Oral lichen planus versus oral lichenoid reaction: Difficulties

in the diagnosisIndian J Dent Res, 2009;20(3):361-4

Renata Falchete Do Prado, Luciana Sassa Marocchio, Renata Callestini Felipini

Alfie Fiandra Garcia070620774

Oral Medicine Dept. Faculty of Dentistry University of Indonesia

2011

AbstractLichen 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.

Introduction• Some of the diseases have similarities in clinical

and microscopical caharacteristic

diagnosis is impaired

Oral Lichen Planus & Oral Lichenoid Reactions

Investigated difficulties faced to establish the differential diagnosis between the two pathologies

Lichen planusDescription (Wilson, 1869)

A mucocutaneous disease of unknown etiology represented by a cell-mediated immunopathological response to antigenic alterations of keratinocytes in the skin and mucosa.

Epidemiology

Mainly females (3rd – 7th decades)

Predilection

Buccal mucosa, gingiva and tongue.

Clinical characteristics

Lesions with fine crossed whitegrayish lines (Wickham’s striae)

Risk FactorAnxiety and Depression

Symptoms

Remission and exacerbation

typesTypes (6)

1. Reticular: fine whitish striae cross the buccal mucosa and gingiva;

2. Plaque type

3. Atrophic: erythematous areas surrounded by reticular components

4. Ulcerative: erythematous regions surrounded by reticular elements with a tendency to ulceration

5. Papular

6. Bullous type: The bullae range from a few millimeters to centimeters in diameter. Such bullae are generally short lived and, on rupturing, leave apainful ulcer.

Lichen planus

Lichen planus

Microscopically: disorganization and destruction of the basal layer due to hydropic degeneration, with consequent interruption

in the basal membrane

Epithelial cells affected

Immunocompetent cells affected

Some epithelial cells trigger apoptosis

Formation of civatte bodies

The juxtaepithelial lymphocyte inflammatory infiltrate exhibits a band arrangement

Lichen planusSelf immune disorder

several associations or overlaps with other self-immune pathologies

Pre cancerous lesion (WHO): systemic disorder associated with an increase in the risk ofcancer.

Malignant transformation: ranging from 0.4 to 5.6%.

Follow upEarly diagnosis of malignancies

Lichenoid reactions

exhibit similar clinical and microscopic alterations as the LP

Pinkus (1973):Published the first microscopic description

TriggeredSpecific etiological agents, such as: 1.Dental materials2.Drugs3.Flavoring agents

Lind (1986): Term LR to refer to clinical lesions related with amalgam restorations.

Lichenoid reactions

Pathogenesis:Tissue alteration caused by antigen fixation in the keratinocyte

Recognized and destructed by cells of the immune system

EtiologyDental Material

Restorative dental material : Resin (Blongren, et al) & metallic material (amalgam, cobalt, nickel, gold)

Amalgam: sensitivity to the amalgam mercury (replacing the restorations) and corrosion

Methyl methacrylate (Ali, et al)Causing burning mouth syndrome\

Orthodontic wires (Dunlap, et al)

Etiology

Drugs

Non steroidal anti inflammatory drugs(fenclofenac, fenilbutazone, and salsalate)

→erosive type

Antihypertensive drugs(methyldopa, propranolol, practolol, oxprenolol, and amlodipine)

Antimalarial drugs (quinine and quinidine)

Antimicrobial drugs,(penicillin, tetracycline, cyclosporine, prednisolone, indomethacin, and

pyridoxine

Etiology

Lithium (antidepression),

Hypoglycemic drugs

Triggered by drugs: there maybeperiod of latency from the onset ofdrug intake to the appearance of lesions.

Gold salts (rheumatoid arthritis/liqueur)

Drugs

Lichenoid reactions

Flavoring Agent

(on food and dentrifices)

Candies with cinnamon flavour

Mouthrinses with cinnamon flavour

menthol oil and peppermint

cinnamaldehyde

Diagnosis

Clinical examination of cause-effect relationship

Careful and detailed anamnesis

Hypersensitivity test → replace material

Dietary habits Routine or occasional drugs

Oral Hygiene

Routine Follow up to eliminate the possibility of OLP/malignancies

Discussion:Therapeutic Approach

Removal of etiological agent: Amalgam: replaced, Drug: replaced by another

Therapy of choiceImmunocompetent drugs

Corticosteroids: topical or systemic & Cyclosporine

Alternative therapyRetinoids

Topical etretinate and systemic isotretinoinAdverse effect: hairloss & mucosal drying

PUVA

Conclusion

Attention should be given to the difficulty in establishing the differential diagnosis by clinicians unaware of the two diseases

The treatments for both pathologies are distinct ;one of them should be more carefully followed due to the possibility

of malignant transformation

the definitive diagnosis should beestablished as early as possible.