• Due to corticosteroid therapy that is
prescribed for other medical purposes
• Adrenal or pituitary tumors may also be the
source of endogenous hormones‐cushing’s
• Young adult females

Clinical Features
• Signs of this disease develop slowly
• Most consistent clinical observation is
weight gain, in central areas of body

Clinical Features
• “Buffalo hump"‐ accumulation of fat in
dorsocervical spine region
• “Moon facies ‐round facial appearance due
to fat deposition in facial area

Clinical Features
• Other common findings include:
– red‐purple abdominal striae
– hirsutism
– poor healing*
– osteoporosis
– hypertension
– mood changes (especially depression)
– hyperglycemia with thirst and polyuria
– muscle wasting with weakness

Diagnosis &Treatment
• >> 20mg of prednisone
• Free cortisol in urine
• Assay of ACTH & cortisol with dexamethasone
• ACTH & Cortisol falls without tumor
• No change with tumor
• Cause: systemic corticosteroid therapy
• Cortisol is critical to body function with stress

Treatment
• Tumors ‐ resected, non‐surgical cases
• drugs inhibiting cortisol synthesis‐ketoconazole/
aminoglutethimide
• Alternate day therapy/steroid sparing drugs
• Drop in cortisol levels signals pituitary gland to
produce ACTH
• ACTH stimulates adrenal gland to produce
cortisol‐ FEEDBACK LOOP

Treatment
• ACTH production is suppressed in patients
on long‐term steroids
• Acute hypodrenocorticism (addison’s disease)
• Highly stressful situation, gland may not
produce ACTH

Treatment
• When stressful dental and/or surgical
procedures are planned, corticosteroid
dosage may need to be adjusted
• A medical consultation is warranted

• Insufficient production of adrenal
hormones – cortisol, due to destruction of
adrenal cortex
(primary)
• Non functioning pituitary‐ ACTH
(secondary)

Causes are diverse and include:
• autoimmune destruction
• infections (TB and deep fungal, especially in
AIDS patients
• rarely, metastatic tumors, sarcoidosis,
amyloidosis

Clinical Features
• Insidious onset of fatigue, irritability, depression,
weakness, & hypotension
• Generalized hyperpigmentation of skin
("bronzing" )‐ more prominent on sun‐exposed
skin , due to beta lipoproteins or ACTH stimulus
on melanocytes
• GI upset with anorexia, nausea, diarrhea, weight
loss, and salt craving

Clinical Features
• Young patients ‐ Addison’s with
hypoparathyroidism & mucocutaneous
candiasis‐autoimmune
polyendocrinopathy‐candidiasisectodermal
dystrophy syndrome should be
considered

Clinical Features
• Oral manifestations include diffuse or patchy,
brown macular pigmentation of mucosa caused
by excess melanin production, may preceede skin
pigmentation
• Diag ‐ rapid ACTH stimulation test
• <<20microg/dl of free cortisol‐adrenal insufficiency
• Primary‐>>100ng/L of plasmaACTH
• Secondary‐ plasma ACTH (9‐52ng/L or low)

Treatment and Prognosis
• Corticosteroid replacement therapy
• 5‐7.5mg of prednisone/day in div doses
• Body’s need for corticosteroid hormones
increases during stress, dosage must be adjusted
accordingly
• < 1hr dental procedure no adj
• >>1hr dental/surgical procedure >>dose
• Before patients death within 2yrs now normal life
span

• Common disorder of carbohydrate
metabolism
• Decreased/deranged production of/
increased tissue resistance‐ insulin
• Increase in blood glucose level
(hyperglycemia)
• Lowered tissue resistance to infection

Two types:
• 1)Insulin‐dependent diabetes mellitus
(IDDM)/type I/juvenile‐onset diabetes
• 2)non‐insulin‐dependent diabetes mellitus
(NIDDM)/type II/adult‐onset diabetes

Clinical Features

• Insulin deficiency, glucose cannot be
absorbed into cells, remains in blood
• Normal glucose levels 70 ‐120 mg/dL
• diabetics, levels often 200‐400 mg/dL
• >>300mg/dl renal reabsorption fail

Clinical Features
• Lose weight, with increased food intake
(polyphagia)
• Frequent urination (polyuria)‐osmolarity,
thirst, and increased water intake
(polydipsia)
• Average age at diagnosis 14

• NIDDM 40+ at diagnosis
• 80‐90% obese
• Decrease number of insulin receptors or
abnormal postbinding molecular events
• Show "insulin resistance"

COMPLICATIONS
• Microangiopathy
• Occlusion‐ small vessels, producing
peripheral vascular disease
• Decrease in tissue perfusion results in
ischemia
• Ischemia predisposes to infection as does
impaired neutrophil chemotaxis

COMPLICATIONS
• Extremities affected, gangrene
• Vascular occlusion of coronaries,
myocardial infarction
• Microvascular occlusion retinal vessels,
blindness
• Kidney failure, renal blood vessel
involvement

Oral Manifestations
• Limited to patients with IDDM
• Periodontal disease, occurs more
frequently and progresses more rapidly

Oral Manifestations
• Diabetic sialadenosis: nontender, bilateral
parotid gland enlargement
• More susceptible to oral candidiasis
• Erythematous candidiasis of the dorsal
tongue papillae 30

Oral Manifestations
• Zygomycosis poorly controlled IDDM
• Increased prevalence of benign migratory
glossitis in IDDM
• Xerostomia, one third of diabetics

Treatment and Prognosis
• Diabetes mellitus: common, complex
medical problem with many complications
• Prognosis is guarded
• Consultation with the patient’s physician:
IDDM and poor glucose control, active
infections, or extensive oral surgical
procedures

• Inflammatory, immunologically mediated
condition of unknown cause
• Mainly distal portion of small bowel and
proximal colon
• Anywhere in GI tract, from mouth to anus
• Extraintestinal sites: skin, eyes and joints
• Oral lesions may precede GI lesions in 30%

– Can affect any portion of the GI tract
– Skip lesions
– Transmural involvement
– Noncaseating granulomatous inflammation

• Affects rectum primarily and eventually
affects entire colon in a retrograde manner
• No skip lesions
• Mucosa and submucosa affected only
• No granulomatous inflammation

• Most patients teenagers when first
becomes evident / 60yrs
• GI signs and symptoms include: abdominal
cramping and pain, nausea, and diarrhea

• Diffuse or nodular swelling of oral soft
tissues
• Cobblestone appearance of mucosa

• Deep, granulomatous‐appearing ulcers
• Ulcers, linear and in buccal vestibule.
• Aphthous ulcerations may also occur

Histopathologic Features
• Microscopic examination of tissue from
intestine or oral mucosa shows nonnecrotizing
granulomatous inflammation
Treatment and Prognosis
• Sulfasalazine or prednisone, depending on
the degree of involvement, sys thalidomide
in refractory cases

• Rare condition
• Unusual oral expression ‐ IBD, ulcerative
colitis or Crohn's disease
• C/F‐Yellowish, linear, serpentine pustules
on erythematous oral mucosa
• Primarily affect buccal and labial mucosa ,
soft palate, V. tongue

Clinical Features
• “Snail‐track" ulcerations
• Oral lesions may appear concomitantly with
bowel symptoms
• Intestinal signs and symptoms of
inflammatory bowel disease are of most
concern
• Tx‐ Sulphasalazine & systemic
corticosteroids