|Year : 2015 | Volume
| Issue : 1 | Page : 19-24
Applications of Corticosteroids in Dentistry
Jatan Sanghavi1, Amita Aditya2
1 Department of Orthodontics and Dentofacial Orthopedics, Sinhgad Dental College and Hospital, Pune, Maharashtra, India
2 Department of Oral Medicine and Radiology, Sinhgad Dental College and Hospital, Pune, Maharashtra, India
|Date of Web Publication||19-Oct-2015|
Reader, Department of Oral Medicine and Radiology, Sinhgad Dental College and Hospital, Pune, Maharashtra
Source of Support: None, Conflict of Interest: None
Corticosteroids, since their introduction in the 1940s, have become one of the most widely prescribed class of drugs. They belong to a class of chemicals that includes steroid hormones that are produced naturally in the adrenal cortex of vertebrates and analogous to those that are synthesized in laboratories. They have been used extensively in managing many oral diseases, due to their excellent anti-inflammatory and immuno-modulatory effects. However, considering their potential and significant side-effects, they are sometimes termed as the "double-edged sword" in the field of medicine. Their successful use depends upon the comprehension of the disease process. This includes an appropriate diagnosis, a clear view of the desirable treatment outcome and understanding of whether the treatment is aimed at the management of a chronic disease or enhanced resolution of a short-term condition. The possible beneficial effects of systemic corticosteroids must be weighed against probable risks. This article is aimed at reviewing the use of corticosteroids in the treatment of various oral conditions and lesions, and deriving a certain protocol for the same.
Keywords: Corticosteroids, dentistry, oral lesions
|How to cite this article:|
Sanghavi J, Aditya A. Applications of Corticosteroids in Dentistry. J Dent Allied Sci 2015;4:19-24
| Introduction|| |
Corticosteroids have been in regular clinical usage for a range of inflammatory and immune-mediated conditions for over half a century. Their initial recognition and subsequent development from clinical observations about 80 years ago lead to the Nobel Prize award in Medicine to Kendall, Reichstein and Hench in 1950. This certifies to their extreme importance in physiological homeostasis and in clinical medicine.  An extract of animal adrenocortical tissue could counteract human adrenal failure, which was the first clinical evidence, was demonstrated in 1930. By 1940, it became evident that there are two categories: Those that cause retention of sodium and fluid and those that counteract shock and inflammation. Intra-articular and oral administration of cortisone and hydrocortisone began in 1950-51. Several attempts in research to produce cortisone semi-synthetically showed some success by 1952. Between 1954 and 1958, six synthetic steroids were introduced for systemic anti-inflammatory therapy. By 1960, all of the toxic effects of long-term corticosteroid administration had been reported. In addition, protocols to withdraw such drugs while reducing the symptoms of cortical insufficiency were made. To be able to use lower corticosteroid doses, companion use of nonsteroidal anti-inflammatory drugs began in the late 1950s (phenylbutazone was the first). In the 1970s, methotrexate and other anti-metabolites were introduced which lead to a reduction in dosages and limited use of corticosteroids in rheumatic diseases.  Wide applications of corticosteroids in Dentistry can be mainly owed to their excellent anti-inflammatory and immuno-modulatory properties. Glucocorticosteroids exhibit intervention at several points in the immune response and appear to affect many aspects of inflammation. In fact, corticosteroids have evolved and emerged as the mainstay of therapy for numerous oral lesions and conditions.
| Physiology|| |
Corticosteroids are chemically similar to endogenous cortisol which is vital in protein, carbohydrate, and fat metabolism, maintenance of vascular reactivity, and body adaption to stress. , Every day, the adrenal gland normally produces about 24-30 mg of cortisol, but may produce up to 300 mg of cortisol in times of great stress. The secretion of cortisol is regulated by circadian rhythm, a stress-related response, and a negative feedback mechanism between the adrenals, hypothalamus, and pituitary. When supraphysiologic doses of corticosteroids (>30 mg cortisol equivalent) are given for over 14 days, the hypothalamic-pituitary-adrenal axis may become suppressed and may even take up to 12 months to recover. A functional ability to respond to stress, however, has been shown to return within 2 weeks to 1 month. ,
The normal secretion rate of the two principal corticoids in human is:
- Hydrocortisone: 10-20 mg daily (nearly half of this is in the few morning hours).
- Aldosterone: 0.125 mg daily.
| Mechanism of Action|| |
The corticosteroids have wide spread of actions. These include maintenance of fluid electrolytes, cardiovascular and energy substrate homeostasis as well as functional status of skeletal muscles and nervous system. They basically prepare the body to withstand any type of stress. They have both direct and permissive actions. Actions of corticosteroids may be broadly divided into  :
- Glucocorticoids: Affects carbohydrate, protein, and fat metabolism.
- Mineralocorticoids: Affects Na + , K + , and fluid balance.
| Applications in Management of Oral Lesions and Conditions|| |
Recurrent aphthous stomatitis
The drugs that are most commonly adopted for local application orally in recurrent aphthous stomatitis (RAS) are hydrocortisone hemisuccinate (pellets of 2.5 mg) and triamcinolone acetonide (adhesive paste containing 0.1% of the steroid). Gel, pellets, and pastes can be applied directly to the lesion post meals and at bedtime twice or thrice a day or mixed with an adhesive such as orabase before application.
Ulcerations that are located in the areas which are inaccessible can be controlled by topical dexamethasone elixir, 0.5 mg/5 ml held over the area or applied with a saturated gauge pad to the ulcers, 4 times/day for 15 min or betamethasone sodium phosphate rinse by dissolving 0.5 mg in 5 ml of water and asking the patient to rinse for 2-3 min), steroid aerosol (e.g., beclometasone diproprionate), or a high-potency topical corticosteroid, such as clobetasol 0.05% in orabase or fluocinonide 0.05%, in orabase. 
Major aphthous ulcers commonly require systemic treatment as the approach initially. Prednisone therapy 40 mg/day for 1 week is usually adequate to manage the outbreak. Oral prednisone systemically is prescribed most commonly. Systemic prednisone therapy should begin at 1.0 mg/kg a day as a single dose in severe RAS patients and should be tapered after 7-14 days. Intralesional steroids can be employed to treat large indolent major RAS lesions. 
Corticosteroids given locally often controls oro-genital ulcers, and immunosuppressive therapy is reserved for extreme mucocutaneous cases. The mainstay of treatment for Behcet's disease is immunosuppressive therapy. Successful treatment includes anti-inflammatory agents that modify the activity of neutrophils. In the acute phase, prednisone, at doses of 40-60 mg/day, may be beneficial. It may be used alone or in combination therapy with other immunosuppressive agents. 
Oral lichen planus
In treating mild to moderate symptomatic lesions, topical corticosteroids are the chief treatment agents. They are widely used in the therapeutics of oral lichen planus (OLP) to reduce inflammation and pain. Options (in order of decreasing potency) include 0.05% clobetasol proprionate gel, 0.1-0.05% betamethasone valerate gel, 0.05% fluocinonide gel, 0.05% clobetasol ointment or cream, and 0.1% triamcinolone acetonide ointment. Triamcinolone acetonide is used either in orabase or lozenge form.
In widespread OLP, high-potency steroid mouthwashes such as disodium betamethasone phosphate, or clobetasol propionate can be used. 
Intralesional corticosteroid injection for recalcitrant or extensive lesions involves the subcutaneous injection of 0.2-0.4 ml of a 10 mg/ml solution of triamcinolone acetonide via a 1.0 ml 23- or a 25-gauge tuberculin syringe.
Intralesional triamcinolone acetonide in doses of 0.5-1 ml of a 1 mg/ml suspension in the form of bi-weekly injections, or even 3-4 times a week in more severe cases can be used for the treatment of erosions. 
Systemic corticosteroids are used for recalcitrant erosive or erythematous lichen planus where topical therapy has not been effective. Systemic prednisolone is the drug of choice, but should be employed at the lowest possible dose for the least duration (40-80 mg for 5-7 days). It can be used to control the erythema and ulcers in OLP. The oral dose of prednisone is in the range of 10-20 mg/day for moderately severe cases to as high as 35 mg/day (0.5 mg/kg daily) for extreme cases. 
Topical steroid therapy
Oral topical steroids provide symptomatic relief. Clobetasol propionate mouthwashes in aqueous solution may offer another topical approach to this patient population. The mouthwash-solution provides ready accessibility to all lesional areas, and there is good control over the contact time between the lesion and the drug. 
Systemic steroid therapy
Moderate-to-severe oral erythema multiforme can be treated with a short course of systemic glucocorticosteroid in patients without severe contraindications to their usage.
Prednisone may be used in patients with severe lesions at a dose of 40-80 mg/day for 1-2 weeks then tapered rapidly. Initial therapy with systemic prednisone (0.5-1.0 mg/kg/day) or pulse methylprednisolone (1 mg/kg/day for 3 days) has shown effective results. 
Corticosteroids may be employed in the following forms: A paste, an ointment, or a mouthwash administered as monotherapy or as adjunctive therapy with systemic treatment. In patients without progressing oral lesions, moderate to high-potency topical corticosteroids should be applied twice or thrice a day, such as 0.05% fluocinolone acetonide or 0.05% clobetasol propionate. 
Systemic corticosteroid therapy
In patients with severe disease and the spread of lesions is to the dermal surfaces, the systemic corticosteroid is the drug of choice. The first drug used to treat this disease is prednisolone and, almost, all situations, is the first line of treatment. The starting dose is more; a total oral dose of 100-200 mg prednisolone is employed every day until clinical signs abate. The dose can be gradually reduced to a maintenance level of 40-50 mg daily. 
Intralesional corticosteroid therapy
This accelerates the scarring process of a lesion. It may be used to treat persistent lesions. This treatment, which does not give consistent results, involves intralesional injections given every 1-2 weeks; treatment is ceased after 3 injections if there is no improvement. Scarring is often seen along with cutaneous or mucosal atrophy, which is the main drawback of this treatment. 
Mucous membrane pemphigoid
Topical steroid therapy
Lesions that are mild and localized usually respond to topical steroids, including triamcinolone, fluocinonide, and clobetasol propionate. Mild oral lesions should be managed with topical and intralesional steroids. Desquamative gingivitis can often be managed with topical steroids in soft dental splint covering the gingiva, although the clinician must closely monitor the patient for side effects such as candidiasis and effects of systemic absorption. 
Systemic steroid therapy
In patients with high risk, such as with multiple oral lesions, the administration of prednisone 1-2 mg/kg/day, with gradual dose reduction, and immune-suppressors such as cyclophosphamide (0.5-2 mg/kg/day), azathioprine 1-2 mg/kg/day, or mycophenolate mofetil 2-2.5 g/day have shown good results. 
Topical steroid therapy
In patients with the limited or moderate disease, potent topical corticosteroids should be considered. In recent times, low dose topical clobetasol propionate (10-30 g daily) was shown to have similar short-term efficacy but reduced side-effects compared to the high-dose topical regimen (40 g daily clobetasol propionate). 
Systemic steroid therapy
High-dose systemic corticosteroids are the standard initial treatment of bullous pemphigoid to manage the eruptions, and prolonged high-doses are commonly used in severe cases.
Initial doses of prednisolone are 20 mg/day or 0.3 mg/kg/day in localized or mild disease, 40 mg/day or 0.6 mg/kg/day in moderate disease, and 50-70 mg or 0.75-1 mg/kg/day in severe disease are recommended. In patients with limited disease, clobetasol propionate cream alone is used; in patients with moderate disease, clobetasol propionate cream may be combined with dapsone (1.0-1.5 mg/kg/day) and in severe cases, oral prednisolone (0.5 mg/kg/day) may be added. 
Intralesional corticosteroid therapy
Triamcinolone acetonide 3-10 mg/ml can be administered to resistant lesions intralesionally. Experience benefits in injecting correctly, thereby maximizing efficacy and minimizing atrophy. When pemphigoid is not responsive to steroids, or large maintenance doses are required, other "steroid-sparing" agents can be administered. 
Systemic lupus erythematosus
Lesions that are symptomatic can be managed with high-potency topical corticoids or injections of intralesional steroids. Systemically low dose prednisone 10-20 mg/day or a dose of 20-40 mg every alternate day may be required in some cases.
Potent topical steroids and antimalarials are the prime drugs to treat systemic lupus erythematosus. Patients commonly begin with a topical steroid (e.g., betamethasone or clobetasol) applied 2 times a day, and then shift to a lower-potency steroid as soon as possible. Intralesional corticosteroid injection is useful as a supportive therapy for individual lesions. 
Treatment should be conservative, depending upon the severity and probable prognosis in each case. If there are no specific contraindications, immunocompetent patients are administered prednisone at 1 mg/kg/day (maximum 80 mg) for the 1 st week and tapered over the following week. Patients with partial palsy should also be managed as there are chances of around one-fifth of these cases to be progressive in nature.
Ramsay Hunt syndrome
Definitive treatment consists of antiviral therapy. Often, it includes steroids. Adjunctive steroid therapy may help in the treatment of the facial paralysis of Ramsay Hunt syndrome. However, steroid therapy should be employed with proper caution, especially with periocular lesions, because of the fear of dissemination of the VZV infection.
A large prospective study showed that combination therapy with both acyclovir and steroids leads to a better recovery of facial nerve function in comparison to steroids administered alone. 
Post herpetic neuralgia
Corticosteroids are used, which help to treat pain, swelling, and also reduce the risk of recurrence of post herpetic neuralgia (PHN) significantly.
Prednisolone is the drug most commonly prescribed in heavy doses to herpes patients. A moderate dose of prednisone 40 mg daily for 10 days, which is gradually tapered off over the following 3 weeks is a very effective and safe routine in reducing the incidence of PHN.
The use of steroids in combination with an antiviral for uncomplicated herpes zoster is controversial. Steroids increase the resolution of acute neuritis as well as provide a definite improvement in the quality of life in comparison to those patients treated with antivirals alone. The use of oral steroids did not affect the development or duration of PHN though it seems reasonable for steroids to be used adjunctive to antiviral therapy.
The use of oral or epidural corticosteroids concurrently with antiviral therapy has been effective in treating moderate-to-severe acute zoster, but has no effect on the development or duration of PHN. ,
Temporomandibular joint disorders
Toller suggested that intra-articular corticosteroid injections were only useful in adult patients with temporomandibular joint (TMJ) disorders; a single intra-articular injection resulted in resolution of TMJ pain and other symptoms in 62% of adult patients, compared to only 17% of pediatric patients.
Triamcinolone acetonide which has been used for this purpose is absorbed from the injection sites very slowly. The dose ranges between 2 and 40 mg, depending upon the size of the joint to be injected. The dose is usually 10 mg in cases of TMJ. 
Oral prednisone is the first-line acute therapy for temporal arteritis. Vast majority of patients respond to an initial dose of 1 mg/kg/day, or between 40 and 60 mg/day of prednisone. The dose is lowered after 2-4 weeks and slowly tapered over 9 months to 1 year.
Higher doses of 80-100 mg/day are suggested for patients of GCA with visual or neurological symptoms. Intravenous pulse methylprednisolone has been proposed as an induction therapy, especially when vision is at risk. 
| Miscellaneous Uses|| |
Medical emergencies in dental practice
Adrenal crisis prophylaxis
Acute adrenal crisis, with the lack of mineralocorticoids and glucocorticoids, is a medical emergency. Symptoms include abdominal pain, weakness, hypotension, dehydration, nausea, and vomiting. Laboratory findings may include hyperkalemia, hyponatremia, hypoglycemia, uremia, and acidosis.
Exogenous glucocorticoids can lead to suppression of adrenal gland and resultant atrophy. This may cause a decreased glucocorticoid response to stress, and precipitate an adrenal crisis.
- Intravenous fluids (in the form of 5% dextrose in normal saline).
- Primary adrenal insufficiency: Start on 20-25 mg hydrocortisone per 24 h.
- Secondary adrenal insufficiency: 15-20 mg hydrocortisone per 24 h; if borderline fails in cosyntropin test considers 10 mg or stress dose cover only.
- Hydrocortisone should initially be given intravenously. If there is an improvement within 24 h, the hydrocortisone dose can be reduced. This can be changed to an oral formulation whenever the patient is stable. The dose can be declined by one-third to one-half the doses daily until a maintenance dose of 20 mg in the morning and 10 mg in the afternoon or at night is attained. Some patients may need only a dose of 20 mg/day total (i.e., 20 mg every morning, or 15 mg in the morning and 5 mg in the afternoon or at night).
- The condition that precipitated the crisis, such as infection, should be searched. The underlying cause should be treated.
- Patients will not need mineralocorticoid replacement because the renin angiotensin-aldosterone axis is intact. 
Anaphylaxis is the quintessential disease of emergency medicine. Steroids are unlikely to be beneficial in the management of acute anaphylaxis. One of the reasons is their delayed onset of 4-6 h.
With the antihistamines, despite their many theoretical benefits on mediator release and tissue responsiveness, there are no placebo-controlled trials that can confirm how much steroids are effective in the treatment of anaphylaxis. Most clinicians, however, give prednisone 1 mg/kg up to 50 mg orally or hydrocortisone 1.5-3 mg/kg intravenously specific in patients with airway involvement and bronchospasm, based empirically on their crucial role in asthma.
Steroids are fundamental in the management of recurrent idiopathic anaphylaxis. 
Applications in restorative dentistry
Corticosteroid can be used as a dressing agent for deep cavities and exposed pulp tissue so as to control the inflammatory pulp response and decrease postoperative pain. The therapeutic effect of a corticosteroid depends upon its concentration, potency, and ability to diffuse into the connective tissue.
The results of studies that use corticosteroids as a cavity liner support that these medications are effective in decreasing or preventing postoperative thermal sensitivity.
The intracanal use of corticosteroid-antibiotic combination has been reported to effectively control the post treatment endodontic pain. 
Perioperative corticosteroid use in dentoalveolar surgery
Dentists are often advised to use corticosteroids during and after third molar removal and other dentoalveolar surgery for reducing the postsurgical edema.
Dexamethasone has a longer duration of action and is more potent than methyl prednisolone. Methylprednisolone is usually administered via the intramuscular or intravenous route, though the possibility of the topical (intra-alveolar) application has been described, showing a reduction in morbidity and possible side-effects. It is 5 times more potent than cortisol. 
| Special Considerations|| |
Corticosteroids cause the adrenal glands to slow or stop the production of cortisol. Hence, they cannot be discontinued abruptly. The adrenal glands take some time to start producing cortisol again. Tapering the dose of corticosteroids gradually allows the body to start producing its own supply of cortisol again.
| Conclusion|| |
The usage of corticosteroids is vast, yet crucial. No wonder, cortisol (hydrocortisone) is called the "life-protecting hormone" and aldosterone, the "life-saving hormone."
Corticosteroids used in different forms can be given intralesionally, topically, and even systemically. Sometimes it may be given to control edema, whereas, in some situations, it is given because of its immunosuppressive properties. Even though corticosteroids have adverse effects, their anti-inflammatory and immuno-modulatory properties are very beneficiary and supersede them.
It can be said in conclusion that corticosteroids play an important role in the management of lesions affecting the oral mucosa and skin. In addition, its importance in medical emergencies cannot be neglected.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Savage NW, McCullough MJ. Topical corticosteroids in dental practice. Aust Dent J 2005;50 4 Suppl 2:S40-4.
Benedek TG. History of the development of corticosteroid therapy. Clin Exp Rheumatol 2011;29 5 Suppl 68:S-5-12.
Malamed SF, editor. Acute adrenal insufficiency. In: Medical Emergencies in the Dental Office. 6 th
ed. St. Louis: Mosby; 1993. p. 155-65.
Kehrl JH, Fauci AS. The clinical use of glucocorticoids. Ann Allergy 1983;50:2-8.
Glick M. Glucocorticosteroid replacement therapy: A literature review and suggested replacement therapy. Oral Surg Oral Med Oral Pathol 1989;67:614-20.
Wynn RL, Meiller TF, Crossley HL. Drug Information Handbook for Dentistry. 5 th
ed. Cleveland: Lexi-Comp; 1999.
Tripathi DK. Corticosteroids. In: Essentials of Medical Pharmacology. 5 th
ed. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd.; 2003. p. 254-65.
Natah SS, Konttinen YT, Enattah NS, Ashammakhi N, Sharkey KA, Häyrinen-Immonen R. Recurrent aphthous ulcers today: A review of the growing knowledge. Int J Oral Maxillofac Surg 2004;33:221-34.
Field EA, Allan RB. Review article: Oral ulceration - Aetiopathogenesis, clinical diagnosis and management in the gastrointestinal clinic. Aliment Pharmacol Ther 2003;18:949-62.
Reich RF, Kerpel SM. Differential diagnosis and treatment of ulcerative, erosive and vesiculobullous lesions of oral mucosa. Oral Maxillofac Surg Clin North Am 1998;10:95-129.
Gonzalez-Moles MA, Morales P, Rodriguez-Archilla A, Isabel IR, Gonzalez-Moles S. Treatment of severe chronic oral erosive lesions with clobetasol propionate in aqueous solution. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;93:264-70.
Edwards PC, Kelsch R. Oral lichen planus: Clinical presentation and management. J Clin Dent 2002;68:494-9.
Zegarelli DJ. Multimodality steroid therapy of erosive and ulcerative oral lichen planus. J Oral Med 1983;38:127-30.
Jacobson C, Cornell RC, Savin RC. A comparison of clobetasol propionate 0.05 percent ointment and an optimized betamethasone dipropionate 0.05 percent ointment in the treatment of psoriasis. Cutis 1986;37:213-4, 216, 218-20.
Scully C, Bagan J. Oral mucosal diseases: Erythema multiforme. Br J Oral Maxillofac Surg 2008;46:90-5.
Hashimoto T. Treatment strategies for pemphigus vulgaris in Japan. Expert Opin Pharmacother 2008;9:1519-30.
Fassmann A, Dvorakova N, Izakovicova Holla L, Vanuk J, Wotke J. Manifestation of pemphigus vulgaris in the orofacial region. Case report. Scr Med (Brno) 2008;76:55-62.
Fellner MJ, Sapadin AN. Current therapy of pemphigus vulgaris. Mt Sinai J Med 2001;68:268-78.
Bagan J, Lo Muzio L, Scully C. Mucosal disease series. Number III. Mucous membrane pemphigoid. Oral Dis 2005;11:197-218.
Joly P, Roujeau JC, Benichou J, Delaporte E, D′Incan M, Dreno B, et al.
A comparison of two regimens of topical corticosteroids in the treatment of patients with bullous pemphigoid: A multicenter randomized study. J Invest Dermatol 2009;129:1681-7.
Kasperkiewicz M, Schmidt E. Current treatment of autoimmune blistering diseases. Curr Drug Discov Technol 2009;6:270-80.
Panjwani S. Early diagnosis and treatment of discoid lupus erythematosus. J Am Board Fam Med 2009;22:206-13.
Ramsey MJ, DerSimonian R, Holtel MR, Burgess LP. Corticosteroid treatment for idiopathic facial nerve paralysis: A meta-analysis. Laryngoscope 2000;110 (3 Pt 1):335-41.
Kinishi M, Amatsu M, Mohri M, Saito M, Hasegawa T, Hasegawa S. Acyclovir improves recovery rate of facial nerve palsy in Ramsay Hunt syndrome. Auris Nasus Larynx 2001;28:223-6.
Wood MJ, Johnson RW, McKendrick MW, Taylor J, Mandal BK, Crooks J. A randomized trial of acyclovir for 7 days or 21 days with and without prednisolone for treatment of acute herpes zoster. N Engl J Med 1994;330:896-900.
Gray RJ, Davies SJ, Quayle AA. A clinical approach to temporomandibular disorders 7. Treatment planning, general guidelines and case histories. Br Dent J 1994;177:171-8.
Rahman W, Rahman FZ. Giant cell (temporal) arteritis: An overview and update. Surv Ophthalmol 2005;50:415-28.
Arlt W. The approach to the adult with newly diagnosed adrenal insufficiency. J Clin Endocrinol Metab 2009;94:1059-67.
Ring J, Darsow U. Idiopathic anaphylaxis. Curr Allergy Asthma Rep 2002;2:40-5.
Negm MM. Intracanal use of a corticosteroid-antibiotic compound for the management of post treatment endodontic pain. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:435-9.
Micó-Llorens JM, Satorres-Nieto M, Gargallo-Albiol J, Arnabat-Domínguez J, Berini-Aytés L, Gay-Escoda C. Efficacy of methylprednisolone in controlling complications after impacted lower third molar surgical extraction. Eur J Clin Pharmacol 2006;62:693-8.