It has been almost 60 years since corticosteroids were first recognized for their anti-inflammatory and immunosuppressive properties, initially in rheumatologic diseases. The beneficial effects of steroids in rheumatoid arthritis were described in 1949 by Philip S. Hench and colleagues, a discovery for which he received (together with Edward C. Kendall and Tadeus Reichstein) the Nobel Prize in medicine in 1950.1,2
The adrenal glands produce three major classes of hormones, each of which aid in dealing with the multitude of small and large stresses faced by animals and people almost daily. There is no doubt that at least two of these groups - glucocorticoids and mineralocorticoids - are necessary for life.
DHEA IS A METABOLIC INTERMEDIATE IN SYNTHESIS OF ANDROGENS.
cycles of cortisol levels are found in several animal species, including humans. In species that exhibit such cycles, different timing of diurnal maxima and minima has been observed, not only in different species but also, in some cases, within the same species.In humans, the amount of cortisol present in the blood undergoes diurnal variation; the level peaks in the early morning (approximately 8 am) and reaches its lowest level at about midnight-4 am, or three to five hours after the onset of sleep. Information about the light/dark cycle is transmitted from the retina to the paired suprachiasmatic nuclei in the hypothalamus. This pattern is not present at birth; estimates of when it begins vary from two weeks to nine months of age.Changed patterns of serum cortisol levels have been observed in connection with abnormal ACTH levels, clinical depression, psychological stress, and physiological stressors such as hypoglycemia, illness, fever, trauma, surgery, fear, pain, physical exertion, or temperature extremes. Cortisol levels may also differ for individuals with autism or Asperger's syndrome.
Cortisol also exerts permissive actions. This refers to the fact thatthe action of some hormones requires the presence of cortisol. For example,cortisol must be present in order for glucagon and catecholamines to exert their calorigenic action, and for catecholamines to exert their lipolytic effect.
Because-peripheral adipocytes are less sensitive to insulin,corticosteroids action predominate,whereastruncaladipocytes respond mainly to enhanced insulin levels under the influence of corticosteroids.
Cortisol maintains the responsiveness of vascular smooth muscle to catecholamines and therefore participates in blood pressure regulation. This is another example of a permissive action of cortisol. In adrenal insufficiency, vascular smooth muscle becomes unresponsive to catecholamines. The decreased responsiveness, together with the associated hypovolemia caused by mineralocorticoid deficiency, can result in severe hypotension.
Corticosteroids inhibit phospholipase A2* This leads to reduction in PG levels in the stomach* Cytoprotective effect of PGs is thereforelost peptic ulcer.(this is not due to destruction of these cells but due to their sequestration in tissues)* Misoprostol ( A prostaglandin E1, analogue) may be used to replenish the depleted stomach PGS.* Misoprostol causes a) diarrhoea. b) abortion
cortisol-induced collagen loss in the skin is ten times greater than in any other tissue
Corticosteroidspenetrate cells and bind to a high affinity cytoplasmic receptor protien-> a structural change occurs in the steroid receptor complex that allows its migration into the nucleus and binding to specific sites on the chromatin->trancription of specific m-RNA->regulation of protien synthesis .
Like most steroids, cortisol is metabolized in the liver. It has a half life of 60-90 minutes in the circulation. Most of the cortisol is reduced to dihydrocortisol and then to tetrahydrocortisol which is conjugated to glucuronic acid . Some cortisol is converted to cortisone.Note that cortisone is an active glucocorticoid but that it is formed in the liver, not in the adrenal. The tetrahydroglucuronide derivatives of cortisol and cortisone are water soluble and are excreted in the urine.Oral boiavailabilty of synthetic corticoids is high.
Pulse therapy with high dose methy-pred (1 g infused i.v. every 6-8 weeks)in autoimmune diseases.with good results and minimal suppression of pituitary-adrenal axis.the initial effect of this is due to its antiinflammatoryaction,while long term benefit is due to temporary switchin of immunodamaging process as a cosequence of lymphopenia and deceased IG synthesis.
Not used clinically coz of low oral bioavailability and difficulty in regulating doses.
as in severe TB,severeleprareaction,pneumoocystiscarinii in AIDS patient.
Dexa used to test hpa.at dose which donot contribute to steroid metabolite in urine.responsiveness tested by measuring daily urinary steroid metabolite excretion.
Osteoporosis arrested by ca supplement,vit d ,bisphosphonate,estrogen-androgen replacement)
Moderate dose of short acting steroids given at 48 hrs interval did not cause HPA suppresion.whereas same total amount given in 4 divided 12 hourly doses pruduced marked HPA depression.alternate day therapy resultsnin less immunosupression-lower risk of infection.the long acting steroids (dexa) are not suitable for alternate day therapy.onlyprolem with alternate day therapyare incapacitated on the “off”day.
1. Adams and Siderius ' have reported on five patients with postoperative shock in whom they felt the diagnosis of adrenal insufficiency was justified. one patient had persistent hypotension and tachycardia.In the immediate postoperative period the hypotension became severe, despite adequate blood, fluid, and electrolyte therapy. Levarterenol (Levophed) bitartrate was given continuously but was ineffective. On the third postoperative day hydrocortisone sodium succinate (Solu-Cortef) was given intravenously, and the blood pressure rose sharply and gradually stabilized. The patien received a total of 250 mg. on the third day and 200 mg. on the fourth day. No levarterenol was required. The patient recovered and was discharged on the 14th postoperative day.
Patients on steroids who present for surgery may be at increased risk of complications because of:The adrenal suppression caused by steroid therapy.This often poses the greatest risk and deserves particular attention. The disease or condition which required them to take steroids. Corticosteroids are used in a wide variety of conditions. Some of these may also have attached risks for anaesthesia (those for example affecting lungs, neck joints or drug metabolism).Long-term and other side-effects of steroid therapy.There are preoperative, perioperative and postoperative factors to be considered when assessing and managing these risks.
Hempenstallet al. compared cortisollevels in patients having either a generalanaesthetic or sedation for surgical removal of third molar teeth. Cortisol levels remained unchanged in the sedation group but rose significantly after surgery in patients who had a general anaesthetic
Steroids in oral and maxillofacial surgery
Endocrine system maintains
The concept that hormones acting on
distant target cells to maintain the stability
of the internal milieu was a major advance
in the historical events of physiological
understanding of human body.
Ernest Henry Starling
(1866-1927)was the first to use the term
hormone(from Greek ὁρμή, "impetus")
This is especially important in
oral surgery because many of
the patients attending the our
clinics face stressful
Awareness is therefore
necessary of -the risks and
difficulties that may arise
during the surgical
management of patients with
endocrine disorders; and the
most common oral
History of steroid therapy
It has been almost 60 years since corticosteroids were first
recognized for their anti-inflammatory and immunosuppressive
properties, initially in rheumatologic diseases( in 1949) by
Philip S. Hench and colleagues, a discovery for which he received
(together with Edward C. Kendall and Tadeus Reichstein) the
Nobel Prize in medicine in 1950. Currently,corticosteroids are
the drugs with one of the broadest specturm of clinical
E D W A RD C. KE N D A L L
The development of cortisone as a therapeutic agent
Nobel Lecture, December 11, 1950
From the time, ages ago, when cortisone was
first made in the adrenal cortex it has continued
to serve as a powerful agent in health and
disease.. What physiologic processes are modified
by cortisone and how this influence is exerted are
matters still locked within this hormone of the
adrenal cortex. Said Shakespeare’s soothsayer, "In
Nature’s infinite book of secrecy a little I can
The term “corticosteriods”(also called simply steroids) refers both
-to the hormones produced in outer layer(cortex) of adrenal glands
-to the modified forms of these hormones that are used as drugs.
Despite the name , corticosteroids should not be confused with
anabolic steroids , substances that mimic the virilizing effects of
testosterone and are some times used illegally by athletes to build up
When you think about the adrenal
glands, you should think about
stress. Stress can take many forms:
taking an examination, recovering
from a broken bone, running away
from an invading army, starvation.
For human males, there is even
considerable stress associated
even with shopping .
The two adrenal glands are located immediately anterior to the kidneys, encased in a
connective tissue capsule and usually partially buried in an island of fat. Their
combined weight is about .01-.02% of total body weight in both males and females.
Inspection of a mammalian adrenal gland that has been sectioned reveals two distinct
An inner medulla, which is a source of the catecholamines epinephrine and
norepinephrine. The chromaffin cell is the principle cell type. The medulla is richly
innervated by preganglionic sympathetic fibers and is, in essence, an extension of the
sympathetic nervous system.
An outer cortex, which secretes several classes of steroid hormones (glucocorticoids
and mineralocorticoids, plus a few others). Histologic examination of the cortex reveals
three concentric zones of cells that differ in the major steroid hormones they secrete.
Adrenal cortex makes and secretes over 30 different steroid hormones
(collectively called corticosteroids).Corticoids are 21 carbon
compounds having a cyclopentanoperhydro-phenanthene(steroid)
nucleus. Since adrenal cortical cells store only minute quantity of
hormone ,rate of release is governed by the rate of biosynthesis.
The hypothalamic-pituitary-adrenal (HPA) axis is a feedback loop that
includes the hypothalamus, the pituitary and the adrenal glands. The main
hormones that activate the HPA axis are corticotropin-releasing factor (CRF),
arginine vasopressin (AVP) and adrenocorticotropin hormone (ACTH). The
loop is completed by the negative feedback of cortisol on the hypothalamus
ACTH is secreted in irregular pulses throughout the day which cause parallel
increases in plasma cortisol . Both the frequency and the amplitude of the
pulses are the greatest in the early morning.
This early morning increase in ACTH release is initiated by the release of CRH
(corticotropin releasing hormone) and starts approximately a couple of
hours before waking.
The lowest levels of ACTH in blood occur just before or after falling asleep. This
results in the characteristic diurnal rhythm in ACTH and cortisol secretion
Cortisol is one of the few hormones
essential for life. Adrenalectomy in
humans is always fatal unless
administered.Exactly why adrenal
insufficiency results in death is not
well understood, but in view of the
widespread actions of the
glucocorticoids, it is not surprising
that they are needed for life
•Effect on BP
•Effect on bronchial muscles
(e . g . sympathomimetic amine)
Mineralocorticoid Actions: Electrolyte and water
As a result, blood glucose increases(hyperglycemia,a diabetes like state).
The metabolic effects of glucocorticoids may be counterbalanced by those of other
hormones, particularly insulin, the secretion of which is stimulated by the rise in blood
Promote adipokinetic agents activity(lipolysis)
Redistribution of Fat
Moon face , fish mouth , buffalo hump
↓ Intestinal absorption
OSTEOPOROSIS-spongy bones are
more sensitive(e.g., vertebrae, ribs etc)
Restrict capillary permeability
Maintain tone of arterioles & Myocardial
Na+ sensitize blood vessels to the
action of catecholamines &
angiotensin-(permissive role in
development of hypertension ,should be
used cautiously in hypertensives)
Optimum level of corticosteroid is needed for
normal muscular activity.
Hypocorticisim : ↓ work capacity &
weakness(due to hypodyanamic circulation)
•excess mineralocorticoid action -
hypokalemia – weakness
•excess glucocorticoid action - muscle
wasting & myopathy -
excitability,High doses lower seizure
threshold-cautious use in epileptics
maintain glucose, circulation and
↑ section of gastric acid &pepsin&↓ in
PG levels in the stomach--
Cytoprotective effect of PG lost--result-
Misoprostol ( A prostaglandin
E1, analogue) may be used to replenish
the depleted stomach PGS
Lymphoid tissue and Blood cells
• ↑ rate of destruction of lymphoid cells(T
cells are more sensitive than B cells)
↑ number of RBCs,platlets,neutrophils in
circulation. ↓ lymphocytes,eosinophils and
basophils blood count come back normal
after 24 hours.
Irrespective of type of injury the attending inflammatory response is ↓ed.The cardinal
signs of inflammation –redness,heat,swelling and pain are suppressed.
In early events:↓acute inflammatory response, reduced exudation, ↓ in numbers and
activity of leucocytes, ↓ in inflammatory mediators
In late events:↓numbers and activity of mononuclear cells and fibroblasts, ↓ proliferation
of blood vessels, less fibrosis-thus ↓ chronic inflammation but also ↓ healing
Causes greater suppression of CMI (graft rejection & delayed hypersensitivity)
↓Transplant rejection: ↓antigen expression from grafted tissues, ↓sensitisation of T
Which makes the basis of use in autoimmune diseases and organ transplantation.
Growth & Cell division
Delays the process of healing
and scar formation.
Retards the growth of
•Most potent and most effective
•Effects not seen immediately
(delay 6 or more hrs)
•Inhaled corticosteroids are used
for long term control in bronchial
Effects on stress
ACTH and cortisol secretion are increased by stressful stimuli including surgery
, trauma, pain, apprehension, infection, hypoglycemia and hemorrhage. The increase in
cortisol production is necessary for survival, and stresses that are normally tolerated can
become fatal in adrenal insufficiencyRapid deterioration resulting in organ damage and
shock/coma/death can occur, especially in children.
Cortisol response to a minor (dashed line) and major (solid line) surgery
This process takes 30-60 min.So effects of corticosteroids are not immediate ,and once the
appropriate proteins are synthesized-effects persist much longer than steroid itself
Mechanism of action
Basal Cortisol Production = 8-25 mg/24hrs
Cortisol Production can be 6-fold in
Metabolism by liver enzymes
excretion by urine
plasma t1/2 of cortisol 60-90 min in
biological t1/2 is longer-effects persist
long after steroid is removed from
Hydrocortisone undergoes high
first pass metabolism,has low oral:
parentral activity ratio.Oral
bioavailability of synthetic
corticoids is high.
Transport: Transcortin 75%
Free form 20%
SYNTHETIC STEROIDS have largely replaced the natural compound
s in therapeutic use ,because they are potent,longer acting,more
selective,for glucu/mineralo action and have high oral activity.
Mineralocorticoids - Preparations
Drug Anti-inflam. Salt
Preapartions & dose
Fludrocortisone 10 150 100 mcg tab.
DOCA 0 100 10 mg /ml inj.,used
occasionally for replacemen
t therapy in addison’s
disease2-5 mg sublingual ,
10-20 mg i.m. once or twice
Aldosterone 0.3 3000 Not used clinically
Replacement therapy(for endocrine diseases)
Pharmacotherapy( for non-endocrine diseases)
Uses of steroids therapy
Long term use is potentially hazardous.keep dose to
minimum which is found by trial & error; Needs
Single dose: No harm ,can be used to tide over
Few days therapy (even high doses)unlikely to be
Incidence of side effects related to duration of
Use is only palliative (except replacement therapy)
infection,severe trauma or any stress during
Abrupt cessation of prolonged high dose(>2-3
weeks) leads to adrenal insufficiency
1.Acute adrenal insufficiency:
Amount of fluid infused-governed by-b.p.
2.Chronic adrenal insufficiency: (addison’s disease):
Hydrocortisone given orally,Supplemented with –a mineralocorticoid (fludrocortisone)
3.Congenital adrenal hyperplasia
Familial disorder due to def.of of 21- hydroxylase &11 - hydroxylase enzyme.
Treatment:hydrocortisone 0.6 mg /kg/day in divided doses .
1.arthritis: rheumatoid ,osteoarthritis , rheumatic fever , gout
2.Collegen diseses:SLE,polyarteritis nodosa,dermatomyostitis,nephrotic
May be life saving
Started with high dose-tapered to maintainance dose when remission occurs.
3.Severe allergic reactions: anaphylaxis,angioneurotic edema,urticaria,serum
Even i.v. inj takes 1-2 hours to act,So not a substitute to adr.in anaphylaxis and
angioedema of larynx.
4.Autoimmune diseases :
Hemolytic anaemia , trombocytopenia , MS, active chronic hepatitis , myasthenia
Status asthmaticus ,Severe chronic asthma:as a supplement to bronchodilators.
6.Other lung diseases:
Aspiration pneumonia,pulmonary edema ,for lung maturation in foetus ,to
prevent RDS in cases of premature delivery.
7.Infective diseases :
Under effective chemotherapeutic cover , corticosteroids are indicated only in
serious infective diseases to tide over crisis or to prevent complication.
Inflammatory ocular diseases-may prevent blindness.
Life saving in-pemphigus vulgaris,exfoliative dermatitis,stevens johnson sysndrome.
Ulcerative colitis,crohn’disease,coeliac diseses
Due to tumors,tubercular meningitis,Dexa or beta-methasone preferred .
ALL,hodgkin’s,other lymphoma,secondary role in breast carcinoma,symptomatic relief
in advance malignancy.
13. Liver diseases
• Subacute hepatic necrosis & chronic active hepatitis: Improves survival rates
• Alcoholic hepatitis: reserved for pts. with severe illness
15.Organ tranplant and skin allograft:
High dose corticosteroids +other immunosuppressants to prevent rejection followed by
low maintenance dose.
With chemotherapy(antiemetic),Bell’s palsy,Thrombocytopenia,Spinal cord
To locate the source of androgen production in hirusitism
Mineralocoricoids:sodium and water retention,edema,↑ b.p.
1.cushing habitus cutaneous atrophy occurs with topical use
Precipitation of diabetes.
Susceptibility to infection.(opportunistic)
Peptic ulceration(silent perforation of ulcers)
Osteoporosis(spongy bones)(r/g evidence of osteoporosis –
indication of withdrawal of therapy)
Posterior subcapsular cataract(in children)
Suppression of HPA axis
Longer the duration of therapy, slower the withdrawal
Less than 1 week: withdrawal in few steps
Rapid withdrawal: 50% reduction of dose every day
Slow withdrawal: 2.5 – 5 mg prednisolone reduced at an interval
of 2-3 days
Longer period & high dose:
Half the dose weekly until 25 mg prednisolone or equivalent is
Later reduce by about 1mg every 3-7 days.
HPA axis recovery may take months or up to 2 years
In The patients with steroids therapy for long time,the adrenal cortex atrophies and
stoppage of exogenous steroids precipitates a withdrawal syndrome-
Malaise,fever,weakness,pain in muscles and joints and reactivation of disease.
Subjected to stress these patients may go into acute adrenal insufficiency.
So any patient who has received >20-25 mg/day hydrocortisone or equivalent for
longer than2-3 weeks should be put on a scheme of gradual withdrawal .
Such patients may need protection with steroids if a stressful situation developes
upto one year after withdrawal.
If a patient on steoids develops an infection –the steroids should not be discontinued
despite its propensity weaken host defence.Rather,the dose may have to be increased
to meet the stress of infection.
Use shorter acting
steroids(hydrocortisone,prednisolone) at the
lowest possible dose.
Use steroids for the shortest peroids of time
Give entire daily dose at one time in
Switch to alternate day therapy if possible.
If appropiate ,use
vial)prep.of steroid with poor systemic
1.Moonface’ – excess adipose tissue in face
2 ‘Buffalo Hump’ – excess cervical adipose
4 Excess adipose tissue in trunk
5 Thin limbs
6 Thinning of skin on limbs
7 Bruising on extremities
8 Amenorrhea, decreased libido
9 Osteoporosis, fractures easily
10 Hirsutism 11 Acne 12 Mood swings
There are no specific oral
manifestations,but,though it may be hard
to believe ,patients have been referred to
dentists,for suspected cause of the swollen
Cushing syndrome-clinical features
Dental management in these patients consists in ---LA is preffered for pain control.
pathological fractures during surgical treatments
complications such as hypertension,CVS problems, hyperglycemia, depression and
If the steroid dose is reduced too quickly
after replacement therapy in post
surgical patients with cushing
pain,hypotentionscaly desquamation of
facial skin,paticularly of forehead,is a
1⁰-due to adrenal disesae(addision’s disease)
2⁰-following use of systemic steroids
addision;’s disease- (autoimmune)
c/f-hypotention,hypogyycemia,hyperpigmentation,vulnerable to any
stress such as
infection, trauma, surgery, aneasthesia, fatigue, weakness, lethargy,weigh
Rᵪ-most patients are treated with oral hyrocortisone and fludrocortisone
Dental aspects:risk of ppt hypotensive collapse,prefer LA for pain control
(over concious sedation and GA),oral hyperpigmentation
Life-threatening emergency characterised by collapse ,
bradycardia,hypotension,profound weakness,hypoglycemia,vomiting,and dehydration
The early indicators of an adrenal-crisis onset can be vague and non-specific.
Lay patient flat and leg raised
Give 200 mg hydrocortisone i.v. and summon medical assistance
Take blood for glucose and electrolyte estimation
Give glucose if there is hypoglycemia(25 mg orally or i.v.)
Put up an infusion of NS or glucose –saline.
Give I litre. For two hours together with 200mg hydrocortisone sodium
succinate,repeating this at 4-6 hourly intervals as req. and monitor b.p.
Determine and deal with underlying cause,control of pain &infection
Steroids supplementation must be continued for 3 days after the b.p.has retuned to
Systemic steroids are often effective in the
treatment of oral lesions due to
noninfectious inflammatory disease.
Topical use: non-infections, ulcerative
diseases in oral cavity. Inhibit the
inflammatory reaction, redness and edema,
Systemic use: third molar extraction, minor
and major surgery to reduce
joint disorders,oral submucous fibrosis
Surgical management of a
patient on steroid therapy
Barely three years later after the
discovery of steroids , Fraser and
coworkers reported the death of a
34-year-old man after routine
orthopedic surgery due to
shock, adrenal insufficiency, and
circulatory collapse. The patient
had been on corticosteroids for
rheumatoid arthritis, but the
treatment had been stopped prior
Surgery-activation of HPA axis
Surgery is one of the most potent stressors that can cause activation of the HPA axis. The
degree of activation depends on the type and duration of surgery and anesthesia, with
many other variables adding to the picture, including analgesics, antihypertensive
medications, infections, and age.
The maximum stimulation of the HPA axis is occur during reversal of anesthesia and in
the immediate postoperative period.
Significant hypotension which cannot be explained
by acute blood loss, myocardial
infarction, anesthesia, drugs, or electrolyte
imbalance should suggest the possibility of an acute
adrenal insufficiency. This is especially true if the
blood pressure does not respond promptly to blood
transfusions or vasopressors.
It is suggested that an increase in capillary
resistance and potentiation of the effect of
vasoconstrictors on blood vessels may be factors in
the blood pressure response to adrenal
Adams, R., and Siderius, N.: Postoperative Acute Adrenal Cortical Insufficiency, J. A. M. A.
165:41-44 (Sept. 7) 1957 56
Lack of increase in cortisol production during stress would cause the host to
succumb to it. On the other hand, too much cortisol would be detrimental,
causing increased tissue breakdown, poor wound healing, and
Given this background, it is clear that any patient who has inadequate
cortisol production in response to surgical stress will fare poorly in such a
situation. This patient will need to be recognized, and his acute steroid
requirement will have to be estimated and supplemented.
Adrenocortical function may be suppressed if:
The patient is currently on daily systemic corticosteroids at doses above 7.5 mg
Cortisteroids has been taken regularly during the past 30 days.
Corticosteroids have been taken for more than one month during past one year.
Although the evidence for the need of steroid cover may be questionable,medicolegal
and other considerations suggest that one should act on the side of caution and fully
inform and discuss with patient,take medical advice in case of doubt,give a steroid cover
unless confident that collapse is unlikely.
B.p. must be carefully watched during surgery and especially during
recovery.,and steroid supplementation must be given if b.p. starts to fall.
Drugs especially sedative and GA ,are a hazard and it is extremely
important to avoid hypoxia,hypotention and haemorrhage
Patient may also require special management as a result of
diabetes,hypertention ,poor wound healing and infections.
Procedure No steroids for
previous 12 months
during previous 12
No cover required Give usual oral
steroids dose in
50mg i.v. preop
Double oral steroids
dose in morning or
50 mg i.v.
Consider cover if
large doses of
steroids were given
Give usual steroids
dose in morning
50 mg i,.v. preop +
i.m. 6 hourly for 24 h
Double oral steriod
dose in morning
50mg i.v.preop +
i.m.6 hourly for 24
Consider cover if
large doses were
Same+i,.m 6 houly
for 72 h
Same +i.m. 6 hourly
for 72 h+normal
ROUTINE DENTAL PROCEDURES
Conducting treatment in the morning.
Control of anxiety and emotional stress.
Use long-acting anesthetics.
Treatment of postoperative pain.
Minimum use of NSAIDs
Aseptis surgery ,Antibiotic prophylaxis
Prevention of iatrogenic fracture during surgery .
topical steroids for use in mouth predispose to oral candidiosis.
Gersema L, Baker K. Use of corticosteroids in oral surgery.J Oral Maxillofac Surg. 1992
Perioperative use of corticosteroids has been advocated for reduction of pain, edema, and
trismus following oral surgical procedures. It was demonstrated that corticosteroids
reduced the amount of inflammation , especially edema. No significant adverse reactions
were noted. Based on these studies, the use of perioperative corticosteroids appears to be a
safe and rational method of reducing postoperative complications following the removal of
impacted third molars
Oral submucous fibrosis: etiology, pathogenesis, and future researchR. Rajendran1. Bulletin of
the World Health Organization, 1994, 72 (6): 985-996
Immunomodulatory drugs and systemic application of glucocorticoids and placental extract are
commonly used. By opposing the action of soluble factors released by sensitized lymphocytes
following activation by specific antigens, glucocorticoids act as immunosuppressive agents .
These also prevent or suppress inflammatory reactions, thereby preventing fibrosis by
decreasing fibroblastic proliferation and deposition of collagen.
Emerging intra-articular drug delivery systems for the temporomandibular joint.
Mountziaris PM, Kramer PR, Mikos AG.Methods. 2009 Feb;47(2):134-40.
Intra-articular injections of corticosteroids and hyaluronic acid are currently used to treat
chronic painof TMJ.The most common treatment strategy is either a single injection or a
series of two injections spaced 14 days apart .A single corticosteroid injection is beneficial
for patients with severe TMJ pain, while further injections do not provide added pain relief,
and may increase the risk of joint degeneration and other complications
Kondoh T et al ..Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Dec;98(6):651-6
Aim was to compare the the clinical outcome of intra-articular irrigation and corticosteroid
injection into the superior joint compartment (SJC) of patients and conventional closed
reduction with IMF with fresh mandibular condyle fractures. Clinical outcome was
determined by clinical examination of jaw motion, joint pain, and occlusal changes.
It was concluded that the modified treatment protocol involving intra-articular
corticosteroid injection is a more effective and quick-acting modality than conventional
closed reduction with IMF for functional recovery and control of clinical symptoms of
patients with unilateral fresh condylar fractures
Say “NO” to the mis-use!!
A patient consults a general dental practitioner for burning sensation in the mouth
The dentist looks into the mouth, finds red patches on the buccal mucosa and tongue
prescribes a topical steroid.
Within few days the burning sensation increases manifold times making life miserable for
Such events are not uncommon in today’s practice. This patient probably had oral
candidiasis predisposed by some underlying factor (e.g. diabetes). The use of a steroid
further increased the immune suppression locally, resulting in the flare up of the fungal
This is a clear case of misuse of steroid
USE TOPICAL STEROIDS WISELY!!
Althoughthe practitioners have learnt (as students) that steroids are “double edged
weapons” many of them consider steroids as panacea
Steroids are used by every practitioner irrespective of their speciality. Steroids can be
administered in various forms, but its use or misuse is generally restricted to topical
preparations in dentistry(KENACORT)
Some general practitioners use them for any ulcer or even an area of erythema in the oral
Unfortunately these preparations can also be bought over the counter
.... It doesn’t end there. The patient uses the preparation till he feels better and stops or
keeps using it for an unlimited period without consulting the dentist again
To make the situation worse, the patient recommends its use to anyone who has an ulcer in
the mouth. Although nothing catastrophic is going to happen, such misuse for prolonged
periods can result in unexpected and unwanted effects and delay in the correct diagnosis
and proper management.
Somasundaram Elangovan,A RETHINK ON THE USE OF TOPICAL STEROIDSe-Journal of
Dentistry July - Sep 2011 Vol 1 Issue 3 65
In Addison’s disease: We must conduct treatment
in the morning and control of anxiety. In
patients with corticotherapy, we must evaluate
the necessity to administer additional
In Addisonian crises: we should interrupt dental
procedure. Unexplained hyponatremia and
hyperkalemia in the setting of hypotension
unresponsive to catecholamine and fluid
administration… should receive 100mg
In hyperadrenocorcism: we must prevent infection
and pathological fractures.
•Jabbour SA. Steroids and the surgical patient. Med Clin North Am. 2001
•Hume DM, Bell CC, Bartter F. Direct measurement of adrenal secretion during operative
trauma and convalescence. Surgery. 1962 Jul;52:174-187.
•Kehlet H. A rational approach to dosage and preparation of parenteral glucocorticoid
substitution therapy during surgical procedures. A short review. Acta Anaesthesiol
•Kehlet H. Clinical course and hypothalamic-pituitary-adrenocortical function in
glucocorticoid-treated surgical patients. Copenhagen: FADL; 1976.
•Somasundaram Elangovan,A RETHINK ON THE USE OF TOPICAL STEROIDSe-Journal of
Dentistry July - Sep 2011 Vol 1 Issue 3
•Steroid cover for dental patients on long-term steroid medication: proposed clinical
guidelines based upon a critical review of the literatureN. Gibson1 and J. W.
Ferguson2.British Dental Journal 2004; 197: 681–685
Oral submucous fibrosis: etiology, pathogenesis, and future researchR. Rajendran1.
Bulletin of the World Health Organization, 1994, 72 (6): 985-996
•Crispian Scully and Roderick A. Cowson,5TH edition-medical problems in dentistry
Chapter-7,endocrine disorder II,p-85-92.
•Salem M, Tainsh RE Jr, Bromberg J, et al. Perioperative glucocorticoid coverage. A
reassessment 42 years after emergence of a problem. Ann Surg. 1994
Mitotane:structure similar to DDT, used in inoperable adrenal
Metyrapone: inhibit 11 -hydroxylase
Aminoglutethamide: inhibit conversion of cholesterol to
pregnolone, medical adrenelectomy
Trilostane: inhibit conversion of pregnolone to progesterone;
used in Cushing’s syndrome
Ketoconazole: anti-fungal, inhibit CYP450 enzymes, inhibit
steroid synthesis in ad.cortex and testis; used in Cushing’s
syndrome & Ca.prostate
Mifepristone: glucocorticoid receptor antagonist; anti-
progesterone, used in Cushing’s syndrome 70
The effect of anabolic steroids on muscle mass is caused in at least two ways:first, they increase the
production of proteins; second, they reduce recovery time by blocking the effects of stress hormone
cortisol on muscle tissue, so that catabolism of muscle is greatly reduced. It has been hypothesized
that this reduction in muscle breakdown may occur through anabolic steroids inhibiting the action
of other steroid hormones called glucocorticoids that promote the breakdown of muscles.
Anabolic steroids also affect the number of cells that develop into fat-storage cells, by favouring
cellular differentiation into muscle cells instead. Anabolic steroids can also decrease fat by
increasing basal metabolic rate(BMR), since an increase in muscle mass increases BMR
Major effects of steroid abuse can include liver damage; jaundice; fluid retention; high blood
pressure; increases in "bad" cholesterol. Also, males risk shrinking of the testicles, baldness,
breast development, and infertility. Females risk growth of facial hair, menstrual changes,
male-pattern baldness, and deepened voice. Teens risk permanently stunted height,
accelerated puberty changes, and severe acne. All users, but particularly those who inject
the drug, risk infectious diseases such as HIV/AIDS and hepatitis.
Most anabolic steroids are synthetic substances similar to the male sex hormone testosterone
This short review should underscore the primary problems associated with the
development of ‘guidelines’ defining the appropriate use of intra-articular corticosteroid
injection: there is just too little science evaluating short and long term efficacy, assessing
the most efficient technique for drug delivery and the most effective formulation, and
documenting the risks associated with repeated articular injection.
Nonetheless, it is clear that intra-articular injection of the TMJ with local anesthetic and
corticosteroid may be useful with some forms of temporomandibular joint disease including
juvenile rheumatoid arthritis and uncomplicated TM joint arthralgia associated with acute
inflammation and osteoarthritis. However, as is noted by JJ Buescher in the American
Family Physician (http://www.aafp.org/afp/2007/1115/p1477.html), “repeated intra-
articular corticosteroid injections are not recommended”