Systemic and Topical Steroids in the Management of Oral Mucosal Lesions

Abstract

From the time of its introduction in the 1040s, glucocorticoids have provided a panacea for many diseases. The therapeutic benefit of corticosteroids lies in their anti-inflammatory and immunosuppressive properties which makes them highly effective in the management of oral mucosal lesions. This article aims to present to the clinician, the plethora of options available as steroid therapy and enables one to choose based on the underlying disease and the properties of the drug.

INTRODUCTION

Glucocorticoids have revolutionized the management of several diseases since they were introduced more than half a century ago. Corticosteroids include the endogenous steroid hormones produced from the adrenal cortex as well as those synthetically produced for pharmacotherapeutics.[1] While the therapeutic benefits of steroids are many, their adverse reactions, as well as long-term effects, must be noted while treating a patient. Topical and systemic steroids find use in the management of various mucosal diseases such as lichen planus, pemphigus, oral submucous fibrosis, and so on. Conversely, the dental clinician might on occasions, be confronted with a patient who is on long-term steroid therapy for systemic diseases such as arthritis or lupus. The management of the dental condition of such patients should be planned keeping in mind, the effect of long-term steroid therapy and its bearing on the dental treatment.

PHARMACOLOGY OF STEROIDS

The adrenal cortex secretes glucocorticoids, mineralocorticoids (collectively referred to as corticosteroids), and sex hormones. The first two are synthesized from cholesterol.

Corticosteroids are classified as hydrocortisone, prednisone, triamcinolone, dexamethasone, clobetasol, and mometasone.

Glucocorticoids influence the metabolism of lipids, carbohydrates, proteins, calcium, and electrolytes. While the physiologic and metabolic effects of corticosteroids are many, the pharmacological utility mainly lies in its anti-inflammatory and immunosuppressive effects. Glucocorticoids suppress all types of inflammation and allergic reactions. Glucocorticoids bring about these effects by inhibition of white blood cell function, stabilization of lysozyme membrane, inhibit plasminogen activation, and reduce the synthesis of inflammatory mediators such as prostaglandins and leukotrienes.

Glucocorticoids may be administered systemically (oral and parenteral) as well as topically. They are metabolized in the liver and following conjugation are excreted through the urine. The metabolism of synthetic steroids is slower and hence their action is prolonged.

Systemic and topical steroids find application in a number of inflammatory and immune mediated mucosal conditions. We have discussed the role of them in some of the commonly encountered mucosal conditions.

RECURRENT APHTHOUS STOMATITIS

Recurrent aphthous stomatitis (RAS) is perhaps one of the most commonly encountered painful mucosal conditions. RAS is usually preceded by localized burning sensation in the area of concern a day or two before ulceration. The ulcers themselves are painful, superficial, well defined, and round to oval with pseudomembrane covering and surrounding erythematous halo. RAS can clinically present in three forms: Minor aphthae account for a majority of the cases of aphthae (75%–85%).[2] They are usually under a centimeter in diameter and heal uneventfully in a week or two. Major aphthae usually occur on the mucosa overlying the minor salivary glands. They usually appear after puberty, commonly involve the lips, soft palate and throat; take weeks to months to heal with resultant scarring.[3]

Herpetiform aphthae constitute a meager 5%–10% of all RAS cases. They present as small (3–5 mm) crops of ulcers resembling herpes simplex infection and the ulcers coalesce. The etiopathogenesis of RAS is unclear. The diagnosis of RAS is by far clinical with care to be taken to rule out any underlying disease. The management of RAS is symptomatic. Triamcinolone acetonide (1% in an adhesive base) is preferred for topical application, four times daily.[4] Severe cases may require high potency topical preparations such as Fluocinonide, Betamethasone, or Clobetasol held directly over the lesion in a gauze. In addition, intralesional injection of Betamethasone, Dexamethasone, or Triamcinolone may be justified in cases where the ulcers are continuous with no periods of remission.[3]

ORAL LICHEN PLANUS

It is a chronic inflammatory condition with unclear pathogenesis involving the T-cells. Clinically, similar lesions caused due to drugs are termed Oral Lichenoid drug reactions. Oral Lichen Planus (OLP) may present as reticular, papillary, atrophic, erosive, bullous, or plaque-like forms. The erosive-atrophic forms are symptomatic.[5] While a cure for lichen planus is yet elusive, steroids play a pivotal role in their symptomatic management. Topical steroids are the mainstay while systemic corticosteroids must be used in the event acute exacerbation or multiple, extensive lesions.[6,7] 0.025% Fluocinonide, topical Betamethasone, fluticasone propionate spray, topical mometasone furoate microemulsion, clobetasol propionate in orabase, triamcinolone acetonide (mouthwash, topical, intralesional) have all shown to be effective in the symptomatic management of OLP. 0.1% Fluocinolone acetonide has been proven to be more effective than triamcinolone in the management of OLP.[8] Systemic corticosteroids are to be considered in recalcitrant cases of erosive lichen planus; Prednisolone at the lowest effective dose (40–80 mg for 6–7 days).[9] If the need to continue systemic steroids for more than 2 weeks arises, withdrawal must be tapered by reducing 5 mg per week to prevent precipitating an adrenal crisis.[10]

ORAL SUBMUCOUS FIBROSIS

Oral submucous fibrosis (OSF), a potentially malignant condition of the oral cavity resulting in increasing loss of tissue mobility, marked rigidity and an eventual inability to open the mouth, has the prevalence rate of 2.01% and a reported malignant transformation rate of 2.3%–7.6%.[11,12,13,14,15] Steroids help in OSF by reducing inflammation, ergo preventing fibrosis by reducing the proliferation of fibroblasts and laying down collagen. Intralesional injections of dexamethasone, (4 mg/ml) with hyaluronidase are given biweekly for 20 weeks. Other steroids used intralesionally includes triamcinolone (10 mg/ml) with hyaluronidase bi-weekly for 4 weeks. These help in improving mouth opening.[16] In addition, systemic prednisone (30–40 mg/day for 14–28 days and then tapered) or hydrocortisone (100 mg/day) may be helpful in alleviating burning sensation.

ERYTHEMA MULTIFORME

Erythema multiforme is a dermatologic hypersensitivity reaction to infectious agents such as herpes and some medications. Herpes simplex virus is believed to be etiologic in more than 50% of the cases. Management involves first treating the suspected infection or withdrawing the offending drug. Steroids have an adjuvant role. Topical clobetasol propionate an adhesive paste or mouthwash may be used. Systemically, prednisone may be used or dexamethasone pulse therapy may be advocated to avoid long-term use of systemic steroids.[17]

PEMPHIGUS

Pemphigus is a chronic mucocutaneous disease where painful blisters are seen, often presenting first in the oral cavity.[18] Being an autoimmune disease, management is often directed at symptomatic management and controlling the disease process. When the lesions of Pemphigus are mild, 0.05% fluocinolone acetonide, or 0.05% clobetasol propionate is advised. Severe cases are treated with a high dose of 100–200 mg of prednisone till symptomatic regression has occurred. Dose is gradually reduced to be maintained at around 50 mg/day.[19]

MUCOUS MEMBRANE PEMPHIGOID

Mucous membrane pemphigoid (MMP) also called cicatricial pemphigoid is a vesiculobullous autoimmune disease affecting the skin and mucosa. High doses of steroids are required to control the disease given its aggressive and unyielding nature.[20] Topical steroids have a limited role to play in MMP and may be used to control gingival desquamation. The first line of treatment is prednisolone (1–2 mg/kg/day) followed by gradual tapering and combining immunosuppressants. If dose above 100 mg/day is required, pulsed intravenous corticosteroids are recommended.[18,21]

BULLOUS PEMPHIGOID

It is a autoimmune vesiculobullous disease with subepidermal blistering. Topically, 0.05% clobetasol propionate has been found to be effective. Severe disease demands systemic steroids. Prednisone 20 mg/day is recommended. Unyielding cases may be given intralesional triamcinolone acetonide (3–10 mg/ml).[17]

LUPUS ERYTHEMATOSUS

It may be acute (systemic) or chronic (discoid). Oral ulcerations of lupus are transient and seen during periods of flare up. Topical betamethasone or clobetasol is indicated.[17] Systemically, prednisone (10–20 mg/day) or on alternate days may be required. Intralesional triamcinolone may also be useful in specific cases.[22,23]

CONCLUSION

Steroids provide the quintessential “Magic Bullet,” a one stop panacea for almost all diseases. However, it remains a double edged sword. It does provide quick, effective results in many diseases. However, it is imperative that the clinician keeps in mind, the indications, contraindications and special precautions that must be exercised while dabbling with steroids and must be aware of the dose modifications and alterations that must be customized to each patient according to the disease process and the patient condition and response. With judicious use, steroids will continue to help in relieving human suffering safely.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.