Wednesday 14 December 2011
Saturday 26 November 2011
Two years with PUBMED by Joshua E.
Two years with PUBMED
Dear Colleagues,
Seasons greetings to one and all
It is about two years since our journal has been listed with PubMed and various other International indexing agencies. In the year 2011, the academic climate in the Indian Dental field has undergone rapid changes. These changes have provoked an unprecedented interest and an increased volume of article submission to our journal. Consequently, we have responded by increasing the frequency as well as the number of manuscripts published per issue by at least four-fold, without compromising on the quality.
With an increase in the volume of articles, the responsibilities of the editorial team as well as the peer reviewers increase all the more. In spite of several check points, mistakes are liable to take place at many stages. Inadvertent or 'Intentional' errors committed by authors of several submissions have been identified and rectified. Notwithstanding these attempts, few errors might have crept in. The Journal publishes the accepted manuscripts in good faith, trusting that the article submitted is original, including the script, and not borrowed from any other source. I, therefore, urge the authors to read and revise their manuscripts several times before submission and abide by the guidelines provided for manuscript submission. I would like to bring to your kind attention that issues with plagiarism and text copying will be viewed seriously and may even warrant blacklisting for three years, if found in the earlier stage, and retraction even after publication. Soliciting in any form for publications shall not be entertained. I request all the authors to keep the high standards set for academic publications.
To increase the quality of the Journal of Oral and Maxillofacial Pathology (JOMFP) as well as to increase the citation rate, it has been decided that only original research articles of contemporary interest will be published from the next issue. However, interesting cases and series that are novel, which open up the understanding of a disease process will be considered. The number of case reports will be restricted to less than 25% of all manuscripts. I request all the members and potential authors to consider these facts while preparing their manuscripts. Submission of high quality photographs with sharp images, in focus, with a clear background and appropriate lighting is mandatory. Markings (arrow / bullets) can be incorporated inside the image itself. Only histopathological images with high resolution and clarity will be considered.
The reviewers have been the backbone of JOMFP. I take this opportunity to thank each one of them personally, especially for sparing their valuable time, and look forward for their continued support and dedication in the years to come.
I am confident that with support from all of you, JOMFP will be a much sought after Journal in our field.
Looking forward to meeting you all in Hyderabad.
Dear Colleagues,
Seasons greetings to one and all
It is about two years since our journal has been listed with PubMed and various other International indexing agencies. In the year 2011, the academic climate in the Indian Dental field has undergone rapid changes. These changes have provoked an unprecedented interest and an increased volume of article submission to our journal. Consequently, we have responded by increasing the frequency as well as the number of manuscripts published per issue by at least four-fold, without compromising on the quality.
With an increase in the volume of articles, the responsibilities of the editorial team as well as the peer reviewers increase all the more. In spite of several check points, mistakes are liable to take place at many stages. Inadvertent or 'Intentional' errors committed by authors of several submissions have been identified and rectified. Notwithstanding these attempts, few errors might have crept in. The Journal publishes the accepted manuscripts in good faith, trusting that the article submitted is original, including the script, and not borrowed from any other source. I, therefore, urge the authors to read and revise their manuscripts several times before submission and abide by the guidelines provided for manuscript submission. I would like to bring to your kind attention that issues with plagiarism and text copying will be viewed seriously and may even warrant blacklisting for three years, if found in the earlier stage, and retraction even after publication. Soliciting in any form for publications shall not be entertained. I request all the authors to keep the high standards set for academic publications.
To increase the quality of the Journal of Oral and Maxillofacial Pathology (JOMFP) as well as to increase the citation rate, it has been decided that only original research articles of contemporary interest will be published from the next issue. However, interesting cases and series that are novel, which open up the understanding of a disease process will be considered. The number of case reports will be restricted to less than 25% of all manuscripts. I request all the members and potential authors to consider these facts while preparing their manuscripts. Submission of high quality photographs with sharp images, in focus, with a clear background and appropriate lighting is mandatory. Markings (arrow / bullets) can be incorporated inside the image itself. Only histopathological images with high resolution and clarity will be considered.
The reviewers have been the backbone of JOMFP. I take this opportunity to thank each one of them personally, especially for sparing their valuable time, and look forward for their continued support and dedication in the years to come.
I am confident that with support from all of you, JOMFP will be a much sought after Journal in our field.
Looking forward to meeting you all in Hyderabad.
Two Years with PUBMED by Joshua E.
Dear Colleagues,
Seasons greetings to one and all
It is about two years since our journal has been listed with PubMed and various other International indexing agencies. In the year 2011, the academic climate in the Indian Dental field has undergone rapid changes. These changes have provoked an unprecedented interest and an increased volume of article submission to our journal. Consequently, we have responded by increasing the frequency as well as the number of manuscripts published per issue by at least four-fold, without compromising on the quality.
With an increase in the volume of articles, the responsibilities of the editorial team as well as the peer reviewers increase all the more. In spite of several check points, mistakes are liable to take place at many stages. Inadvertent or 'Intentional' errors committed by authors of several submissions have been identified and rectified. Notwithstanding these attempts, few errors might have crept in. The Journal publishes the accepted manuscripts in good faith, trusting that the article submitted is original, including the script, and not borrowed from any other source. I, therefore, urge the authors to read and revise their manuscripts several times before submission and abide by the guidelines provided for manuscript submission. I would like to bring to your kind attention that issues with plagiarism and text copying will be viewed seriously and may even warrant blacklisting for three years, if found in the earlier stage, and retraction even after publication. Soliciting in any form for publications shall not be entertained. I request all the authors to keep the high standards set for academic publications.
To increase the quality of the Journal of Oral and Maxillofacial Pathology (JOMFP) as well as to increase the citation rate, it has been decided that only original research articles of contemporary interest will be published from the next issue. However, interesting cases and series that are novel, which open up the understanding of a disease process will be considered. The number of case reports will be restricted to less than 25% of all manuscripts. I request all the members and potential authors to consider these facts while preparing their manuscripts. Submission of high quality photographs with sharp images, in focus, with a clear background and appropriate lighting is mandatory. Markings (arrow / bullets) can be incorporated inside the image itself. Only histopathological images with high resolution and clarity will be considered.
The reviewers have been the backbone of JOMFP. I take this opportunity to thank each one of them personally, especially for sparing their valuable time, and look forward for their continued support and dedication in the years to come.
I am confident that with support from all of you, JOMFP will be a much sought after Journal in our field.
Looking forward to meeting you all in Hyderabad.
Two years with PUBMED
Monday 10 October 2011
Friday 16 September 2011
Plagiarism and scientific writing: a personal commentary
http://onlinelibrary.wiley.com/doi/10.1111/j.2041-1626.2011.00099.x/full
Irulandy Ponniah
Department of Oral and Maxillofacial Pathology, Tamil Nadu Government Dental College and Hopsital, Chennai, India.
Abstract There have been a number of papers that have addressed the issue of plagiarism. Nevertheless, the charges of plagiarism usually merit little attention with experts, because it is still not clear what sort of copying actually constitutes plagiarism. Another problem that eludes consensus is whether plagiarism was committed with or without intention. This paper discusses certain issues relating to plagiarism and differentiates between intentional and unintentional forms of plagiarism.
Irulandy Ponniah
Department of Oral and Maxillofacial Pathology, Tamil Nadu Government Dental College and Hopsital, Chennai, India.
Abstract There have been a number of papers that have addressed the issue of plagiarism. Nevertheless, the charges of plagiarism usually merit little attention with experts, because it is still not clear what sort of copying actually constitutes plagiarism. Another problem that eludes consensus is whether plagiarism was committed with or without intention. This paper discusses certain issues relating to plagiarism and differentiates between intentional and unintentional forms of plagiarism.
Writing is an art that develops with practice, and it can be further enhanced by repetition. However, writing a publishable paper is not an easy task. Reading articles to understand the use of lexis and syntax in science writing and the nature of citations can nevertheless help to a great extent. Further, when the subject matters are clear, the thought process will emerge and the synthesis of language will become spontaneous. However, plagiarism is inevitable when one resorts to reproducing the language of others. Butler reports that the detection of plagiarism becomes easier with software to scan manuscripts submitted to journals.1 According to Butler, plagiarism can range from copying a few paragraphs to the outright copying of others. Even so, what constitutes plagiarism is an issue where there is no consensus due to the subjective nature of assessment. This is one reason why experts who deal with plagiarism conclude that it is unintentional, without being explicit about intentional copying.
According to the Office for Research Integrity, the word “plagiarism” describes theft or misappropriation of others works, including ideas and language.2 The use of others’ language involves substantial textual copying (word for word) of another’s work, with or without attribution.2,3 However, limited use of same or closely-matching phrases does not amount to textual copying when it is pertinent to the paper.2 It is prudent to discuss the nature of citations in the published articles to determine whether plagiarism was intentional or due to an inadvertent error.
In an article by Pino-Neto et al.,4 the discussion section reads: “Ramon et al. described two sibs born to a consanguineous couple who presented with a previously undescribed syndrome of mental deficiency, epilepsy, cherubism, fibrous dysplasia of the mandible, gingival fibromatosis, and stunted growth”. The literature revealed that a similar description, subsequently published after Pino-Neto et al.,4 was also found in other articles.5–7 The same information can also be found at Online Mendelian Inheritance in Man (OMIM ID 266270; http://www.ncbi.nlm.nih.gov/omim/266270).
A closer look at the above sentence is necessary to determine whether the interpretation and citation are appropriate. Unlike Ramon syndrome, mental retardation, epilepsy, hypertrichosis, and gingival fibromatosis represent idiopathic or hereditary gingival fibromatosis.8 Thus, the only denominator to distinguish Ramon syndrome and hereditary gingival fibromatosis is the presence or absence of cherubism.
In this context, a review of the report by Ramon et al.9 shows that of the two patients (9 and 12 years of age) reported, the 9-year-old boy presented with epilepsy, mental retardation, stunted growth, gingival fibromatosis, and cherubism, whereas the 12-year-old boy had only mild mental retardation and gingival fibromatosis. There was no mention of fibrous dysplasia of the mandible as part of the disease complex in the Ramon et al.9 article, as stated by Pino-Neto et al.4 Although the three articles have attributed the right source (i.e. Ramon et al.), two findings were inconsistent with the original report, that is, “two siblings” with Ramon syndrome and “fibrous dysplasia of the mandible”. It shows that the authors’ did not read the original source properly, which points to ignorance, rather than intention.
Scientific writing is a form of argumentation that requires substantiation of inference by citing existing facts, either for or against the conclusion.10 Therefore, citations are needed to verify the source, and to compare and establish the relationship between the source and the authors’ representation of it.11 Unsupported statements or sentences will be considered as the authors’ own.11 For example, “Unfortunately, some situations may occur that delay immediate replantation. Where such situations exist, the tooth should be stored in a medium that maintains periodontal ligament cell viability until definitive dental treatment can be accomplished”. This statement lacks an in-text citation, and as such, forms the authors’ own. However, with the exception of the underlined words, the passage was also found in another article. This raises the issue of whether a similar idea expressed in the same words by people at various points of time is textual copying. Having a unique idea is not unusual, but the overlap of words in a given sentence suggests that it is unlikely to be mere coincidence. This is based on the fact that a similar passage was also found in two other articles, but with proper source attribution (search the later part of the quoted statement “the tooth…can be accomplished” in Google).
It is clear from the above illustrations that unsupported texts need not necessarily be original. This form of writing has the potential to amount to textual plagiarism, especially when there is substantial overlap with other work.2,3 However, a search of the sentence “Apoptotic keratinocytes are no longer able to perform this function” from certain articles in Google will show that even with significant copying, authors are given benefit of doubt for plagiarism when the original source is credited or if the author is a novice. This writing genre, according to Abasi and Akbari,12 does not constitute intentional plagiarism, but can be termed “patch writing”. Writing a review article, however, requires critical analysis of relevant sources to advance an argument in order to seek new lines of enquiry, rather than to take recourse in transgressive textual appropriation of source.
As I alluded to earlier, the assessment of plagiarism is subjective, and readers should judge what constitutes intentional plagiarism by searching the sentences “Diagnosis in dentistry may be defined as the process whereby the data obtained” or “the replacement of lost or deficient tissues involves the use of prosthetic materials” in the Google search.
The purpose of scientific writing is to disseminate and contribute knowledge to the existing literature, but it is more important to refrain from plagiarism, and efforts should be directed to curb such practices at infancy.
References
- 1
- 2 ORI provides working definition of plagiarism. Office of Research Integrity, ORI Newsletter, Vol 3, Number 1, December 1994. Available from: http://ori.dhhs.gov/publications/newsletters.shtml. (Assessed June 25, 2011).
- 3
- 4
- 5
- 6
- 7
- 8
- 9
- 10 Writing guide: parts of an argument. Available from: http://writing.colostate.edu/guides/documents/argueparts/printformat.cfm?printformat=yes. (Assessed June 25, 2011).
- 11
- 12 , . Are we encouraging patchwriting? Reconsidering the role of the pedagogy context in ESL student writers’ transgressive intertextuality. English for Specific Purposes 2008; 27: 267–84.
Tuesday 21 June 2011
1. Bansal R, Bansal R. Regenerative endodontics: A state of the art. Ind J Dent Res 2011;22:122-131.
Abstract – p.122//Bansal et al 2011 | Abstract – p.255//Murray et al 2004 |
Scientific advances in the creation of restorative biomaterials, in vitro cell culture technology, tissue grafting, tissue engineering, molecular biology and the human genome project provide the basis for the introduction of new technologies into dentistry. | Scientific advances in the creation of restorative biomaterials, in vitro cell culture technology, tissue grafting, tissue engineering, molecular biology, and the human genome project provide the basis for the introduction of new technologies into dentistry. |
Abstract – p.122//Bansal et al 2011 | Jhaveri A, 2009//DrBicuspid.com** |
Non-vital infected teeth have long been treated with root canal therapy (for mature root apex) and apexification (for immature root apex), or doomed to extraction. | Nonvital infected teeth have long been treated with root canal therapy and apexification, or doomed to extraction. |
** http://www.drbicuspid.com/index.aspx?sec=sup&sub=rst&pag=dis&ItemID=301812 Assessed: June 19, 2011 | |
Abstract – p.122//Bansal et al 2011 | Jhaveri A, 2009//DrBicuspid.com** |
Although successful, current treatments fail to re-establish healthy pulp tissue in these teeth. But, what if the non-vital tooth could be made vital once again? | Although largely successful, current treatments fail to re-establish healthy pulp tissue in these teeth. But what if the nonvital tooth could be made vital once again? |
** http://www.drbicuspid.com/index.aspx?sec=sup&sub=rst&pag=dis&ItemID=301812 Assessed: June 19, 2011 | |
Abstract – p.122//Bansal et al 2011 | Jhaveri A, 2009//DrBicuspid.com** |
That is the hope offered by regenerative endodontics, an emerging field focused on replacing traumatized and diseased pulp with functional pulp tissue. | That's the hope offered by regenerative endodontics, an emerging field focused on replacing traumatized and diseased pulp with functional pulp tissue. |
** http://www.drbicuspid.com/index.aspx?sec=sup&sub=rst&pag=dis&ItemID=301812 Assessed: June 19, 2011 | |
Abstract – p.122//Bansal et al 2011 | p.711//Nakashima M et al 2005 |
The purpose of this article is to review these biological procedures and the hurdles that must be overcome to develop regenerative endodontic procedures. | The purpose of this article is to review the biological principles of tissue engineering and the hurdles that must be overcome to develop regenerative endodontic procedures. |
Sunday 5 June 2011
Oral Lichen Planus
HOW TO WRITE "ABSTRACT AND CONCLUSION FOR A REVIEW."
Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365. | Roopashree MR et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734. | Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365. |
ABSTRACT: Both antigen-specific and non-specific mechanisms may be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8+ cytotoxic T-cells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase (MMP) activation in OLP lesions. These mechanisms may combine to cause T-cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T-cell migration, and keratinocyte apoptosis in OLP. OLP chronicity may be due, in part, to deficient antigen-specific TGF-b1-mediated immunosuppression. The normal oral mucosa may be an immune privileged site (similar to the eye, testis, and placenta), and breakdown of immune privilege could result in OLP and possibly other autoimmune oral mucosal diseases. Recent findings in mucocutaneous graft-versus-host disease, a clinical and histological correlate of lichen planus, suggest the involvement of TNF-a, CD40, Fas, MMPs, and mast cell degranulation in disease pathogenesis. Potential roles for oral Langerhans cells and the regional lymphatics in OLP lesion formation and chronicity are discussed. Carcinogenesis in OLP may be regulated by the integrated signal from various tumor inhibitors (TGF-b1, TNFa, IFN-g, IL-12) and promoters (MIF, MMP-9). We present our recent data implicating antigen-specific and non-specific mechanisms in the pathogenesis of OLP and propose a unifying hypothesis suggesting that both may be involved in lesion development. The initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown. | ABSTRACT: Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology. OLP presents as white striations, white papules, whiteplaques, erythema, erosions, or blisters affecting predominantly the buccal mucosa, tongue and gingiva. Both antigen-specific and non-specific mechanisms are hypothesized to be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8+ cytotoxic Tcells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase activation in OLP lesions. These mechanisms may combine to cause T cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T cell migration and keratinocyte apoptosis in OLP. The various hypotheses proposed for pathogenesis of oral lichen planus are discussed in this review. | Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology. OLP presents as white striations, white papules, white plaques, erythema, erosions, or blisters affecting predominantly the buccal mucosa, tongue, and gingivae (Vincent et al., 1990; Silverman et al., 1991). |
Ismail SB et al. Oral lichen planus and lichenoid reactions: etiopathogenesis, diagnosis, management and malignant transformation. J Ora Sci 2007;49:89-106. | Roopashree MR et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734. | Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365. |
Conclusion: |
Saturday 4 June 2011
Oral Lichen Planus
Text similarity with different context orientation.
Sugarman PB, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;13:350-365. | Roopashree MR, et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734. |
THE EPITHELIAL BASEMENT MEMBRANE As discussed above, epithelial basement membrane changes are common in OLP and include breaks, branches, and duplications (Jungell et al., 1989a; Zhou et al., 2001). Keratinocytes contribute to the structure of the epithelial basement membrane by secreting collagen IV and laminin V into the basement membrane zone (Marinkovich et al., 1993). Presumably, apoptotic keratinocytes are no longer able to perform this function. Hence, keratinocyte apoptosis triggered by intra-epithelial CD8+ cytotoxic T-cells may result in epithelial basement membrane disruption in OLP. Conversely, evidence from the involuting mouse mammary gland model suggests that keratinocytes require a basement-membrane-derived cell survival signal to prevent the onset of apoptosis (Pullan et al., 1996). Hence, epithelial basement membrane disruption may trigger keratinocyte apoptosis in OLP. An intriguing question in OLP is which came first — keratinocyte apoptosis or epithelial basement membrane disruption? Both mechanisms may be involved in the pathogenesis of OLP, e.g., basement membrane disruption may trigger keratinocyte apoptosis, and apoptotic keratinocytes may be unable to repair the disrupted basement membrane. Such a cyclical mechanism may underlie disease chronicity. | The epithelial basement membrane Keratinocytes contribute to the structure of the epithelial basement membrane by secreting collagen IV and laminin V into the basement membrane zone. Also evidence from the involuting mouse mammary gland model suggests that keratinocytes require a basementmembrane- derived cell survival signal to prevent the onset of apoptosis (3). Thus basement membrane is required for keratinocyte survival and keratinocyte for normal basement membrane production (Fig. 3). Apoptotic keratinocytes are no longer able to perform this function. Hence, keratinocyte apoptosis triggered by intra-epithelial CD8+ cytotoxic T cells may result in epithelial basement membrane disruption in OLP, which allows the non-specific T lymphocytes present in the sub epithelial zone to migrate into the epithelium. Both keratinocyte apoptosis and basement membrane disruption may be involved in the pathogenesis of OLP, e.g., basement membrane disruption may trigger keratinocyte apoptosis, and apoptotic keratinocytes may be unable to repair the disrupted basement membrane. Such a cyclical mechanism may underlie disease chronicity (3, 5). |
Oral Lichen Planus
Same text but with different contextual interpretation.
123
Sugarman PB, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;13:350-365. | Lodi G, et al. Current controversies in oral lichen planus: Report of an international consensus meeting. Part 1. Viral infections and etiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;1:40-51. | Roopashree MR, et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734. |
The lichen planus antigen is unknown, although the antigen may be a self-peptide, thus defining lichen planus as a true autoimmune disease. The role of autoimmunity in disease pathogenesis is supported by many autoimmune features of OLP, including disease chronicity, adult onset, female predilection, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in OLP patients, and the presence of auto-cytotoxic T-cell clones in lichen planus lesions (Sugerman et al., 1992, 1993, 2000b). We suggest that keratinocytes express lichen planus antigen but only at the lesion site, i.e., the clinical distribution of lichen planus lesions is determined by the distribution of the lichen planus antigen. Hence, an early event in lichen planus lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent. Subsequently, intra-epithelial CD8+ cytotoxic T-cells recognize the lichen planus antigen associated with MHC class I on lesional keratinocytes and trigger keratinocyte apoptosis. | LP has a well-defined clinical distribution and there is a clear demarcation between lesional and nonlesional tissue. A possible explanation for this pattern of presentation is that keratinocytes express the LP antigen, but only at the lesion site. In other words, the clinical distribution of lichen planus is determined by the distribution of the antigen. Hence, an early event in LP lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent. Following altered keratinocyte antigen expression, antigen-specific CD41 and CD81 T cells may be either (1) on routine surveillance in the epithelium and encounter the keratinocyte antigen by chance (‘‘chance encounter’’ hypothesis) or (2) attracted to the epithelium by keratinocyte-derived chemokines (‘‘directed migration’’ hypothesis). The ‘‘chance encounter’’ hypothesis is supported by findings of CD81 T cells in normal human epidermis141,142 and basal cell degeneration in the absence of a dense inflammatory infiltrate in LP lesions.143 Conversely, the ‘‘directed migration’’ hypothesis is supported by findings of constitutive chemokine receptor expression by naı¨ve T cells144 and a dermal T-cell infiltrate prior to the appearance of intraepithelial lymphocytes and epithelial damage in LP lesions.145 In this context, keratinocyte antigen expression6chemokine production are primary events in oral LP lesion formation, followed by keratinocyte apoptosis triggered by antigen-specific CD81 cytotoxic T cells (Fig 1). | The lichen planus antigen is unknown, although the antigen may be a self-peptide, thus defining lichen planus as a true autoimmune disease. An early event in lichen planus lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent (3). |
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