Assessment of the Relationship between Expression of p63 with Different Clinical Types of Oral Lichen Planus: A Retrospective Immunohistochemistry Study. Dent Hypotheses [serial online] 2022 [cited 2023 Feb 5];13:132-5. Available from: http://www.dentalhypotheses.com/text.asp?2022/13/4/132/363440
| Introduction|| |
Oral lichen planus (OLP) is a widespread lesion of the skin and mucous membranes with persistent inflammatory development that is thought to be induced by immune response reactivity to skin or mucous alterations.
It is critical to consider the appearance of oral lichenoid lesions for its diagnostic process, which must differentially diagnose from hypersensitivity responses stimulated by antigens from drug action or by immediate communication with allergic components that can reach the oral cavity, with heavy metals, copper, and gold, which are the most common mixtures.
The pathogenesis of lichen planus is unclear. However, immunological elements, genetics, drugs, and hepatitis C may all play a role in its development. Because studies indicated that this condition might progress to a malignant consequence in the long run, the world health organization (WHO) classified it as a precancerous condition.
OLP manifests as white streaks, white sludge, and desquamation affecting the oral mucosa, with erosional and atrophic variants exhibiting the most prevalent malignant development. There are several carcinogenic rates for OLP.
p63, a signaling pathway, is essential for epithelial cell growth, development, and morphogenesis. Rather than a direct association between oncogenesis and carcinogenic transformation, the purpose of p63 in epithelial tissue may be to preserve stem cell activity. Thus, p63 may play an important role in the carcinogenic conversion of oral potentially malignant disorders.
The p63 gene, which is found on chromosome 3q27-29, encodes six distinct proteins, three of which are full-length (TAp63a, TAp63b, and TAp63c) and three of which lack the N-terminus transactivational region. The p63 isoforms play an important part in the development of ectodermally related elements such as mucosal surfaces, salivary glands, dentition, and skin.
However, we aimed to assess the relationship between expression of p63 with different clinical types of OLP.
| Materials and Methods|| |
The study protocol approved by local ethical committee of the Baghdad University (approval number: 294721). Forty-four OLP samples were collected from the oral pathology laboratory, oral diagnostic department, Baghdad University. Formalin-fixed, paraffin-embedded epithelial tissues from each patient were obtained, together with patient medical records (age, sex, and clinical type) from oral and maxillofacial reports. Two pathologists evaluated H&E-stained tissue fragments from each patient to confirm the diagnosis. Prostate tissue was utilized as positive control to determine the intensity of study samples in each immunohistochemical run. Prostate samples collect randomly from the laboratory of Ghazi al-Hariri Surgical Specialities Hospital, Baghdad, Iraq.
P63-PRM114P (PathnSitu Biotechnologies, Secunderabad, India) used as primary monoclonal antibodies. One 5 mm sample was placed on a positive charge glass slide to improve tissue adherence during immunohistochemical staining. Positive control slides have 5 mm thick tissue sections. The antibody was diluted (1:50) and applied to tissue sections for 30 to 60 minutes at room temperature. Phosphate buffered saline (PBS) (Sigma-Aldrich, Saint Louis, MO, USA) was used to wash, dry, and rinse the segments three times (5 minutes for each).
Negative controls were healthy tissue samples which processed with PBS. A drop of soluble rabbit anti-mouse antibody added and was left overnight at 37°C for 15 minutes before being rinsed and dehydrated. Polymer was treated with secondary antibodies at 37°C for 15 minutes, then washed with PBS and dried.
The intensity of immunohistochemistry activity was calculated utilizing the following criteria: weak intensity: one positive cell, moderate intensity: two positive cells, and strong intensity: three or more positive cells (magnification 20×).
Data analyzed by chi-squared tests using MedCalc 20.104 (MedCalc Software Ltd., Ostend, Belgium). A P-value of 0.05 was considered significant.
| Results|| |
The mean age of participants was 52.82 ± 12 (95% confidence interval: 49.14–56.49) years. There was no significant relationship between age and expression of p63 (P = 0.64). 40.9% of participants were male. No significant relationship found between gender and expression of p63 (P = 0.65).
The findings of immunohistochemical staining indicated brown nuclear positivity of p63 in all study participants [Figure 1] and [Figure 2]. Expression of p63 was not significantly related to the clinical type of OLP (P = 0.98) [Figure 2].
|Figure 1 (A) Photomicrograph of oral lichen planus (OLP), H&E stain; (B) positive controls of p63 reactivity in human prostate tissue; (C) positive nuclear expression of P63 in OLP (Mild +); (D) positive nuclear expression of p63 in OLP (Sever +++), (magnification 20×)|
Click here to view
|Figure 2 Distributions of p63 expression among different clinical types of the OLP lesions|
Click here to view
| Discussion|| |
The p63 gene (consists of 15 exons spanning ∼270 kb) encodes multiple proteins that are essential to several of aspects of cell biology including: cell expiry and survival, lineage specification, proliferative potential, differentiation, DNA harm reaction and metabolism. In addition, p63 is related to human illness including cancer.
Several studies examined relationship between p63 and OLP. Ebrahimi et al., showed decreased expression of p63 in OLP in comparison to the normal tissue using monospecific antibodies.
Decreased expression of p63 and increased expression of p53 in OLP, which also in been observed in epithelia exposed to ultraviolet, may act as a protecting mechanism, enabling removal of DNA-damaged cells.Furthermore, p63 associated proteins for instance b-catenin, E-cadherin, and EGFR reduced in OLP. Autoantibodies against p63 found in sera of patient suffering from OLP, suggesting autoimmune response as an etiologic factor for OLP.
A recent review stated that with respect to the currently available data it cannot be concluded whether OLP lesions are at an increased risk of malignant development.
Nevertheless, it is well-known that OLP has different clinical presentations. To our knowledge this is the first study aimed to assess expression of p63 among diverse clinical types of OLP. We could not found significant relationship between expression of p63 among different clinical types of oral lichen planus. Yet, p63 expressed in all clinical types of OLP.
However, with respect to the limited sample size of this single-center retrospective study, some larger scale studies among different populations are need to reach to a definitive conclusion regarding relationship between expression of p63 among different clinical types of oral lichen planus.
| References|| |
Di Como CJ, Urist MJ, Babayan I et al.
p63 expression profiles in human normal and tumor tissues. Clin Cancer Res 2002;8:494-501.
Parsa R, Yang A, McKeon F, Green H. Association of p63 with proliferative potential in normal and neoplastic human keratinocytes. Journal of Investigative Dermatology 1999;113:1099-105.
Agha-Hosseini F, Mirzaii-Dizgah I. p53 as a neoplastic biomarker in patients with erosive and plaque like forms of oral lichen planus. J Contemp Dental Pract 2013;14:1.
Müller S. Oral lichenoid lesions: distinguishing the benign from the deadly. Mod Pathol 2017;30:54e67.
Montebugnoli L, Farnedi A, Marchetti C, Magrini E, Pession A, Foschini MP. High proliferative activity and chromosomal instability in oral lichen planus. Int J Oral Maxillofacial Surg 2006;35:1140-4.
Sá CT, Fonseca LM, Cardoso SV, Aguiar MC, Carmo MA. p53 immunoexpression in oral squamous cell carcinomas from different anatomical sites: a comparative study. Int J Morphol. 2006;24:231-8.
Sugerman PB, Sabage NW. Oral lichen planus: causes, diagnosis and management. Aust Dent J 2002;47:290-7.
Ismail SB, Kumar SK, Zain RB. Oral lichen planus and lichenoid reactions: etiopathogenesis, diagnosis, management and malignant transformation. J Oral Sci 2007;49:89-106.
Yong M, Yang L, Suyila Q et al.
Expression and clinical implications of P53, P63, and P73 protein in malignant tumor of the parotid gland. Turk J Med Sci 2014;44:875-82.
Takeda T, Sugihara K, Hirayama Y, Hirano M, Tanuma JI, Semba I. Immunohistological evaluation of Ki‐67, p63, CK19 and p53 expression in oral epithelial dysplasias. J Oral Pathol Med 2006;35:369-75.
Ou HD, Löhr F, Vogel V, Mäntele W, Dötsch V. Structural evolution of C‐terminal domains in the p53 family. EMBO J 2007;26:3463-73.
Fisher ML, Balinth S, Mills AA. p63-related signaling at a glance. J Cell Sci 2020;133:jcs228015.
Ebrahimi M, Wahlin YB, Coates PJ, Sjöström B, Nylander K. Decreased expression of p63 in oral lichen planus and graft-vs.-host disease associated with oral inflammation. J Oral Pathol Med 2006;35:46-50.
Ebrahimi M, Nylander K, van der Waal I. Oral lichen planus and the p53 family: what do we know? J Oral Pathol Med 2011;40:281-5.
Ebrahimi M, Boldrup L, Wahlin YB, Coates PJ, Nylander K. Decreased expression of the p63 related proteins beta-catenin, E-cadherin and EGFR in oral lichen planus. Oral Oncol 2008;44:634-8.
Ebrahimi M, Wahlin YB, Coates PJ, Wiik A, Roos G, Nylander K. Detection of antibodies against p63 and p73 isoforms in sera from patients diagnosed with oral lichen planus. J Oral Pathol Med 2007;36:93-8.
[Figure 1], [Figure 2]