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REVIEW ARTICLE Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 3  |  Page : 361-364
Oral lichen planus versus oral lichenoid reaction: Difficulties in the diagnosis


1 Department of Biosciences and Oral Diagnosis at São José dos Campos Dental School, São Paulo State University (UNESP), São José dos Campos, São Paulo, Brazil
2 Oral Pathology at the Dental School of University of São Paulo, (USP-FO), São Paulo, Brazil
3 Pathology and Clinical Propedeutics at Araçatuba Dental School, São Paulo State University (UNESP), Araçatuba, São Paulo, Brazil

Click here for correspondence address and email

Date of Submission26-Jun-2008
Date of Decision01-Apr-2009
Date of Acceptance30-Apr-2009
Date of Web Publication30-Oct-2009
 

   Abstract 

Lichen planus (LP) is a mucocutaneous disease with well-established clinical and microscopic features. The oral mucosa and skin may present clinical and microscopic alterations similar to those observed in LP, called lichenoid reactions (LRs), which are triggered by systemic or topical etiological agents. The difficulties faced to establish the differential diagnosis between the two pathologies were investigated in the literature. It was observed that the etiology of LP is still under discussion, with a tendency to self-immunity, while the etiology of LRs is related to the contact with specific agents, such as metallic restorative materials, resins, and drugs, allowing the establishment of a cause-effect relationship. In this case, the disease is caused by the antigen fixation in the epithelial cells, which are destructed by the immune system. Based on these data, protocols are suggested for this differentiation. The important role played by the integration between the clinician and the oral pathologist in the diagnostic process is highlighted. The treatment of LP comprises mainly the utilization of corticosteroids and the LR is treated by removal of the causal factor. Differentiation between the two diseases allows an effective and correct therapeutic approach.

Keywords: Diagnosis, lichen planus, lichenoid reactions, literature review, therapy

How to cite this article:
Do Prado RF, Marocchio LS, Felipini RC. Oral lichen planus versus oral lichenoid reaction: Difficulties in the diagnosis. Indian J Dent Res 2009;20:361-4

How to cite this URL:
Do Prado RF, Marocchio LS, Felipini RC. Oral lichen planus versus oral lichenoid reaction: Difficulties in the diagnosis. Indian J Dent Res [serial online] 2009 [cited 2017 Sep 25];20:361-4. Available from: http://www.ijdr.in/text.asp?2009/20/3/361/57375
Both clinically and in the anatomopathological analysis, the diagnosis between different diseases may be impaired by clinical and microscopic similarities, as observed in the oral lichenoid reaction (LR) and oral lichen planus (LP). The difficulties faced to establish the differential diagnosis between the two pathologies were investigated in the literature.


   Lichen Planus Top


Wilson, [1] in 1869, described the disease and named it LP, a mucocutaneous disease of unknown etiology represented by a cell-mediated immunopathological response to antigenic alterations of keratinocytes in the skin and mucosa. [2]

The disease affects mainly females in the third to seventh decades of life. The most frequent location is the buccal mucosa, gingiva and tongue. [3] The most known clinical characteristics of LP are lesions with fine crossed white-grayish lines, called Wickham's striae. [4]

The oral LP is classically described in six types: Reticular clinical type, in which fine whitish striae cross the buccal mucosa and gingiva; atrophic type, in which erythematous areas are surrounded by reticular components; ulcerative type, exhibiting erythematous regions surrounded by reticular elements with a tendency to ulceration; papular type; and, rarely, bullous type. [4],[5]

The oral LP presents periods of remission, when the signs and symptoms are reduced or disappear, and periods of exacerbation, which may only be related to emotional distress. [6] The study conducted by Vallejo et al. [7] revealed that anxiety and depression are risk factors that may influence the development of LP. Picardi et al. [8] reported that patients with oral LP presented higher levels of anxiety and depression compared with the control group, thus, constituting factors that worsen the manifestations of the disease.

Microscopically, there is disorganization and destruction of the basal layer due to hydropic degeneration, with consequent interruption in the basal membrane, which is a product of the affected epithelial cells. [9] Because immunocompetent cells are affected, some epithelial cells are stimulated to trigger the process of programmed cell death (apoptosis), leading to the formation of Civatte bodies. [10] The juxtaepithelial lymphocyte inflammatory infiltrate exhibits a band arrangement. [3],[11] Hyperparakeratinization and hyperorthokeratinization are common findings and may be clinically coincident with the Wickham's striae. [3],[4],[11]

Even though it does not meet the classical criteria of self- immunity, there is a tendency in the literature to classify LP as a self-immune disorder due to the several associations or overlaps with other self-immune pathologies, such as lupus erythematosus, whose definitive diagnosis may be reached in the follow-up. [12]

The WHO [4] considers the LP as a pre cancerous lesion, a systemic disorder associated with an increase in the risk of cancer. [4] Its malignant transformation is controversial, [13] ranging from 0.4 to 5.6%. [14],[15] While this issue is still discussed, patients with LP should be strictly followed-up to allow the early diagnosis of a possible malignant lesion. [13]


   Lichenoid Reactions Top


The oral mucosa or skin may exhibit similar clinical and microscopic alterations as the LP, the so-called LRs. [4],[11],[16],[17]

Pinkus, [17] in 1973, published the first microscopic description of these reactions. Only in 1986 did Lind [16] employ the term LR to refer to clinical lesions related with amalgam restorations. They are triggered by specific etiological agents, such as dental materials, [16],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31] drugs, [32],[33],[34] and flavoring agents [35],[36],[37],[38],[39] thus allowing the establishment of a cause-effect relationship from a clinical standpoint.

In this case, the tissue alteration is caused by the antigen fixation in the keratinocytes, which are recognized and destructed by cells of the immune system. [3],[10]

Restorative dental materials play a fundamental role in the appearance of LR in the oral mucosa. The reaction to resin materials was reported by Blongren et al., [20] who successfully treated reticular erythematous lesions and white papules on the lip of seven patients by replacing the restorative material. The findings of Backman et al. [40] recently added a new probable etiological agent for the LR after observing that these lesions were in contact with the dental calculus. However, according to the authors, the hypothesis of interaction between the restorative dental materials and the dental plaque should not be ruled out as an etiological agent of LR. Ali et al. [18] investigated the relationship between the LR present in inflammatory fibrous hyperplasia and the hypersensitivity to methacrylate, observing 23% of patients with positive cutaneous tests and resolution of the complaint of burning mouth after removal of the prosthesis.

Among the metallic materials, with emphasis to amalgam, the reports of Ostman et al. [26],[27] should be highlighted, which reported oral LR due to sensitivity to the amalgam mercury by replacing the restorations. Laine et al. [24],[25] conducted careful immunological studies and observed true allergy to mercury. The products of corrosion of these metallic materials were also mentioned by Bolewska et al., [41] who concluded that they might give rise to lesions in patients with a higher sensitivity or susceptibility to develop a reaction. Stenman et al. [30] reported cases of LR in the oral mucosa caused by contact with cobalt, nickel, gold, and palladium due to corrosion of the amalgam restorations. Other authors, as published by Dunlap et al., [21] reported patients developing oral LRs after placement of orthodontic archwires.

In two extensive literature reviews, Mc Cartan et al. [32] and Halevy et al. [33] indicated the drugs that might induce the LR. Non steroidal antiinflammatory drugs were listed, especially inducing the erosive type of oral reaction, especially fenclofenac, fenilbutazone, and salsalate. [42] The reports also include antihypertensive drugs, especially methyldopa, propranolol, practolol, oxprenolol, and amlodipine, [43] as well as the antimalarial drugs quinine and quinidine. LRs were also observed after utilization of antimicrobial drugs, mainly penicillin, tetracycline, cyclosporine, prednisolone, indomethacin, and pyridoxine. [33] Ketoconazole was also reported. [34] Other drugs, such as lithium, [34] prescribed for patients with depression, and hypoglycemic drugs were also related with LRs.

It should also be highlighted that when LRs are triggered by drugs, there may be a period of latency from the onset of drug intake to the appearance of lesions and the ingestion of some substances without therapeutic purposes was also related with the lesions. [33] Both the therapeutic application of gold salts for the treatment of rheumatoid arthritis and the ingestion of a liqueur containing gold salts reveal this situation. [44] The LR is not the only oral lesion induced by drugs. Abdollahi et al. [45] conducted a literature review and observed that the utilization of different drugs gave rise to several oral lesions, including LR, multiform erythema, hairy tongue, halitosis, salivary disorders, taste disturbances, and others.

The literature also mentions that flavoring agents commonly present in foods and dentifrices may trigger the LR. Allen et al. [34] observed lichenoid lesions with a characteristic microscopic aspect associated with the habit of chewing gum or eating candies with cinnamon flavor, with disappearance of symptoms when the habit was discontinued. Miller et al. [37] described focal LR caused by cinnamon candies and diffuse lesions due to utilization of mouthrinses with cinnamon flavor, with lichenoid microscopic characteristics. Morton et al. [38] reported contact sensitivity to menthol oil and peppermint in patients with burning mouth syndrome, recurrent ulceration, and lichenoid lesions. Thyne et al. [39] reported the case of a patient with ulcers in the oral mucosa and lips, with a positive cutaneous test to cinnamaldehyde, a flavoring agent present in toothpastes.

The LR is diagnosed by clinical examination due to the need of a cause-effect relationship. This may be achieved by a careful and detailed anamnesis on the dietary habits, routine or occasional use of drugs, and oral hygiene. When the involvement of dental materials in the etiology of LR is suspected, the material should be replaced or polished, which should lead to disappearance of the lesions.

Hypersensitivity tests employed for identification of patients that might benefit from the replacement of dental materials are widely reported in the literature. [19],[23],[24],[25],[26],[27],[28] The large number of patients testing negative in hypersensitivity tests may be related to the absence of corrosion products in these tests. The long-term follow-up of patients with LR is fundamental in order to identify the remission of LP coinciding with the removal of a possible etiological agent as well as to rule out the presence of other pathologies.

The microscopic characteristics of the LR may not be differentiated from the LP, [3],[11],[46] highlighting the importance of a detailed anamnesis. The pathologist requires the indication of a cause-effect relationship by the clinician in order to provide a diagnosis of LR.


   Discussion Top


Therapeutic approaches

After knowledge on the etiology of the LR, the treatment comprises removal of the etiological agent. When caused by oxidation of an amalgam restoration, it should be replaced by other material; if caused by a drug, it should be replaced by another; when triggered by a flavoring agent, the ingestion of food or utilization of the toothpaste should be avoided.

Immunocompetent drugs are the therapy of choice for the treatment of LP. Because the etiology is unknown, the treatment is symptomatic and aims to interrupt the immune response. Some important actions of corticosteroids, which make them the therapy of choice during treatment, are the reduction in lymphocytic exudate, maintenance of cell membrane integrity, inhibition of phagocytosis, and stabilization of lysosomal membranes. [47] They may be applied topically, by intralesional injection, or systemically. [48] Cyclosporine is an elective inhibitor of proliferation and function of T lymphocytes, reducing the production of cytokines and gamma interferon. Although effective, its high cost makes it a second choice. [48] The alternative treatment with retinoids, such as topical etretinate and systemic isotretinoin, is widely reported in the literature. However, these drugs present adverse effects such as hair loss and mucosal drying. [48],[49] The systemic griseofulvin is largely discussed, however does not allow complete remission of lesions. [48],[50] Both the antiviral drug interferon and the levamisole have been successfully used. [51]

The literature demonstrates the utilization of cryotherapy in the treatment of LP for cosmetic purposes. [48] The therapy with PUVA, which is an acronym for psoralen (a light-sensitizing medication) combined with exposure to ultraviolet light A (UVA) comprises the topical or systemic administration of a photosensitizing drug and local application of UVA radiation, with successful results in the treatment of LP. [52] Periods of remission and exacerbation of LP in periods of emotional imbalance are observed. [48] The multidisciplinary treatment is very important, especially in the presence of cutaneous and psychological involvement.

After a detailed review, Al Hashimi et al. [53] suggested the following protocol for correct management of the patient with suspected oral LP. Initially, the diagnosis should be confirmed by biopsy if the clinical aspects are not sufficient. These authors advocate the treatment with topical corticosteroids, associated or not with antifungal drugs, indicating systemic therapy only in more severe cases affecting other mucosal regions.


   Conclusion and Clinical Significance Top


Attention should be given to the difficulty in establishing the differential diagnosis by clinicians unaware of the two diseases or who do not follow their patients for the period required for their differentiation as well as if the microscopic diagnosis of LR may not be reached due to lack of indication of a cause-effect relationship. The high rate of microscopic diagnosis of LP compared with the low frequency of microscopic diagnosis of LR highlights this concern. Because the treatments for both pathologies are distinct and considering that one of them should be more carefully followed due to the possibility of malignant transformation, the definitive diagnosis should be established as early as possible.

 
   References Top

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Correspondence Address:
Renata Falchete Do Prado
Department of Biosciences and Oral Diagnosis at São José dos Campos Dental School, São Paulo State University (UNESP), São José dos Campos, São Paulo
Brazil
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9290.57375

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    Abstract
    Lichen Planus
    Lichenoid Reactions
    Discussion
    Conclusion and C...
    References

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