3. IntroductionIntroduction
Adrenal gland is the source of diverse groups ofAdrenal gland is the source of diverse groups of
hormones essential to metabolic controlhormones essential to metabolic control
,regulation of body’s response to stress.,regulation of body’s response to stress.
The medullary portion secretes epinephrine andThe medullary portion secretes epinephrine and
norepinephrine.norepinephrine.
Cortex produce a number ofCortex produce a number of
substances,collectively calledsubstances,collectively called
CORTICOSTEROIDSCORTICOSTEROIDS
4. General physiologyGeneral physiology
Corticosteroids are not stored toCorticosteroids are not stored to
adrenal glands but are continuouslyadrenal glands but are continuously
synthesized and secretedsynthesized and secreted
There is a negative feedbackThere is a negative feedback
mechanismmechanism
5. Absorption,fate andAbsorption,fate and
excretionexcretion
ACTH is destroyd by proteolytic enzymes in gut,ACTH is destroyd by proteolytic enzymes in gut,
hence given parentrlly.hence given parentrlly.
Rapidly metabolisedRapidly metabolised
The quantitative response is greater when givenThe quantitative response is greater when given
in morning than in evening and when givenin morning than in evening and when given
slowly and for longer periods than when givenslowly and for longer periods than when given
rapidly and for shorter periodsrapidly and for shorter periods
6. HORMONESHORMONES
3 distinct groups of steroid3 distinct groups of steroid
hormones:-hormones:-
ZonaZona glomerulosaglomerulosa-aldosterone,-aldosterone,
desoxycorticosteronedesoxycorticosterone
ZonaZona fasciculatafasciculata-cortisone,hydrocortisone-cortisone,hydrocortisone
ZonaZona reticularisreticularis-dehydroepiandrosterone-dehydroepiandrosterone
7. PharmacologicalPharmacological
actionsactions
Metabolic effects:-Metabolic effects:-
Carbohydrate and protein metabolismCarbohydrate and protein metabolism
Fat metabolismFat metabolism
Calcium metabolismCalcium metabolism
Skeletal musclesSkeletal muscles
Action on cardiovascular systemAction on cardiovascular system
Action on central nervous systemAction on central nervous system
On G.I.TOn G.I.T
Antiinflammatory actionAntiinflammatory action
8. Mechanism of actionMechanism of action
Antiinflammatory action- suppressAntiinflammatory action- suppress
clinical features of inflammation a localclinical features of inflammation a local
heat,redness,swelling,tendernessheat,redness,swelling,tenderness
MECHANISMMECHANISM
InflammationInflammation
Sensitized lymphocytesSensitized lymphocytes
Interaction with sensitizedInteraction with sensitized
antigensantigens
9. Production of soluble factors likeProduction of soluble factors like
lymphokines,one being migration inhibitorylymphokines,one being migration inhibitory
factor(MIF)factor(MIF)
Local accumulation of macrophages atLocal accumulation of macrophages at
inflammation siteinflammation site
Effect of MIF blockedEffect of MIF blocked
10. General clinicalGeneral clinical
applicationapplication
Emergency therapy-anaphylaxisEmergency therapy-anaphylaxis
and asthmaand asthma
Replacemental therapy-inReplacemental therapy-in
adrenal insufficiencyadrenal insufficiency
Organ transplant proceduresOrgan transplant procedures
Suppression of immuneSuppression of immune
response-immunologicallyresponse-immunologically
mediated diseasemediated disease
12. aphthous ulcers or recurrent aphthousaphthous ulcers or recurrent aphthous
stomatitisstomatitis) are painful mouth ulcer(s) usually) are painful mouth ulcer(s) usually
appear after a gradual burning or tingling sensation.appear after a gradual burning or tingling sensation.
usually found on the movable, non-keratinized (lessusually found on the movable, non-keratinized (less
protected) tissues in the mouth, including the innerprotected) tissues in the mouth, including the inner
surface of the lips, the cheeks, under the tongue, andsurface of the lips, the cheeks, under the tongue, and
back of the throat.back of the throat.
For more serious cases prescribe corticosteroids.
dexamethasone, used topically as a solution
,rinsed and spit out twice a day for five days.
prednisone orally, in tablet form, starting at 40
milligrams per day then tapered for 10 days.
13.
14. Oral lichen planusOral lichen planus
Topical corticosteroid-clobetasolTopical corticosteroid-clobetasol
propionate-0.05%-3-4 times per daypropionate-0.05%-3-4 times per day
Flucocinomide0.05%-3-4 times per dayFlucocinomide0.05%-3-4 times per day
Moderate cases-intralesional injection-Moderate cases-intralesional injection-
triamcinolone-10-20mgtriamcinolone-10-20mg
Severe-prednisolone-30-60mg then taper-Severe-prednisolone-30-60mg then taper-
20 to 30 mg – 10 to 20mg.20 to 30 mg – 10 to 20mg.
16. erythema multifOrmeerythema multifOrme
In moderate to severe caseIn moderate to severe case
Prednisolone initial dose-40 to 80 mg/dayPrednisolone initial dose-40 to 80 mg/day
then taperthen taper
Recurrent infections-400 mg b.dRecurrent infections-400 mg b.d
18. pemphiguspemphigus
Steroids-mainstay of treatmentSteroids-mainstay of treatment
Prednisone-1 to 2 mg/kg/dayPrednisone-1 to 2 mg/kg/day
Only oral involvement-low doseOnly oral involvement-low dose
prednisolone orprednisolone or
Topical and systemic steroid combination-Topical and systemic steroid combination-
betamathasone-0.01%-3 to 4 times/daybetamathasone-0.01%-3 to 4 times/day
22. Pulpal hypersensitivity-Pulpal hypersensitivity-
Resulting from operativeResulting from operative
trauma,bacterial invasion of pulp,trauma,bacterial invasion of pulp,
exposure of dentin- glucocorticoids canexposure of dentin- glucocorticoids can
be used as a component of endodonticbe used as a component of endodontic
sealer as antiinflammatory agentsealer as antiinflammatory agent
tempOrOmanDibulartempOrOmanDibular
jOint DisOrDers-jOint DisOrDers-
Intraarticular injection of glucocorticoidIntraarticular injection of glucocorticoid
such as prednisolone or dexamethasonesuch as prednisolone or dexamethasone
used to relieve temporary or permanentused to relieve temporary or permanent
symptomssymptoms..
23. Post operative sequalaePost operative sequalae
Mainly glucocorticoids used – edema,Mainly glucocorticoids used – edema,
trismustrismus
After dental surgical proceduresAfter dental surgical procedures
AnAphylActic And otherAnAphylActic And other
AllergiesAllergies
Urticaria,contact dermatitis,allergicUrticaria,contact dermatitis,allergic
rhinitis, conjuctivitis,serum sickness,etcrhinitis, conjuctivitis,serum sickness,etc
24. Oral submucous fibrosisOral submucous fibrosis
Corticosteroids cause a dose dependentCorticosteroids cause a dose dependent
enhancement of fibroblast collagenenhancement of fibroblast collagen
phagocytosis.phagocytosis.
Topical –hydrocortisone(0.05%)Topical –hydrocortisone(0.05%)
Betamethasone(.1%)Betamethasone(.1%)
Intralesional injection-triamcinoloneIntralesional injection-triamcinolone
suspension-3mg/ml-2-3ml/day.suspension-3mg/ml-2-3ml/day.
25. CRESOPHENE, Solution for dental use
Composition: Active ingredients: Dexamethasone Acetate 0.111 %
and Thymol
5.00 % in a solution for dental use
Therapeutic Indications: Root canal antisepsis before filling.
Posology and Method of Administration: For local dental use only. After avulsion
of the gangrened pulp and
thorough reaming, insert a solution – impregnated cotton plug into the canal. Prior to
insertion wring out the
plug to eliminate excess solution.
Temporarily seal the canal with non-compressive impervious cement. Leave in
place for 3 to 5 days.
If necessary, repeat the procedure after debriding and reaming the root canal using
the usual methods.
Contraindications: Allergy to any constituent, particularly corticosteroids
and phenols.
30. CONTRA INDICATIONSCONTRA INDICATIONS
Peptic ulcerPeptic ulcer--Corticosteroids, whichCorticosteroids, which
block COX-2 but not COX-1,12 are notblock COX-2 but not COX-1,12 are not
ulcerogenic when used alone,. Whenulcerogenic when used alone,. When
corticosteroids are used in combinationcorticosteroids are used in combination
with NSAIDs, the risk of ulcer formationwith NSAIDs, the risk of ulcer formation
is much greater.is much greater.
Another mechanismAnother mechanism -decreases synthesis of-decreases synthesis of
PGI2 and PGE2.PGI2 and PGE2.
31. DiabetesDiabetes-- precipitates hyperglycaemiaprecipitates hyperglycaemia
andand glycosuriaglycosuria
HerpesHerpes --suppression of host response maysuppression of host response may
allow disseminatioan of herpes.allow disseminatioan of herpes.
o OsteoporosisOsteoporosis--decreases calciumdecreases calcium
absorption from intestine, increases renalabsorption from intestine, increases renal
excretion of calcium, increased boneexcretion of calcium, increased bone
resorpion.resorpion.
32. Ocular diseasesOcular diseases --increasesincreases
intraocular pressure, causes reversibleintraocular pressure, causes reversible
damage-post subcapsular cataractsdamage-post subcapsular cataracts
Fungal infections –Fungal infections –antiinflammatory-antiinflammatory-
decreases body’s reaction to infectious agent isdecreases body’s reaction to infectious agent is
depressed.depressed.
Tuberculosis-Tuberculosis- latent tuberculosis reactivatedlatent tuberculosis reactivated
after initiation of glucocorticoid therapy.after initiation of glucocorticoid therapy.
36. Primary adrenocorticalPrimary adrenocortical
inSufficiency, alSo knowninSufficiency, alSo known
aS addiSon’S diSeaSeaS addiSon’S diSeaSe
idiopathic nature (most commonlyidiopathic nature (most commonly
autoimmune), but also results fromautoimmune), but also results from
hemorrhage, sepsis, infectious diseaseshemorrhage, sepsis, infectious diseases
(such as tuberculosis, human(such as tuberculosis, human
immunodeficiency virus, cytomegalovirusimmunodeficiency virus, cytomegalovirus
and fungal infection), malignancy,and fungal infection), malignancy,
adrenalectomy, amyloidosis or drugsadrenalectomy, amyloidosis or drugs
37. ADRENAL CRISISADRENAL CRISIS
The most significant acute adverse outcome of AIThe most significant acute adverse outcome of AI
is adrenal crisis. This event can occur when ais adrenal crisis. This event can occur when a
patient with AI, most commonly in the form ofpatient with AI, most commonly in the form of
Addison’s disease, is challenged by stress (forAddison’s disease, is challenged by stress (for
example, illness, infection or surgery), and, inexample, illness, infection or surgery), and, in
response, is unable to synthesize adequateresponse, is unable to synthesize adequate
amounts of cortisol and aldosterone. Thisamounts of cortisol and aldosterone. This
potentially life-threatening emergency usuallypotentially life-threatening emergency usually
evolves slowly during a few hours and then isevolves slowly during a few hours and then is
manifested by severe exacerbation of themanifested by severe exacerbation of the
condition, including profuse sweating,condition, including profuse sweating,
hypotension, weak pulse, cyanosis, nausea,hypotension, weak pulse, cyanosis, nausea,
vomiting, weakness, headache, dehydration,vomiting, weakness, headache, dehydration,
fever, sunken eyes, dyspnea, myalgias,fever, sunken eyes, dyspnea, myalgias,
arthralgia, hyponatremia and eosinophilia.arthralgia, hyponatremia and eosinophilia.
38.
39. CONCLUSIONCONCLUSION
Corticosteroids form the mainstay ofCorticosteroids form the mainstay of
treatment in allergic and inflammatorytreatment in allergic and inflammatory
diseases and oral inflammationsdiseases and oral inflammations
Dose of corticosteroids should always beDose of corticosteroids should always be
tapered.tapered.
Corticosteroid therapy should not beCorticosteroid therapy should not be
discontinued abruptly because abruptdiscontinued abruptly because abrupt
withdrawl will lead to signs ofwithdrawl will lead to signs of
adrenocortical insufficiency.adrenocortical insufficiency.
40. References.References.
Burket’s- oral medicineBurket’s- oral medicine
Arvindo ghomes-oral medicineArvindo ghomes-oral medicine
Carranza-periodonticsCarranza-periodontics
Neelima anil malik-oral surgeryNeelima anil malik-oral surgery
Yagella,dowd-pharmacologyYagella,dowd-pharmacology
K.d. tripathi-pharmacologyK.d. tripathi-pharmacology
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