Corticosteroids in Dentistry Seminar by Dr Pratik

Corticosteroi
ds
SEMINAR I I
PRESENTER : DR PRATIK PIPALIA

Corticosteroi
ds
SEMINAR II
PRESENTER: DR PRATIK PIPALIA
PPT available at
https://www.dropbox.com/s/unzzzyaotqhs1vz/Steroids%20seminar%20Dr%20Prat
ik.pptx

Introduction
History
Functional anatomy and histology of adrenal
glands
Biosynthesis of steroids
Fate of steroids
Mineralocorticoids (source, action, regulation)
Glucocorticoids (source, action, regulation)
Mechanism of action at cellular level
Contents 4

5Classification of steroids
Uses in medicine
Steroids in dentistry
Adverse effects
Drug interactions
Precautions
Pathologies of adrenal gland

Introduction
 The adrenal gland is the source of a diverse group
of hormones essential for metabolic control,
regulation of water and electrolyte balance, and
regulation of body’s response to stress.
 Using cholesterol as a substrate, the adrenal
cortex produces a large number of substances
collectively known as corticosteroids.
6

History
 By the middle of 19th century it was demonstrated
that adrenal glands were essential for life
 Later, it was appreciated that the cortex was more
important than the medulla
 A number of steroidal active principles were
isolated and their structures were elucidated by
kendall and his coworkers in the 1930s.
7

 However, the gate to their great
therapeutic potential was
opened by Hench (1949) who
obtained striking improvement
in rheumatoid arthritis by using
cortisone.
 The nobel prize was awarded
the very next year to kendall
and Hench.
 Currently, corticosteroids are
drugs with one of the broadest
spectrum of clinical utility.
8

Functional anatomy and
histology of adrenal glands
9

Zones of adrenal cortex Hormones
Zona glomerulosa Aldosterone
Desoxycorticosterone
Zona fasciculata
Cortisone
Cortisol
Zona reticularis
Dehydroepiandrosterone
Androstenidione
Traces of estrogens
12
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam

Cholesterol
Pregnenolone
Progesterone
11- Deoxy corticosterone
Corticosterone
Aldosterone
17α Hydroxy
pregnenolone
17α Hydroxy
progesterone
11 Desoxyhydro
cortisone
Hydrocortisone
Dehydroepiandrosterone
Androstenidione
Testosterone
Biosynthesis of steroids 13

Mineralocorticoids
Aldosterone
11- Deoxy
corticosterone
Glucocorticoids
Cortisol
Corticosterone
Cortisone
14
K Sembulingam

Rate of secretion of the
principal steroids
Glucorticoids
10-20 mg daily
Mineralocorticoids –
0.125 mg daily
Textbook of Medical Physiology 11th Edition,
Arthur C. Guyton, John E. Hall - 2006
15

 Regulation by
Hypothalamus (CRH) &
Pituitary (ACTH)
 Negative feedback
effect from plasma
cortisol levels
 Pulsatile secretion of
ACTH based on
Circadian rhythm
 Neural effects on HPA
axis due to emotional /
physical stress
16
REGULATION OF SECRETION

Fate of corticosteroids 17
Degraded mainly in liver
Conjugated to form glucuronides and to a lesser
extent form sulphates
25% - excreted in bile and feces
75% - excreted in urine

18
MECHANISM OF ACTION
plasma memb
Corticosteroids
CYTOPLASMIC
RECEPTOR
PROTEIN
GLUCOCORTICOID
RESPONSE
ELEMENT
Nucleus
Transcription of
m - RNA
New protein
synthesis
TOTAL
TIME
30 – 60 mins

Mineralocorticoids
 Source : Zona glomerulosa
 Functions: 90% of mineralocorticoid activity is
provided by aldosterone
 Aldosterone – life saving hormone
20
K Sembulingam

On Na+ metabolism
•Increase in the
reabsorption of
sodium from renal
tubules
Actions 21
K Sembulingam

22
On ECF volume
• Na reabsorption from renal tubules
• Simultaneous water reabsorption
• Increase in ECF volume
K Sembulingam

23
On BP
• Increases ECF volume
• Increases BP
K Sembulingam

24
On K+ ions
•Increase in the
excretion of
potassium from renal
tubules
K Sembulingam

25
On H+ ion concentration
• Causes tubular secretion
of hydrogen ions
• Essential to maintain
acid - base balance
K Sembulingam

26
On intestine
•Greatly enhances
sodium absorption
from the intestine
K Sembulingam

Increase in K+ concentration
Decrease in Na+ Concentration
Decrease in ECF volume
Decrease in K+ concentration
Increase in Na+ Concentration
Increase in ECF volume
Juxtaglomerular
apparatus
Excretion of K+
Retention of Na+
Retention of water
kidneysLungs
AldosteroneAdrenal cortex
angiotensinogen
Angiotensin - 1
Angiotensin - 2
Renin
Converting
enzyme
Stimulation
Feedback
inhibition
Regulation of aldosterone secretion
27
K Sembulingam

Glucocorticoids
Source : zona fasciculata
Functions:
Cortisol – Life protecting hormone
Hormone Glucocorticoid activity
Cortisol 95%
Corticosterone 4%
Cortisone 1%
29
K Sembulingam

Actions: 30
On carbohydrate metabolism
• Increases blood glucose
level in two ways,
Promotes gluconeogenesis
Inhibits glucose uptake and
utilization by peripheral
cells
K Sembulingam

31
On protein metabolism
• Promote catabolism of
protein in cell
• Increase plasma
amino acid and protein
content in the cell.
K Sembulingam

32
On fat metabolism
• Causes mobilization and redistribution of
fat
• Actions are
• - Mobilization of fatty acids from adipose
tissue
• - Increase the concentration of fatty acids
in blood
• - Increases the utilization of fat for energy
K Sembulingam

33
On mineral metabolism
• Enhances sodium retention
• Slightly increase potassium
excretion
• Decreases blood calcium by
inhibiting absorption from
intestine
K Sembulingam

34
On water metabolism
•Accelerate the
excretion of water
K Sembulingam

35
On muscles
•Increase the release
of aminoacids from
muscles by
catabolism of proteins
K Sembulingam

36
On blood vessels
• Decreases the number of
circulating eosinophills in
retculoendothelial cells
• Decrease the number of
basophils and lymphocytes
• Increase the number of
neutrophills, RBCs and platelets.
K Sembulingam

37
On vascular response
• Glucocorticoids is essential
for the constrictor action of
adrenaline and noradrenaline
• In adrenal deficiency, the
blood vessels fail to respond
to Adr and NA leading to
vascular collapse.
K Sembulingam

38
On CNS
• Essential for normal
functioning
• Insufficiency causes
personality changes like
irritablity and lack of
concentration
K Sembulingam

39
Permissive action of
glucocorticoids
• The action of some hormones are
executed only in the presence of
glucocorticoids.
• Eg: Calorigenic effect of glucagon
• Lipolytic effect of catecholamines
• Pressor effects of catecholamines
• Bronchodialation by catecholamines
K Sembulingam

Lipocortin
Recruitment of WBC & monocyte-
macrophage into affected area &
elaboration of chemotactic
substances
ELAM & ICAM in endothelial cells
TNF from phagocytic cells
IL1 from monocyte-macrophage
Expression of cyclooxygenase II
40
Anti-inflammatory actions
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)

41
Phospholipids
Arachidonic acids
lipoxygenase Cycylooxygenase
Leukotriene
Prostaglandins,
Thromboxane
Prostacyclins
Phospholipase A2
Lipocortin
Corticosteroids

On resistance to stress 42
Physical or mental stress
Increases ACTH
Increase in glucocorticoid
secretion
High resistance to body
against stress

43
Anti allergic action
• Suppress all types of
hypersensitivity and allergic
phenomena.
• Suppression of recruitment of
leucocytes at the site of contact
with antigen and of inflammatory
response to immunological injury.

44
Immunosuppresive
effects
• Suppress the immune system of
the body by decreasing the
number of circulating T
lymphocytes
• Prevent release of interleukin-2
by T cells

Emotion, stress, trauma
Hypothalamus
Corticotropin releasing factor
Anterior pituitary
ACTH
Adrenal cortex
Cortisol
Feedbackinhibition
Regulation of cortisol secretion 45

Mechanism of action at
cellular level
46

Translocation of glucose transporters
from plasma membrane to deeper sites
Decreased glucose
uptake and utilization
in peripheral tissues
47
Mechanism of action at
cellular level

48
Induction of hepatic
gluconeogenetic enzymes
Increased production
of glucose from
aminoacids

49
Induction of hepatic glycogen
synthetase
Deposition of
glycogen in
hepatocytes

50
Site specific changes in sensitivity
of adipocytes to GH, Adr, insulin
Altered
distribution of
body fat

51
Decreased expression of POMC
gene in pituitary corticotropes
Decreased
production of
ACTH

52
Induction of lipocortins in macrophages,
endothelium and fibroblasts
Lipocortins inhibit
phospolipase A2 –
decreased production
of PGs,LTs&PAF

53
Negative regulation of genes for cytokines in
macrophages, endothelial cells and
lymphocytes
Decreased production of IL-
1,2,3,6,TNFα,GM-CSF,
Interferon – γFibroblast
proliferation and T lymphocyte
function are suppressed.
chemotaxis interfered.

54
Decreased production of acute phase reactants
from macrophages and endothelial cells
Complement
function is
interfered.

55
Decreased production of ELAM-1
and ICAM-1 in endothelial cells
Adhesion and
localization of
leukocytes is
interfered.

56
Inhibit IgE mediated histamine
and LT-C4 release from basophils
Effects of antigen –
antibody reaction
not mediated

Classification of steroids based on
their relative activity
Glucocorticoids:
Short acting
(t1/2 < 12 hr)
• Hydrocortisone
• Cortisone
Intermediate
acting:
(t1/2 12 – 36)
• Prednisole
• Methyl prednisole
• Triamcinolone
Long acting:
(t1/2 > 36 hrs)
• Paramethasone
• Dexamethasone
• Betamethasone
58

Mineralocorticoids
• Desoxycorticosterone
acetate(DOCA)
• Fludrocortisone
• Aldosterone
59

60
Potency Examples
Highest
0.05% Clobetasol propionate
0.05%Betamethasone dipropionate
High
0.1% Halcinonide
0.25% Desoximethasone
0.05% Fluocinonide
0.5% Triamcinolone acetinode
0.05% Betamethasone dipropionate
0.05% Diflorasone diacetate cream
Intermediate
0.2% Fluo-cinolone acetonide
0.05% Desoxymethasone
0.025% Betamethasone benzoate
0.2% Hydrocortisone valerate
Low
0.025% Fluo-metholone
0.025% Triamcinolone acetonide
0.03% Fluocinolone pivalate
0.01% Betamethasone valerate
Lowest
0.25-2.5% Hydrocortisone
0.5% Prednisolone
0.2% Betamethasone
Handbook of Applied therapeutics 8th Edition, 2007

Agent Anti-
inflammatory
Topical Equivalent
oral dose
(mg)
Forms
Available
Hydrocortisone 1 1 20 O, I, T
Cortisone 0.8 0 25 O
Prednisolone 5 4 5 O, I
Triamcinolone 5 5 4 O, I, T
Flu-prednisolone 15 7 1.5 O
Betamethasone 25-40 10 0.6 O, I, T
Dexamethasone 30 10 0.75 O, I, T
61
According to
Potency
Basic and Clinical Pharmacology LANGE-11th Edition

Some Commonly
Prescribed Steroids
62

63
Triamcinolone
Kenacort, Tricort, k
enalog, Tess
buccal paste
Oral:1,4,8mg syrup
Topical:0.1% eye drops, ointment
Parentral: 3,10,40 mg/ml for I.M,
intraarticular, intralesional injections

64
Dexamethasone
Decadron,
Dexasone,
Wymesone
Oral:0.25,0.5,0.75,1,2,4,6mg
tablets
Topical:0.1% eye drops, ear
drops, skin ointment
Parenteral: 4,8,10,20 mg/ml
for IV, IM, intralesional and
intraarticular.

65
Betamethasone
Betnesol, Betn
ovate, Betnes
ol
forte, Betawin
forte, Walacort
, Stemin
Oral: oral drops – 0.5 mg/ ml,
tablets – 0.5 to 1 mg.
Topical – 0.1% eye drops,
ointment,0.05% nasal drops,
0.12% skin creams
Parenteral:4 mg/ml for IM, IV,
intralesional, intraarticular

66
Hydrocortisone
Wycort, Hycort,
Unicort,
Cipcorlin,
Efcorlin
Oral:5mg,10mg,20mgtab
Topical:
1%eye drops
0.025%nasal drops
0.25-2.5%skin cream
Parenteral:25, 50 mg/ml for
IV,IM,SC Injections

67
Cortisone
Corlin,
Cortone
Oral: 5, 10, 25 mg
tablets
Parentral:22,25
mg/ml of solution

68
Prednisolone
Wysolone,
Prelone,
Nucort,
Cecort,
Oral:5,10, 20 mg tablets,
15mg/5 ml syrup,
5mg/ml suspension as
pediatric drops
Parenteral:25,50 mg/ml
IM,IV,Intralesional

In medicine
In dentistry
69
Uses

Medicine 70
Replacement
therapy
Pharmacotherapy

Acute adrenal
insufficiency
• Hydrocortisone
or
dexamethasone
are given i.v, first
as a bolus
injection and then
as infusion along
with istonic saline
and glucose
solutions.
Chronic adrenal
insufficiency :
• Hydrocortisone
given orally is the
most commonly
used drug with
adequate salt
and water
allowance
Congenital adrenal
hypoplasia :
• 0.6 mg/kg daily in
divided doses
round the clock
Replacement therapy: 71

Pharmacotherapy:
 Single dose (even excessive) is not harmful can be
used to tide over mortal crisis even when benefit is
not certain.
 Short courses (even high doses) are not likely to
be harmful in the absence of contraindications.
Starting doses can be high in severe illness
72

 Long term use is potentially hazardous: keep the
dose to minimum which is found by trial and error,
even partial relief may have to be tolerated.
 No abrupt withdrawal after a corticoid has been
given for > 2 to 3 weeks: may precipitate adrenal
insufficiency
73

Arthritis
Rheumatoid arthritis
Osteoarthritis
Rheumatic fever
Gout
74

Collagen diseases
SLE
Polyarteritis nodosa
Dermatomyositis
Nephrotic syndrome
Glomerulonephritis
75

Severe allergic reactions
Used for short periods in
anaphylaxis
Angioneurotic edema
Utricaria
Serum sickness
76

Autoimmune disorders
Autoimmune hemolytic anemia
Thrombocytopenia
Active chronic hepatitis
Myasthenia gravis
77

Bronchial asthma
Status
asthmaticus
Severe chronic
asthma
78

Infective diseases
Severe forms of tuberculosis
Severe lepra reaction
Certain form of bacterial meningitis
Pneumocystitis carini pneumonia with
hypoxia in AIDS patients.
79

Eye diseases
Effective in diseases of anterior chamber
Allergic conjuctivitis
Iritis
keratitis
80

Skin diseases
Eczematous skin diseases
Pemphigus vulgaris
Exfoliative dermatitis
Steven johnsons syndrome
81

Intestinal diseases
Ulcerative
colitis
Chron’s
disease
82

Others 83
Cerebral edema
Malignancies
Organ transplantation and skin allograft
Shock
To test the adrenal pituitary axis

Steroids in
Dentistry
 Used primarily to decrease postoperative edema and
manage oral inflammatory diseases
84

Steroids in oral surgery 85
Prevention of postoperative
pain, edema, trismus after 3rd
molar surgery
Prevention of postoperative
edema after orthognathic
surgery
Prevention of alveolar osteitis

steroids in Endodontics
 Steroids are used as intracanal medicaments in endodontics
 Ledermix is corticosteroid- antibiotic intracanal paste
 Painful teeth with acute apical periodontitis that had been
dressed with ledermix paste gave rise to less pain and it has
proved to be an effective intracanal medicament for the
control of postoperative pain associated with acute apical
periodontitis with a rapid onset of pain reduction
86
International Endodontic Journal,Volume 36
Issue12, Pages 868 - 75

Corticosteroi
ds in Oral
Medicine
87

Corticosteroi
ds
SEMINAR II SESSION-2
PRESENTER: DR PRATIK PIPALIA
CHAIR PERSON: DR ALI I M

Mineralosorticoid Lifesaving
.. Why ??
 Without mineralocorticoids, potassium ion concentration of the
extracellular fluid rises markedly, sodium and chloride are
rapidly lost from the body, and the total extracellular fluid
volume and blood volume become greatly reduced.
 The person soon develops diminished cardiac output, which
progresses to a shock like state, followed by death.
 This entire sequence can be prevented by the administration of
aldosterone or some other mineralocorticoid
92

93Sources of cholesterolEgg Yolk
Dairy Products, ice
cream cheese, butter
Oil, ghee, soyaben oil,
sun flower oil
Red
Meat, pork, beef, mutton

Lipids
Total Lipid Range mg% Mean
Total Lipid 350-800mg% 570
Cholesterole 150-250 200
HDL 30-6 45
LDL 70-200 135
VLDL 1/5th of TG
Phospholipid 125-400 210
Triglycerol 75-175 140
Free Fatty acids 5-15 10
94

How exactly stress induces
increases Corticosteroid
production?
 At the hypothalamus, fear-signaling impulses activate both
the sympathetic nervous system and the modulating
systems of the HPA axis.
 E/NE will positively feedback to the pituitary and increase
the breakdown of POMCs(Pro-opiomelanocortin ) into ACTH
95

96
Steroids in Oram Medicine
Adverse effects
Drug interactions
Precautions
Pathologies of adrenal gland
Content

Corticosteroi
ds in Oral
Medicine
97

98• Eg: Erosive LP
• RASUlcerative, Vesiculoerosive
diseases
• Eg: CGCG
Benign lesions
• Eg: Mucocele
Salivary gland disorders
• Eg: Osteoarthritis
• Rheumatiid arthritisTMJ Disorders
• Eg. Post herpatic neuralgia
Neuralgia Treatment
• OSMF
Miscellanous

Ulcerative Vesiculoerosive
diseases
 Immunologically mediated diseases that affect the oral
mucosa present with inflammation and loss of epithelial
integrity, through cellular and/or humoral immunity-
mediated attack on epithelial connective tissue targets.
 The main clinical features are ulceration and reddening,
with pain that can be severe and debilitating.
99

 Corticosteroids play a central role in the treatment
of vesiculoerosive lesions.
 However, the frequency and severity of the
adverse effects associated with the use of
systemic corticosteroids have led to the increased
use of topical corticosteroids (TCs)
10
0

10
1
short course of
TCs
Accelerate
remission without
adverse effects
Recurrent aphthous
stomatitis (RAS), some
cases of erythema
multiforme (EM), and
Drug-induced ulceration.
TCs must be used
for longer, less
predictable periods
Severe RAS, Erosive
oral lichen planus
(OLP), specific forms of
EM, and mucous
membrane pemphigoid
(MMP)
Scully et al., 1999; Chan et al., 2002
Criteria for use

10
2
very severe
cases of
ulceration
Short course of systemic
corticosteroids followed
by maintenance regimen
of TCs and or can also
be started
simultaneously with the
systemic therapy
Pemphigus
vulgaris ,10-30%
of Pemphigoid
patients, Erosive
lichen planus
Inevitably be treated with
systemic corticosteroids
and/or other
immunosuppressant
therapies
Laskaris and Angelopoulos, 1981;
Nisengard and Neiders, 1981; Fine et al., 1984;
Domloge-Hultsch et al., 1994; Dayan et al., 1999

Protocols for use
 When a TC is prescribed, and especially when a prolonged
course is predicted, the basic rule is that a TC of a potency
appropriate to the severity of the clinical symptoms should be
used, at the lowest possible concentration and frequency,
with maintaining the effectiveness of the treatment.
 It should always be taken into account that these drugs do
not cure the disease but rather control or relieve the
symptoms.
10
3
JDR April 2005 vol. 84 no. 4 294-301

The key factors
10
4
JDR April 2005 vol. 84 no. 4 294-301
The specific diagnosis
The severity of the oral disease
The presence or absence of extra-oral
lesions
The medical history of the patient

Factors that influence the
effectiveness of TCs:
10
5
JDR April 2005 vol. 84 no. 4 294-301
The intrinsic potency of
the drug
which can be significantly
increased by the halogenation of
the steroid; esterification, which
makes the drug more lipophilic
and gives it greater penetrability
(Regezi and Sciubba, 1999).

10
6
JDR April 2005 vol. 84 no. 4 294-301
The contact time
between the drug and
lesion and the vehicle
used to apply it;

10
7
JDR April 2005 vol. 84 no. 4 294-301
Concentration
which can increase its clinical
effectiveness, although no
additional advantage is
obtained beyond certain
limits.
(Regezi and Sciubba,
1999).

Success of a topical medicine
10
8
Two main factors
Number of applications
per day
High-potency
(2-3 times)
Low potency
(5-10 times)
The vehicle
used
Various
vehicles
JDR April 2005 vol. 84 no. 4 294-301

Various vehicles.
10
9
JDR April 2005 vol. 84 no. 4 294-301
Orabase (Stoy, 1966),
Cyanoacrylate (Jasmin et al., 1993),
Bioadhesive patches made of cellulose
derivatives (Mahdi et al., 1996),
Gels (Regezi and Sciubba, 1999), and
Denture adhesive paste (Lo Muzio et al., 2001).

 Patients prescribed TC in an adherent vehicle
should be instructed to
 Apply a small amount to the target area after
meals, and
 Not to eat or drink for at least 30 min.
 It is best not to rub the TC in, because this can
produce irritation.
11
0
JDR April 2005 vol. 84 no. 4 294-301

 For small and accessible erosive lesions, or those
located on the gingiva and palate, the lesions can
be treated by the
 Use of an adherent paste in a tray,
 Which allows for accurate control over the contact
time and
 Ensures that the entire lesional surface is exposed
to the drug.
11
2
JDR April 2005 vol. 84 no. 4 294-301

Systemic steroids for ulcerative
vesiculobullous diseases
11
3

major aphthae or severe
multiple minor aphthae
 Prednisone therapy should be started at 1.0 mg/kg/day
in patients with severe RAU and should be tapered after
1 to 2 weeks.
11
4
Natah SS, Konttinen YT. IJOMS 2004;33:221-34.

11
5
Minor EM 20 – 40 mg/day for 4 – 6
days
Severe or rapidly
progressing
lesions
60 mg/day slowly
tapered by 10 mg/day
over 6 weeks
Erythema multiforme
Indian J Ophthalmol Jan-Feb 2010;58(1):64-66

Pemphigus Vulgaris
 Mainstay 1-2mg/kg/d.
 Initial dose of treatment – 0.5 mg/kg/day to 3 mg/kg/d
 Dose that achieves clinical control is maintained for 2-
3 weeks and then gradually tapered.
11
6
Burkit’s Oral Medicine, 11th edition

Pulse therapy
 Also called short term therapy
 High dose therapy involves a 48-72 hrs course of
intensive steroid administration
 Single i.v injection of a supra-physiological dose of
steroid
 Dose of 0.5-2g of prednisolone or equivalent
11
7

Benefits
 Avoids complications & side effects of long term steroid
therapy
 To achieve immunosuppressive effects similar to those
with higher doses of steroids
11
8

12
0Cicatricial pemphigoid
Predisolone – 30
to 60 mg/day
2-3 weeks to
stop new bullae
formation
Tapered by 20%
every 2-3 weeks
until the dose of
10 mg is reached
Dose maintained on
alternate days and
reduced by 5 mg
every 2 weeks, then
stopped

12
1Bullous pemphigoid
Clobetasol propionate
20 -40 mg/day is more
effective for the treatment.
JIAOMR, April-June 2011;23(2):128-131

12
2Lichen planus
Prednisolone
1mg/kg/d for <7
days
Tapered to
10-20mg per day
for 2 weeks
Burkit’s Oral Medicine, 11th edition
JIAOMR, April-June 2011;23(2):128-131

12
3Lupus erythematosus
Predisolone –
20 - 30 mg/day
for 2- 6 weeks
Tapered
gradually

Steroids in the treatment of
benign lesions
12
4
CGCG
HEMANGIOMA

12
5CGCG
Intralesional injection of triamcinolone
can be given in a dose of 1 to 2 mg/kg/d
(maximum of 60 mg).
The treatment interval at 4 to 6 weeks.
J Med Assoc Thai 2008; 91 (Suppl 3): S90-6

12
9
Prednisone at a dose of 20-30
mg/d can be given for 2 weeks
to 4 months
( Fost and Esterly)
Intralesional triamcinolone
acetonide (4 mg/mL)
(Hawkins et al)
Hemangioma

13
0
Steroids in salivary gland disorders
MUCOCELE

13
1Mucocele
 0.05% clobetasol
propionate 3 times a day
for 4 weeks in a mucosal
adhesive base.
 Intralesional injections
have also been tried with
success.
(JOMS 2008;66:1737-9)

13
4
Steriods in neuralgia
POST HERPETIC NEURALGIA

13
5Post herpetic neuralgia
To reduce incidence of post herpetic neuralgia:
 Prednisolone 20 to 30 mg/day for 7 – 10 days
tapered to 10 mg/day for 1 week
(Treatment of oral diseases, George Lascaris)

13
8
Steroids for TMJ disorders
OSTEOARTHRITIS
RHEUMATOID ARTHRITIS

13
9
Rheumatoid
arthritis
Intraarticular injection –
10 to 40 mg/ml
osteoarthritis
Intraarticular injection –
20 mg/ml(2 injections 14
days apart)
Arthritis
Oral Surgery Volume 1 Issue 2, Pages 88 - 95

14
0
Miscellaneous
OSMF
BELL’S PALSY

14
1Bell’s palsy
 Significant improvement can be
achived when Prednisolone is
started within 72 hours of
symptom onset
 1 mg/kg body weight (maximum
70 mg) in divided doses with
meals for six days, and the dose
can be reduced gradually over
the next four days.

14
2OSMF
Predisolone –
20 - 30 mg/day
for 2 – 4 weeks
Gradually taper
Discontinue in 1-
2 months

14
3
Injections of triamcinolone 10mg/ml diluted
in 1 ml of 2% lidocaine with hyaluronidase 1500
IU, biweekly for 4 weeks.
(Borle et al)

14
4
 Biweekly submucosal injections of a combination
of dexamethasone (4mg/ml) and two parts of
hyaluronidase, diluted in 1.0 ml of 2% xylocaine
by means of a 27 gauge needle, not more than
0.2ml solution per site, for a period of 20 weeks.
 Significant relief of burning sensation (88%) and
improvement of trismus (83%) can be seen in
most patients.

14
6Adverse effects
Due to extention of pharmacological action occuring with
prolonged therapy
Mineralocorticoids:
 Sodium and water retention
 Edema
 Hypokalemic alkalosis
 Progressive rise in B.P
 Weight gain
 Fluid and electrolyte disturbance

14
7Glucocorticoid:
GIT:
 Acute erosive gastritis with hemorrhage
 Peptic ulcer
 Intestitial perfortion
 Pancreatitis
Metabolic effects:
 Hyperglycemia
 Ketoacidosis
 Hyperosmolar coma
 Hypophosphatemia

14
8
Cushingoidism:
Prolonged therapy causes
 Central obesity with moon face
 Buffalo hump
 Pink florid striae are liable to appear on the
abdomen, hips and pectoral region and skin may
become friable

14
9
CVS and renal system:
 Hypertension
 Salt and water retention
 Hypokalemic alkalosis
CNS:
 Influence mood, sleep pattern
 Insomnia
 Acute psychotic reactions
 Benign intracranial hypertension
 Epilepsy

15
0
Musculoskeletal effects:
 Proximal myopathy and osteoporosis with
compression fractures of vertebrae
 Acute aseptic necrosis of bone
Eyes:
 Glaucoma

15
1
Suppression of inflammation and immune response:
 Latent infection may flare
 Oppurtunistic infection with low grade pathogens
Retardation of linear growth:
 Occurs in children who receive more than 50 mg
of cortisone per m2 of body surface per day.

Relative Contraindications:
15
2
 Peptic ulcer
 Diabetes mellitus
 Hypertension
 Pregnancy
 Herpes simplex
keratitis
 Tuberculosis
 Osteoporosis
 Psycosis
 Epilepsy
 Renal failure

Drug interactions
15
3
Glucocorticoid dosage decreased:
 Antibiotics (Erythromycin)
 Cyclosporine
 Isoniazid
 Ketakonazole
 Estrogen
Reduce metabolic
clearance

Glucocorticoid dosage increased:
 Cholestyramine
 Antiepileptic Drugs (Barbiturates, Phenytoin,
Carbamazepine)
 Rifampicin
Glucocorticoid dosage needs adjustment:
 Antianxiety and antipsychotic drugs
 Antihypertensives
 Hypoglycemics
 sympathomimetics
15
4

15
5Precautions during therapy
Before starting therapy:
 Enquire and check for hypertension, diabetes
mellitus, peptic ulcer, any infection

15
6During therapy:
 Prescribe drug with food
 Diet low in calories and sodium and rich in
potassium
 Check periodically for weight gain, hypertension,
hyperglycemia

15
7
 Increase dose in case of stress
 Instruct patient not to stop abruptly
While stopping therapy:
 Taper therapy

Rule of 2
Adrenocortical suppression should be suspected if a patient
has received Glucocoticoid therapy through two of the
following methods
 In a dose of 20 mg or more of cortisone or its equivalent
 Via oral or parenteral route or a continuous period of 2
weeks or longer
 Within 6 months -2 years of therapy
15
8
Medical emergencies in dental office, Stanley F.Malamed
Complications in Anesthesia - John L. Atlee; Page-132

Protocol for
Supplementation of Patients
on Glucocorticoid Therapy
Who Are Undergoing Dental
Care (Burket’s 10th ed)
15
9

16
0
Dental
Procedure
Previous
Systemic
Steroid Use
Current
Systemic
Steroid Use
Daily
alternating
Systemic
Steroid Use
Current
topical
Systemic
Steroid Use
Routine
procedures
If prior usage
lasted for > 2
weeks and
ceased < 14–30
days ago, give
previous
maintenance
dose
If prior usage
ceased > 14–30
days
ago, no
supplementation
needed
No
supplementation
needed
Treat on steroid
dosage day; no
further
supplementatio
n needed
No
supplementatio
n needed

16
1Dental
Procedure
Previous
Systemic
Steroid Use
Current
Systemic
Steroid Use
Daily
alternating
Systemic
Steroid Use
Current
topical
Systemic
Steroid Use
Extractions,
surgery, or
extensive
procedures
If prior usage
lasted > 2 weeks
and ceased <
14–30 days ago,
give previous
maintenance
dose
If prior usage
ceased > 14–30
days ago, no
supplementation
needed
Double daily
dose on day of
procedure
Double daily
dose on first
postoperative
day when pain
is anticipated
Treat on
steroid dosage
day, and give
double daily
dose on day of
procedure
Give normal
daily dose on
first
postoperative
day when pain
is anticipated
No
supplementatio
n needed

16
2
Patient requiring extractions
took a 7 day course of 20 mg.
of prednisone for exacerbation
of asthma one week ago
No supplementation
required. Even though the
dose was
supraphysiologic, the
course of time it was taken
was less than 2 weeks
Scenario One
Clinical update by Naval Postgraduate Dental School, Maryland
Vol. 23, No. 7 July 2001

16
3
Patient requiring extractions is taking
10 mg of prednisone for the past year
to treat rheumatoid arthritis
This patient’s HPA axis is
probably suppressed due to
supraphysiologic dose of
corticosteroids for longer than 2
weeks. Supplement with at least
100 mg of cortisol equivalent (25
mg prednisone) in the morning on
the day of the surgery
Scenario Two
Vol. 23, No. 7 July 2001

16
4
Patient requiring extractions is
taking 2.5 mg of prednisone daily
for the past 3 months to treat his
psoriasis
No supplementation required.
Even though the patient has
been on prednisone for over 2
weeks, the dose is
subphysiologic and will not
adversely impact his stress
response
Scenario
Three
Vol. 23, No. 7 July 2001

16
5
was previously taking 50 mg of
prednisone for Crohn’s
disease. He was on a 6-month
course of prednisone but took
his last dose 5 weeks ago
No supplementation
needed. A functional stress
response returns in 14-30
days after the last dose of
steroids
Scenario
Four

16
6
is taking 75 mg of
prednisone daily for the
past 8 weeks to treat
pemphigus
No supplementation
needed as 75 mg of
prednisone is the
maximum dose
equivalent to 300 mg of
endogenous cortisol
Scenario Five
Vol. 23, No. 7 July 2001

Pathology of Adrenal
Gland
16
7

16
8Pathologies of the adrenal gland
Adrenal cortex
HypoactivityHyperactivity

16
9
Hyperactivity
Cushing’s
syndrome
Hyper-
aldosteronism
Adreno-
genital
syndrome

17
0
Due to pituitary
origin
Cushing’s disease
Due to adrenal
origin Cushing’s syndrome
Cushing’s syndrome
 Hypersecretion of glucocorticoids particularly
cortisol

17
1Disproportionate body fat distribution
Moon face
Buffalo hump
Pot belly
Purple striae
Thinning of skin
Pigmentation
Facial redness
Hirsutism
Muscle weakness

17
2
Bone resorption
Hyperglycemia
Hypertension
Susceptiblity to infections
Poor wound healing

17
3
Primary Adrenal cause
Secondary Extra adrenal causes
Hyperaldosteronism
 Hypersecretion of aldosterone

17
4
Hyperaldosteronism
• Increase in ECF volume and
blood volume
• Hypertension
• Severe depletion of
potassium
• Muscle weakness
• Metabolic alkalosis

17
7
Hypoactivity
Addison’s
disease Adrenal crisis
Chronic
adrenal
hyperplasia

17
8
Primary Adrenal cause
Secondary
Failure of anterior
pituitary to secrete ACTH
Addison’s disease
 Failure of adrenal cortex to secrete all the
corticosteroids
Tertiary
Failure of hypothalamus
to secrete CRF

17
9
Pigmentation of skin and mucous membrane
Muscle weakness
Dehydration
Hypotension
Decreased cardiac output
Hypoglycemia
Nausea, vomiting, diarrhoea
Inability to withstand stress

18
0Adrenal crisis
 Common symptom of addison’s disease
characterized by sudden collapse associated
with an increase in need for large quantities of
glucocorticoids.
 Fatal if not treated in time

18
1Adrenal crisis
Causes
• Exposure to even mild stress
Hypoglycemia due to fasting
Surgical operation
Sudden withdrawal of
glucocorticoid treatment

Congenital adrenal
hyperplasia
 Congenital disorder characterized by increase in size of
adrenal cortex.
 Eventhough the size of the gland increases the cortisol
secretion decreases.
 Congenital enzymes necessary for synthesis of cortisol,
particularly 21- hydroxylase.
18
2

In boys:
 Precocious body growth, causing stocky
appearance called infant Hercules
 Precocious sexual development with enlarged
penis even at age of 4 years.
In girls:
 Produces Masculinization
 Female child born with external genitalia of male
type.
18
3

Conclusion
 Corticosteroids play an important role in control of
pain & inflammation associated with numerous
disease states of oral cavity.
 Currently corticosteroids are drugs with one of the
broadest spectrum of clinical utility.
 But it should never be used as a substitute to other
treatments
 Lets keep it mind that these drugs do not cure the
disease but rather control or relieve the symptoms.
 It should be used cautiously as it is two edged
sword.
18
5

Thank You…
18
6
PPT available at
https://www.dropbox.com/s/unzzzyaotqhs1vz/Steroids%20seminar%20Dr%20Prat
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Corticosteroids in Dentistry Seminar by Dr Pratik

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