Corticisteroids/certified fixed orthodontic courses by Indian dental academy

Seminar OnSeminar On
CORTICOSTEROIDS IN DENTISTRYCORTICOSTEROIDS IN DENTISTRY
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

Learning ObjectivesLearning Objectives
 At the end of the session the learner should be
able to:
 Describe the action of corticosteroids
 Enumerate the preparation & dose of corticosteroid
 Discuss the therapeutic uses in dentistry
 Discuss the adverse effects of corticosteroids

CONTENTSCONTENTS
INTRODUCTION
ACTIONS
PHARMACOKINETICS
PREPARATION AND DOSE
THERAPEUTIC USES IN DENTISTRY
ADVERSE EFFECTS
CONCLUSION
REFERENCES

INTRODUCTIONINTRODUCTION
 For more than 50 years, Medicine & Dentistry have
appreciated the importance of adrenal glands in
maintaining the physiological integrity.
 Using cholesterol as a substrate,the adrenal cortex
produces large number of substances collectively known
as corticosteroids.
 They are used in adrenal insufficiency and to suppress
acute or chronic inflammation that accompanies injury and
many diseases.

ACTIONS OF GLUCOCORTICOIDS
 The corticosteroids have a wide spread actions.
 They prepare the body to withstand effects of all kinds of
noxious stimuli and stress.Therefore cortisole is a life-
protecting hormone.
Carbohydrate Metabolism
 Promotes glyogen deposition in liver.
 Inhibit glucose utilization by peripheral tissue.
 This results in hyperglycemia.

Protein Metabolism
 Causes protein breakdown.
 Mobilization of amino acids from peripheral tissues.
 Responsible for side effects like
 Muscle wasting
 Lympholysis
 Loss of osteoid from bone
 Thinning of skin

Fat MetabolismFat Metabolism
 Lipolysis occurs
 Redistribution of body fat
 Subcutaneous tissue loses fat.
 Fat deposition over face,neck and shoulders- “Moon
face”,”Fish mouth”,Buffalo hump”.

Calcium MetabolismCalcium Metabolism
 Inhibits intestinal absorbtion of calcium
 Enhance renal excretion of calcium.
 Loss of calcium from bone indirectly due to loss of
osteoid ( Decreased formation and increased resorption)
Cardiovascular System
 They restrict capillary permeability.
 Maintains tone of arterioles & myocardial contractility.
 They play permissive role in development to
hypertension.

Skeletal MuscleSkeletal Muscle
 Optimum levels of corticosteroid is needed for normal
muscular activity.
 Weakness occurs in both hypo & hypercorticism.
 Excess mineralocorticoid leads to hypokaelemia,which
leads to weakness.
 Excess glucocorticoids leads to muscle wasting and
myopathy,which leads to weakness.

Central Nervous SystemCentral Nervous System
 Mild euphoria
 Maintains the level of sensory perception and normal level
of excitability of neurons.
Stomach
 Secretions of gastric acid and pepsin is increased.
 May aggravate peptic ulcer.

Lymphoid Tissue and Blood cellsLymphoid Tissue and Blood cells
 Glucocortioids increases rate of destruction of lymphoid
cells.
 They increase the number of RBCs,platelet and
neutrophil.
 They decrease lymphocytes,eosinophils and basophils
due to sequestration of cells in tissues.
 Blood count comes back to normal after 24 hours.

Inflammatory ResponseInflammatory Response
 Corticosteroids do not remove the cause of inflammation, the
underlying disease continues to progress while manifestation
are dampened.
 The anti-inflammatory action of corticosteroids are as follows:
 Stabilization of lysosomes so that proteolytic enzymes
responsible for inflammation are not released.
 Prevention of release of histamine and proteolytic enzymes
from the affected tissue.
 Decrease in capillary permeability so that loss of fluids
from plasma into the affected tissue is prevented.
 Inhibition of migration of leucocytes into affected area.

 Suppression of T cells and other leucocytes so that there
is decrease in reaction of tissue which usually enhance
the inflammatory process.
 If inflammation starts,glucocorticoids cause an early
resolution of inflammation and rapid healing.

Immunological & Allergic responseImmunological & Allergic response
 Corticosteroids impairs immunological competence.
 They suppress all types of hypersensitivity and allergic
phenomenon.At high concentration they interfere with
every step of immunological response,but at therapeutic
doses there is no impairment of antibody production or
complement function.
 The clinical effects are due to suppression of recruitment
of leucocytes at the site of contact with antigen and of
inflammatory response to immunological injury.

 They supress cell mediated immunity in which T cells are
primarily involved e.g.,delayed hypersensitivity and graft
rejection.
 There is inhibition of interleukin-1 release from
macrophages,inhibition of interleukin-2 formation and
action,T-cells proliferation is not stimulated and there is
suppression of natural killer cells.

Effect of Resistance on stressEffect of Resistance on stress
 Stress stimulates secretion of ACTH and there is
increase in glucocorticoids level.Corticosteroids enhance
release of amino acid and synthesis of new proteins
necessary for cellular functions.
 They enhance release of fatty acids and supply more
energy during stress.They enhance vascular reactivity to
catecholamines and fatty acids mobilizing action of
catecholamines.
 Corticosteroids prevent severity of other changes in body
caused by stress.

HPA AXIS
Cicardian rhythm
Hypothalamus
Corticotrophic Releasing Hormone(CRF)
Anterior Pitutary
Adrenocorticotrophic hormone(ACTH)
Adrenal Cortex
Cortisol
Regulation of cortisol secretion

PHARMACOKINETICSPHARMACOKINETICS
 All natural and synthetic corticosteroids,except DOCA are
effective by oral route.
 Water soluble esters like hydrocortisone
hemisuccinate,dexamethasone sodium phosphate can be given
IV or IM.
 Water insoluble esters like hydrocortisone acetate,triamcinolone
acetonide cannot be injected IV,but are slowly absorbed from IM
site and produce more prolonged effects.
 Hydrocortisone undergoes high first pass metabolism.

 It is 90% bound to plasma protein,mostly to a specific
corticosteroid binding globulin (Transcortin) as well as to
albumin.
 Steroids are metabolized primarily by hepatic
microsomal enzymes.

PREPARATION AND DOSEPREPARATION AND DOSE

Hydrocortisone(cortisol)
 Used for replacement therapy (20 mg morning + 10 mg
afternoon orally).
 In shock,status asthamicus and acute adrenal insufficiency
(100mg IV bolus + 100mg 8 hourly infusion).
 Trade name: Lycortin-S 100mg/2ml injection
 Wycort 25 mg/ml injection (as acetate or IM / intraarticular
injection)
 Primacort 100,200,400mg /vial injection

Cortisone
 It is inactive and hydroxylated in liver to hydroxycortisone.It
is slightly less potent than hydrocortisone.
 Dose :20-100mg /day oral,IM.
 Trade Name: Corlin 5 mg tablet;25 mg/ml injection.

Prednisolone
 It is four times more potent than hydroxycortisone.It is used
for allergic,inflammatory,autoimmune diseases and in
malignancies.
 Dose : 5-60 mg/day orally
10-40 mg IM ,intraarticular and topical.
 Trade name: Wysolone,Nucort 5,10,20 mg tablet.
 Deltacortil,Hostacortin H 5,10 mg tablet,
20mg /ml( as acetate)for IM ,intraarticular injection.

Methyl prednisoloneMethyl prednisolone
 It is slightly more potent and more selective than
prednisolone.
 Dose: 4-32 mg/day oral.
 Used in pulse therapy(1 gm infused every 6-8 weeks)
used in non-responsive acute rheumatoid arthritis,renal
transplant,pemphigus,etc.
 Trade name: Solu-medrol 0.5 gm( 8 ml) and 1gm (16 ml)
injection,for IM or slow IV injection (as sodium acetate).

TriamcinoloneTriamcinolone
 It is more potent than prednisolone.
 Dose: 4-32 mg/day oral,5-40 mg IM,intra-articular
injection.
 Trade name: Kenacort,Tricort 1,4,8 mg tablet,
10,40 mg/ml ( as acetonide) for IM,intra-articular inj.
Ledercort 4 mg tablet.

DexamethasoneDexamethasone
 Very potent and highly selective glucocorticoids.
 Used for inflammatory and allergic conditions.
 0.5 mg/day oral.
 In shock,cerebral edema 4-20 mg/day IV or IM.
 Trade name:Decadron,Dedan 0.5 mg tab,4 mg/ml (As
sodium phosphate) for IV, IM inj,0.5 mg/ml oral drops.
 Wyemesone,Decdan 0.5 mg tab,4mg/ml inj.

BetamethasoneBetamethasone
 Actions are similar to dexamethasone.
 0.5-5 mg/day oral,4-20 mg IM,IV,inj; also topical.
 Trade name: Betnesol,betacortril,celestone 0.5 mg,1 mg
tab, 4 mg/ml (As sodium phosphate) for IV,IM inj.0.5
mg/ml oral drops; Betnelan 0.5 mg,1 mg tablet.
Paramethasone
 It has intermediate properties between prednisolone and
dexamethasone.
 Dose : 2-20 mg/day,oral

Desoxycorticosterone acetate(DOCA)Desoxycorticosterone acetate(DOCA)
 Has only mineralocorticoid activity.
 It is used for replacement therapy in Additions diseases :
2-5 mg sublingual,10-20 mg IM.once or twice weekly.
 Trade name: Docabolin 10 mg/ml (along with
nandrolone)

FludrocortisoneFludrocortisone
 It is a potent mineralocorticoid having some glucocorticoid activity.
 It is used for replacement therapy in Additions disease.
 50-200 ug/day.
 Idiopathic postural hypotension 100-200 ug/day
 Trade name: Floricort 100 ug tablet
Aldosterone
 It is a most potent mineralocorticoid.But not used clinically coz of
low oral bioavailability & difficulties in regulating doses.

INDICATIONSINDICATIONS
 Arthritis
 Collagen diseases
 Severe allergic reactions
 Autoimmune disease
 Bronchial asthma
 Other lung diseases
 Infective diseases
 Eye diseases
 Skin diseases
 Intestinal diseases
 Cerebral edema
 Malignancies
 Shock

CONTRAINDICATIONSCONTRAINDICATIONS
 Peptic Ulcer
 Diabetes mellitus
 Hypertention
 Viral and fungal infection
 Tuberculosis and other infection
 Osteporosis
 Herpes simplex keratitis
 Psychosis
 Epilepsy
 Renal failure

THERAPEUTIC USES IN DENTISTRYTHERAPEUTIC USES IN DENTISTRY
Oral Ulceration
 Various ulcerative lesions of oral mucosa may be treated
by the application of oral gluocorticoid.
 Relief of symptoms and abbreviation of the clinical course
are usually obtained regardless of the cause of the
ulceration.

PemphigusPemphigus
 In mild lesions of pemphigus topical glucocorticoids are
preferred.
 The benefit of topical glucocorticoids is greatest when the period
of contact with the tissue is maximal.
 Retention at the site of application is difficult in oral cavity.
 Therefore vehicle like carboxymethyl cellulose in a base of
polyethylene resin and mineral oil(orabase) can be used which
will adher to the mucosa and resists dissolution and
displacement.

 Larger dose(Prednisolone 100 mg of /day or 1-2
mg/kg/day)are needed to control the diseases.
 Adjuvants like azathioprine or cyclophosphamide are
added to decrease complications of long term steroids.
(Prednisolone 40-60 mg/day + Azathioprine 100-150
mg/day.

Mucous membrane pemphigoidMucous membrane pemphigoid
 It can often be treated with topical corticosteroids.
 More potent corticosteroids like beclomethasone dipropionate or
betamethasone valerate,can often be used as sprays.
 Such sprays deliver a metered dose of 100 ug/puff and this can be
repeated several times until there is adequate amount of
corticosteroid deposited on the lesion.
 If ocular lesions develop then systemic corticosteroids become
necessary.
 In desquamative gingivitis occlusal splints can be used as carriers
for topical steroids.
 Candida overgrowth with clinical thrush may develop requiring
concomitant topical or systemic antifungal therapy.

Bullous pemphigoidBullous pemphigoid
 In localized lesions high potency topical corticosteroids are
used.
 In severe lesions ,systemic corticosteroids along with
immunosupressives are used.

Lichen Planus
 Topical 0.05% Fluocininide (Lidex) and 0.05% clobestasol
(Temovate) can be used.Topical steroids can be applied to the lesion
using cotton swabs or guaze pads.
 For recalcitrant cases or in severe exacerbation for short period
systemic steroids ( Prednisone 40-80 mg/day) can be used.
 Prednisolone 5mg along with Levamisole 50 mg tablet for first 3 days
of rest followed for 2-3 weeks.
 Intralesional injection of triamcilone acetonide 10 mg/ml can also be
used.

Erythema multiformeErythema multiforme
 Initial dose of 30-40 mg of prednisone or methly
prednisone per day,which is then tapered ,is helpful in
shortening the healing time of erythema multiformi
particularly when therapy is started in early course of
disease.
 Systemic cortiosteroids are life saving in severe cases of
Stevens-Johnsons syndrome.

Contact allergy stomatitisContact allergy stomatitis
 In mild cases removal of the allergen is required.
 In more severe symptomatic cases,application of topical
corticosteroids is helpful to speed healing of painful
lesions.
Recurrent apthous stomatitis
 In severe cases use of high potency topical steroids
fluocinonide,betamethasone or clobetasol placed directly
on the lesion shortens healing time and reduces the size
of the ulcer.
 Intralesional steroids can be used to treat large indolent
major apthous lesions.If apthae is not responding to
topical then,systemic steroids therapy should be
considered.

Behcets SyndromeBehcets Syndrome
 Azathioprine along with prednisone,cyclosporin along with
corticosteroids can be used.
 Systemic steroids are useful in rapidly controlling the disease.
Herpes zoster
 Systemic corticosteroids are used to prevent post-herpetic
neuralgia.
TMJ disorders
 In refractory cases of TMJ pain and in acute pain,intra-articular
injection of prednisolone or dexamethasone may be beneficial.

Pulpal hypersensitivityPulpal hypersensitivity
 Hysensitivity of the dental pulp can result from various
conditions that induce an inflammatory response in the
pulp like operative trauma,invasion of the pulp by bacteria
or their products and exposure of dentine to the oral
environment.
 Glucocorticoids are often used to lessen postoperative
complications,mainly edema and trismus,after dental
surgical procedures.

Anaphylaxis and allergic reactionsAnaphylaxis and allergic reactions
 The immunosupressant and anti-inflammatory effects of
glucocorticoids may be used to treat the manifestations of various
allergic reactions such as:
◦ Urticaria,Contact dermatitis,Angioneurotic edema,Allergic
rhinitis,Insect bite,Drug Reaction and Serum Sickness.
◦ As histamine is an important mediator in most of these
conditions,H1-antihistamine are major drugs in treatment of
milder reations.
◦ Systemic glucocorticoids are useful in more sever responses.
◦ In anaphylaxis even though epinephrine is the drug of
choice,larger doses of glucocorticoid may be beneficial in
reducing bronchospasm and laryngeal edema.

Idiopathic thrombocytopenic purpuraIdiopathic thrombocytopenic purpura
 In adults,prednisolone 60mg/dl should be given untill the
platelet count rise to normal level.Dose should be tapered
untill the drug is withdrawn.
Bell’s palsy
 Systemic steroids or adrenocorticotrophic hormone
injection is useful.
Shock
 Injection hydrocortisone sodium hemisuccinate 100mg
dissolved in 5ml of sterile water is given.

MineralocorticoidsMineralocorticoids
 Important natural mineralocorticoid is
Aldosterone,fludrocortisone and desoxycorticosterone.
 Aldosterone produces sodium retention and increased urinary
loss of potassium.Mineralocorticoids are used in treatment of
Additions disease,hypoaldosteronism,diabetes mellitus and
severe postural hypotention.

ADVERSE EFFECTSADVERSE EFFECTS
 These are extensions of pharmacological action occuring with
prolonged therapy and are a great limitation to use of corticoids in
chronic diseases.
◦ Cushings syndrome : round face,narrow mouth,supraclavicular
hump,obesity of trunks with relatively thin limbs.
◦ Fragile skin,purple striae typically on thighs and lower
abdomen,easy bruising,telengiectasia and hirsutism.Cutaneous
atrophy occurs with topial use also.
◦ Hyperglycemia,glycosuria and precipitation of diabetes.
◦ Muscular weakness-Proximal (shoulder,arms,pelvis,thigh) myopathy
occurs occasionally.

 Suspectibility to infection-Latent tuberculosis may flare.
◦ Opportunistic infection (candida)
 Delayed healing of wounds and surgical incisions.
 Peptic ulceration – Risk is doubled.Bleeding and silent
perforation of ulcer may occur.Dyspeptic symptoms are
frequent with high dose therapy.
 Osteoporosis
Specially involving vertebrae and other flat spongy
bones.
Compression fracture of vertebrae
Spontaneous fracture of long bones especially in elders.www.indiandentalacademy.com

 Radiological evidence of osteoporosis is an indication for withdrawl
of corticosteroid therapy.
 Corticosteroid induced osteoporosis can be prevented by calcium
supplements+ Vitamin D,biphosphonates and by estrogen
/androgen replacement in females/males respectively.
 Avascular necrosis of head of femur,humerus or knee joint is an
occasional abrupt onset complication of high dose corticosteroid
therapy.
 Posterior subcapsular cataract may develop after several years of
use especially in children.
 Glaucoma may develop in susceptible individuals after prolonged
topical therapy.
 Growth retardation in children occurs even with small dose of
corticosteroids,if given for long periods.

 Larger doses inhibit growth hormone secretion.
 Fetal abnormalities: Cleft palate,cardiac septal
defect,neurologic and behavioral disturbances are likely
if corticosteroids are given during pregnancy( 2nd
trimester)
 Psychiatric disturbances
Mild euphoria due to high dose therapy.
Nervousness and decreased sleep and mood
changes.
Rarely a depressive illness may be precipitated

 Supression of hypothalamus-pitutary-adrenal(HPA) axis occurs
depending both on dose and duration of therapy.
 In time,adrenal cortex atrophies and stoppage of exogenous
steroid precipitates a withdrawal symptoms-
malaise,fever,weakness,pain in muscles and joint and reactivation
of the diseases.
 Subjected to stress this patient may go into acute adrenal
insufficiency.

 Measures that minimize HPA axis suppression are :-
◦ Use short acting steroid (hydrocortisone,prednisolone) at
the lowest possible dose.
◦ Use steroids for a shorter period of time.
◦ Give the entire daily dose at one time in the morning.
◦ Switch to alternate day therapy if possible.
◦ If appropriate use local preparations of steroids with poor
systemic availability.

IMPLICATIONS IN DENTISTRYIMPLICATIONS IN DENTISTRY
 Patients treated with large dose of glucocorticoid for long
periods,present special problems in dentistry.
 Such patients are likely to have a decreased resistance to
infection and a poor wound healing response.
 Actual or potential source of infection in the oral cavity,such as
carious teeth and inflamed tissue,should be promptly treated.
 If surgical procedures are necessary,they should be as
conservative,atraumatic and aseptic as possible.

 Preoperative antimicrobial prophylaxis may be indicated in some
cases.
 In patients receiving long-term corticosteroids,the dentist should
for look for osteoporotic changes in the jaw and degenerative
changes in periodontal ligament.
 In dental procedures with minimum stress like periodontal
probing,alloy restoration,minor biopsies,denture and orthodontic
adjustment or scaling and prophylaxis,no increase in
corticosteroids is required.

 For moderately stressful dental procedures (in a suppressed patient)
performed under local anaesthesia that takes less than 1 hour such
as third molar impaction, multiple extraction, incision and drainage of
dental infection, extensive restoration and periodontal surgery,
normal daily dose should be doubled 8 hours before the procedure.
 For procedures taking longer periods of time the preoperative dose
should be tripled. The dose should be tapered back to normal during
the postoperative period.

 For major dental surgery under general anaesthesia like
orthognathic surgery, management of acute facial trauma and
treatment of severe oral infections parenteral administration of
corticosteroids is mandatory.
 IM 100mg cortisone acetate 8 hrs before surgery, followed by IV.
hydrocortisone or its equivalent during the procedure, so that total
dose on the day of operation is 300mg.
 The dose is tapered off over 2-3 day period.

EFFECTS OF STEROIDS ON DNA ACTIVITYEFFECTS OF STEROIDS ON DNA ACTIVITY
 Steroids penetrate the cell membrane and bind to specific
cytoplasmic receptor proteins.
 The resulting complex binds to the nucleus.
 Studies suggest that steroid hormone stimulate the synthesis
of specific proteins by affecting the transcription of structural
or regulatory genes.
 Studies have shown that steroid-receptor complexes bind to
chromatin or DNA bound complexes can be released from
nuclei by DNase but not by Rnase.

CONCLUSIONCONCLUSION
 Corticosteroids have rather limited applications in
dentistry.
 Patients treated with large doses of corticosteroids
present special problems in dentistry.
 Therefore consultation with patient’s physician is
essential for the optimal management of a person who is
receiving or has received long-term corticosteroid
therapy.

ReferencesReferences
 Burkit’s Oral Medicine.10th
edition,2004
 Tripathi K.D. Essentials of medical physiology,5th
edition,2003
 Satoskar.Pharmaology and Pharmaotherapeutics.1998
 Yagiela JA, Dowd FJ ,Neidle EA. Pharmacology and therapeutis
for dentistry,5th
edition
 Crispian Scully.Handbook of oral diseases,revised edition,2001
 Ann E Drummond Reproductive Biology and
Endocrinology2006, 4:16 The role of steroids in follicular growth
 A. R. Fahmy, K. Griffiths, R. Mahler and A. R. Williams Biochem.
J. (1967) 105, 6c The Effect of Steroids on Deoxyribonucleic
Acid Polymerase Activity

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