COMPLICATIONS OF DIABETES

COMPLICATIONS OF DIABETES
By Dr Bashir Ahmed Dar
Professor of Medicine
Chinkipora Sopore Kashmir
Email-- drbashir123@gmail.com

Dr Bashir and Dr yashodhora leading group of medical students to
meet noble prize winner in medicine at KL Malaysia

Precious moments with noble prize winner Prof Barry. J Marshall
for Helicobacter pylori cause for peptic ulcer

Complications of Diabetes
• Short term Complications
–Hypoglycemia
–Diabetic Ketoacidosis
–Non Ketotic hyperosmolar diabetic coma
–Lactic acidosis

Long term Complications
• 1. Dermopathy
• 2. Retinopathy
• 3. Gastroentropathy
• 4. Neuropathy
• 5. Nephropathy
• 6. Myopathy
• 7. Osteopathy

Cutaneous complications of Diabetes
• Bacterial infections
– Cellulitis
– Folliculitis

• Fungal Infections
– Tinea pedis (athlete’s
foot)
– Tinea cruris (jock itch)

– Vaginal yeast infections
– Onychomycosis (fungal
infection of the nails)

• Yellow Nails

• Itching
– Often a result of yeast infection, dry skin, and/or
poor circulation

• Digital Sclerosis
Tight, thick, waxy skin most commonly on the
back of the hand
• Finger joints can become stiff

• Acanthosis Nigricans
Hyperpigmented plaques.
Most commonly found in
armpits, neck, and groin

• Diabetic Dermopathy.
• Light brown, scaly, atrophic
patches
• Usually occur on the
shins.round or oval,
reddish-brown, scaly
papules and plaques,
ranging in size from 0.5
cm.Lesions do not itch,
hurt, or open up.

Diabetic Dermopathy
• Diabetic Dermopathy

• Necrobiosis Lipoidica
Diabeticorum
• Similar to diabetic
dermopathy but spots
are fewer in number
and larger and deeper
• Can be itchy, painful,
and difficult to treat

(Granuloma Annulare)

• Pigmented Purpura
• Brown to red macules
and patches often
coexists with diabetic
dermopathy.

• Diabetic blisters
Bullosis Diabeticorum
• Most commonly on the
backs of fingers, hands,
toes, feet, and
sometimes on legs or
forearms
• Look like burn blisters

• Eruptive Xanthomatosis
• Firm, yellow, pea-like
enlargements in the skin
• Most often on backs of
hands, feet, arms, legs,
and buttocks.

• Diabetic Foot Ulcers

• Peripheral Vascular
Disease
• Diabetics are more
prone to develop
atherosclerosis, which
can result in peripheral
vascular disease
– Claudication
– Delayed healing
– Cold, pale, hairless legs
and feet
– Thick nails
– Ulcers

• Gangrene

Necrobiosis Lipoidica Diabeticorum
• One of the best known cutaneous markers for
diabetes
• Initially presents with well-circumscribed
erythematous papules, which develop into
large, irregularly delineated plaques with a
waxy, yellow center

Necrobiosis Lipoidica Diabeticorum
• The epidermis becomes thin and transparent,
allowing underlying vasculature to become
visible
• The involved peripheral tissue is slightly raised
and has a reddish-blue color
• About 85% of NLD cases occur on the legs
bilaterally
• Lesions can also appear on the face, scalp,
hands, forearms, or abdomen

Necrobiosis Lipoidica Diabeticorum (cont.)

Bullosis Diabeticorum
• Rare
• a distinct marker for diabetes
• usually on the feet and toes, but occasionally
on the hands and fingers
• Bullae are blisters spontaneously appearing
from normal skin. They are usually 0.5 to
several centimeters in size, and contain a
clear, sterile, viscous fluid

Bullosis Diabeticorum (cont.)
• Two major types of bullae, intraepidermal and
subepidermal, have been defined
• Intraepidermal bullae are clear, sterile,
nonhemorrhagic blisters that generally heal on their
own within two to five weeks without scarring or
atrophy. Most patients developing this type of bullae
are men between ages 40 and 75 with long-standing
diabetes, peripheral neuropathy, and good
circulation to the involved extremity

Bullosis Diabeticorum (cont.)
• Subepidermal bullae are the least common of
the two types of bullosis diabeticorum. These
blisters are similar to the intraepidermal
blisters except they occasionally are
hemorrhagic and may heal with scarring and
atrophy

Granuloma Annulare
• Granuloma annulare is identified by its
characteristic annular or arciform plaques that
begin as flesh-colored, red, or reddish-brown
papules symmetrically spread across the
upper trunk, neck, arms, and occasionally the
legs

Acanthosis Nigricans
• Rough, velvety, dark patches of skin on the
back of the neck
• It is now evident that a close association exists
between AN, obesity, and insulin resistance

GIT COMPLICATIONS OF DIABETES
• Gastroparesis
• Delayed gastric emptying
• Intestinal enteropathy (which can cause
diarrhea, constipation, and fecal incontinence)
• Nonalcoholic fatty liver disease.

• Patients with gastroparesis may present with
early satiety, nausea, vomiting, bloating,
postprandial fullness, or upper abdominal
pain.

• Esophageal manifestations of diabetic
neuropathy, including abnormal peristalsis,
spontaneous contractions, and impaired lower
esophageal sphincter tone, result in heartburn
and dysphagia

• The delayed gastric emptying in patients with
gastroparesis is thought to be caused primarily
by impaired vagal control. Other contributing
factors include the impairment of inhibitory
nitric oxide-containing nerves, damage to the
interstitial cells of Cajal, and underlying
smooth muscle dysfunction

• Abnormal internal and external anal sphincter
function caused by neuropathy can lead to fecal
incontinence.
• Nonalcoholic fatty liver disease is generally
diagnosed because of persistent elevation in hepatic
transaminase levels.
• Diabetes is more common in patients with hepatitis
C infection than in the general population.

• Causes of cirrhosis linked to diabetes include
nonalcoholic fatty liver disease,
hemochromatosis, and hepatitis C infection.
• OHD can cause hepatotoxicity.
• The entire GI tract can be affected, including
the mouth, esophagus, stomach, small
intestine, colon, liver, and pancreas, leading to
a variable symptom complex.

Epidemiology of DR
RISK of developing DR:
• Type I or IDDM – 70%
• Type II or NIDDM - 39%

RISK FACTORS:
1.Duration of diabetes
2.Poor control of Diabetes
3.Pregnancy
4.Hypertension
5.Nephropathy
6.Obesity and hyperlipidemia
7.Smoking

Pathogenesis
Microangiopathy which has features of
both microvascular leakage and occlusion
Larger vessels may also be involved

Microvascular leakage
Loss of pericytes results in distention of weak
capillary wall producing microaneurysms
which leak
Blood-retinal barrier breaks down causing
plasma constituents to leak into the retina –
retinal oedema, hard exudates

Microvascular occlusion
Basement membrane thickening, endothelial
cell damage, deformed RBCs, platelet
stickiness and aggregation
Vascular Endothelial Growth Factor (VEGF) is
produced by hypoxic retina
VEGF stimulates the growth of shunt and new
vessels

Classification of DR
I. Non-proliferative DR (NPDR)
. Mild
. Moderate
. Severe
II. Proliferative DR (PDR)
III. Clinically significant macular oedema (CSME)
- May exist by itself or along with NPDR and
PDR

• At least one microaneurysm -
earliest clinically detectable lesion
 Retinal hemorrhages
 Hard or soft exudates
Mild NPDR

Moderate NPDR
• Microaneurysms and/or dot and blot
hemorrhages in at least 1 quadrant
• Soft exudates (Cotton wool spots)
• Venous beading or IRMA (intraretinal
microvascular abnormalities)

Mild and Moderate Non- proliferative DR was
previously known as Background DR

Severe NPDR
Any one of the following 3 features is present
• Microaneurysms and intraretinal hemorrhages
in all 4 quadrants
• Venous beading in 2 or more quadrants
• Moderate IRMA in at least 1 quadrant
Known as the 4-2-1 rule

Severe Non-proliferative DR was known as the
Pre-proliferative DR

Clinically significant Macular
Oedema
• Retinal oedema close to fovea
• Hard exudates close to fovea
• Presents with dimness of vision
• By itself or along with NPDR or PDR

CSME – Hard exudates close to fovea and
associated retinal thickening

Proliferative DR (PDR)
Characterized by Proliferation of new
vessels from retinal veins
• New vessels on the optic disc
• New vessels elsewhere on the retina

COMPLICATIONS OF DIABETIC
RETINOPATHY
• Vitreous hemorrhage
• Tractional retinal detachment
• Rubeosis Iridis
• Glaucoma
• Blindness

Vitreous Hemorrhage
SUBHYALOID HEMORRHAGE

Neovascular Glaucoma
• Complication of rubeosis iridis
• New vessels cause angle closure
• Mechanical obstruction to aqueous outflow
• Intra ocular pressure rises
• Pupil gets distorted as iris gets pulled
• Eye becomes painful and red
• Loss of vision

Blindness
• Non-clearing vitreous hemorrhage
• Neovascular glaucoma
• Tractional retinal detachment
• Macular ischemia

PREVENTION OF COMPLICATIONS
• By early institution of appropriate treatment
• This requires early detection of DR in its
asymptomatic treatable condition
• By routine fundus examination of all Diabetics
(cost effective screening)
• And appropriate referral to ophthalmologist

Mild and Moderate NPDR
- No specific treatment for retinopathy
- Good metabolic control to delay progression
- Control of associated Hypertension, Anemia
and Renal failure
Severe and very severe NPDR
• Close follow up by Ophthalmologist

Clinically significant macular oedema
- Laser photocoagulation to minimise risk of
visual loss
─ Retinal laser photocoagulation as per the
judgment of ophthalmologist (in high risk
eyes)
─ It converts hypoxic retina (which produces
ANGIOGENIC factors) into anoxic retina
Proliferative DR

Screening protocol for Diabetic retinopathy
1. Screening once in a 1 year
• Diabetics with normal fundus
• Mild NPDR
2. Screening once in 6 months
• Moderate NPDR

Referral to Ophthalmologist
• Visual Symptoms
– Diminished visual acuity
– Seeing floaters
– Painful eye
• Fundus findings
- Macular oedema/hard exudates close to fovea
- Proliferative DR
- Vitreous hemorrhage
- Moderate to severe and very severe NPDR
- Retinal detachment
- Cataract obscuring fundus view

Referral to Ophthalmologist
• Presence of Risk Factors
- Pregnancy
- Nephropathy

Simulation of defective vision as experienced by a
Diabetic whose vision has been affected by Diabetic
retinopathy
Normal Defective

DIRECT OPHTHALMOSCOPY
. Examination of the fundus of the eye
. To screen for Diabetic Retinopathy
. After dilatation of both eyes with 0.5%
tropicamide
. Flashlight test, prior to dilatation to detect
eyes with shallow AC
.Procedure will be demonstrated

View of the retina through an
ophthalmoscope

Normal fundus views of Right and left
eye

Mild NPDR – Microaneurysms, Dot and
Blot hemorrhages

Circinate retinopathy – Hard exudates in
a ring around leaking aneurysms

Moderate – Severe NPDR Cotton wool patches
Hemorrhages - 4 quadrants

Severe NPDR
• Cotton-wool patches,
venous segmentation

Very severe NPDR
- Venous beading, -
scars of laser spots,
- Absorbing
hemorrhages

CSME in different stages of NPDR

Proliferative DR – New vessels elsewhere on the
retina along the superior-temporal vessels

PDR – New vessels on disc and New vessels elsewhere
on retina

PDR – with vitreous hemorrhage
Vitreous bleed

Tractional retinal
detachment
Fibro-vascular
proliferation

UROGENITAL COMPLICATIONS OF
DIABETES
• Erectile dysfunction (ED) is a condition that
affects a man's ability to get and sustain an
erection that leads to positive sexual
experiences. Although most men do
encounter trouble having an erection from
time to time, the problem is not generally
thought to be ED unless the symptoms are
consistent for 3 months or more.

DIABETES
• Women may have problems with sexual
response and vaginal lubrication. Urinary tract
infections and bladder problems occur more
often in people with diabetes.
• Damage to these autonomic nerves can
hinder normal function. Reduced blood flow
resulting from damage to blood vessels can
also contribute to sexual dysfunction.

DIABETES
• Retrograde Ejaculation
• Retrograde ejaculation is a condition in which part or
all of a man’s semen goes into the bladder instead of
out the tip of the penis during ejaculation.
Retrograde ejaculation occurs when internal
muscles, called sphincters, do not function normally.
A sphincter automatically opens or closes a passage
in the body.

DIABETES
• With retrograde ejaculation, semen enters the
bladder, mixes with urine, and leaves the body
during urination without harming the bladder. A man
experiencing retrograde ejaculation may notice that
little semen is discharged during ejaculation or may
become aware of the condition if fertility problems
arise. Analysis of a urine sample after ejaculation will
reveal the presence of semen.

DIABETES
• Sexual problems may include
• Decreased vaginal lubrication, resulting in
vaginal dryness
• Uncomfortable or painful sexual intercourse
• Decreased or no desire for sexual activity
• Decreased or absent sexual response

DIABETES
• Decreased or absent sexual response can
include the inability to become or remain
aroused, reduced or no sensation in the
genital area, and the constant or occasional
inability to reach orgasm.

DIABETES
• Common bladder problems in men and women with
diabetes include the following:
• Overactive bladder. Damaged nerves may send
signals to the bladder at the wrong time, causing its
muscles to squeeze without warning. The symptoms
of overactive bladder include
• urinary frequency—urination eight or more times a
day or two or more times a night

DIABETES
• urinary urgency—the sudden, strong need to
urinate immediately
• urge incontinence—leakage of urine that
follows a sudden, strong urge to urinate.

DIABETES
• Poor control of sphincter muscles. Sphincter
muscles surround the urethra—the tube that
carries urine from the bladder to the outside
of the body—and keep it closed to hold urine
in the bladder. If the nerves to the sphincter
muscles are damaged, the muscles may
become loose and allow leakage or stay tight
when a person is trying to release urine.

DIABETES
• Urine retention may also lead to overflow
incontinence—leakage of urine when the bladder is
full and does not empty properly.
• Symptoms of urinary tract infections can include
• a frequent urge to urinate
• pain or burning in the bladder or urethra during
urination
• cloudy or reddish urine
• in women, pressure above the pubic bone
• in men, a feeling of fullness in the rectum

DIABETES
• sexual and urologic problems appear to be more
common in people who
• have poor blood glucose control
• have high levels of blood cholesterol
• have high blood pressure
• are overweight
• are older than 40
• Smoke
• are physically inactive

MUSCULOSKETAL COMPLICATIONS IN DIABETES

Diabetic Muscle Infarction
• Rare
• Painful muscle swelling, usually in thigh
• Mass expands over days to weeks

Neuropathic Arthropathy
(Charcot Joint)
• First described in 1868 by Jean Martin
Charcot in patients with tabes dorsalis
• Destructive arthropathy in diseases which
impair sensory function, but maintain normal
motor function

Charcot Joint
• Most common in MTPs, tarso-metatarsals, tarsus,
ankle and interphalangeal joints
• Single, painless, swollen, deformed joint in
setting of peripheral neuropathy
• Periarticular soft tissues loosen thereby causing
joint laxity and subluxation
• Repetitive microtrauma with weight bearing
damages the joint

Hand Abnormalities
• Carpal Tunnel Syndrome
• Dupuytren’s contracture
• Flexor tenosynovitis
• Limited joint mobility
Each condition present in ~ 20% patients with diabetes

Dupuytren’s Contracture
• Fibrosis in and around the palmar fascia with nodule
formation
• Contraction of the palmar fascia causes flexion
contractures of digits
• The 3rd and 4th finger most commonly effected in
patients with diabetes, compared to the 5th finger in
patients without diabetes
• Present in 15-40% of patients with diabetes
• Prevalence increases with age

Adhesive capsulitis ( frozen shoulder)
• Progressive painful restriction of shoulder movement
• Joint capsule adheres to humeral head
• 3 phases: painful, adhesive, resolution
• 10-30% in diabetics, 2-10% in controls
• 17% patients with adhesive capsulitis have diabetes
• Associated with age and duration of diabetes

Limited Joint mobility
• Diagnosis
“prayer sign”
“table top test”
• To differentiate from Dupuytren’s:
– Limited joint mobility usually involves 4 fingers
– Absence of taut fibrotic bands

Diabetic Sclerodactyly
• Thickening and waxiness of skin
• Usually on dorsa of fingers
• Associated with limited joint mobility
• Similar to skin changes of scleroderma
(absent antibodies, Raynaud’s, calcinosis, ulceration, tapering)

Diabetic neuropathy
• There are two types of diabetic neuropathy
• Diffuse peripheral neuropathy primarily
affects the limbs, damaging the nerves of the
feet and hands.
• Focal—or localized neuropathy affects specific
nerves, most commonly in the torso, leg, or
head.

Autonomic neuropathy
• Autonomic neuropathy is the other form of
diffuse neuropathy and it affects the heart and
other internal organs.

• Diabetic neuropathy can lead to
• muscular weakness,
• Loss of feeling or sensation,
• and loss of autonomic functions such as
• Digestion,
• Erection,
• Bladder control, and sweating

• Impaired urination and sexual function
• Bladder infections
• Stomach disorders, due to the impaired ability of the
stomach to empty (gastric stasis)
• Nausea,
• Vomiting
• and bloating
• Dizziness,

• Lightheadedness,
• and fainting spells
• Loss of appetite
• Abdominal swelling,
• Heat intolerance,
• Impotence,
• Diarrhea,

• Constipation,
• Dizziness with standing,
• Difficulty urinating and urinary incontinence.
• Tachycardia,
• Exercise intolerance,
• Orthostatic hypotension,
• Gastroparesis,
• Erectile dysfunction,

• Sudomotor dysfunction,
• Impaired neurovascular function,
• “brittle diabetes,”
• and hypoglycemic autonomic failure.
• Esophageal enteropathy, gastropathy,
• and fecal incontinence)

Focal neuropathy
• Common symptoms of focal neuropathy include:
• Pain in the front of a thigh
• Severe pain in the lower back
• Pain in the chest or stomach
• Ache behind an eye
• Double vision
• Itching
• Paralysis on one side of the face

Diabetic neuropathy
• In severe diabetic neuropathy loss of
sensation can lead to injuries that are
unnoticed, progressing to infections,
ulceration and possibly amputation.

Diabetic neuropathy
• The exam may include:
• a screening test for lost sensation
• nerve conduction studies to check the flow of
electric current through a nerve
• electromyography (EMG) to see how well muscles
respond to electrical impulses transmitted by nearby
nerves.

Diabetic neuropathy
• ultrasound to show how the bladder and
other parts of the urinary tract are functioning
• sometimes a nerve biopsy may be performed.

Diabetic peripheral neuropathy
• Sensory  Motor (myelin)
• Characteristic features of Peripheral
Neuropathy are
– Bilateral, symmetrical
– Progressive
– Paraesthesias, pain, muscle atrophy
– Glove and stocking type usually affects
distal parts of limbs then ascend
upwards

Chronic Polyneuropathy
Claw foot – Dermopathy & Neuropathy

Diabetic Amyotrophy
Painful muscle wasting

Neuropathic ulcer
Etiology:
 peripheral sensory
neuropathy, Trauma &
deformity.
Factors:
 Ischemia, callus
formation, and edema.

Neuropathic ulcers
FEATURES:
Painless, surrounded by callus
At pressure points.
associated with good foot pulses
May not be associated with gangrene

Nephropathy
• An angiopathy of glomeruli
• Is a micro vascular complication of diabetes
marked by albuminuria and a deteriorating
course from normal renal function to end
stage renal failure. ESRD

Risk factors for nephropathy
• Hypertension
• Hyperglycemia
• Microalbuminuria
• Ethnicity
• Male gender
• Family history
• Cigarette smoking

Nephropathy
• The syndrome was discovered by British
physician Clifford Wilson (1906–1997) and
German-born American physician Paul
Kimmelstiel (1900–1970) and was published
for the first time in 1936.

Nephropathy
• Usually manifests 15–25 years after diagnosis
of diabetes and affects 25-40% of patients
under the age of 30 years.
• The disease is progressive and may cause
death two or three years after the initial
lesions, and is more frequent in men.

Nephropathy
• The glomeruli and kidneys are typically
normal or increased in size initially, thus
distinguishing diabetic nephropathy from
most other forms of chronic renal
insufficiency, wherein renal size is reduced
(except renal amyloidosis and polycystic
kidney disease).

Signs and Symptoms
• Approximately 25% to 40% of patients with
DM 1 ultimately develop diabetic
nephropathy (DN), which progresses
through five predictable stages.

Stage 1 (very early diabetes)
• Increased demand upon the kidneys is indicated by
an above-normal glomerular filtration rate (GFR).
• Hyperglycemia leads to increased kidney filtration
• This is due to osmotic load and to toxic effects of
high sugar levels on kidney cells
• Increased Glomerular Filtration Rate (GFR) with
enlarged kidneys
• All this results in nephromegaly

Stage 2 (developing diabetes)
• Clinically silent phase with continued hyper filtration
and hypertrophy .The GFR remains elevated or has
returned to normal, but glomerular damage has
progressed and leads to next stage that is
chracterised by microalbuminuria with excretion of
albumin in the range of 30-300 mg/day .
• Normal persons excrete less than 30mg/day. at this
stage the disease process is probably reversible.

• Significant microalbuminuria will progress to end-
stage renal disease (ESRD).
• Therefore, all diabetes patients should be screened
for microalbuminuria on a routine basis.
155

Stage 3 (overt, or dipstick-positive diabetes)
• In this stage albumin is more than 300 mg in a 24
hour period. The urine becomes "dipstick positive,”
• Albumin more than 300 mg/24 hour is called
macroalbuminuria (defined as >300 mg/day (200
microgram/min). from this stage the disease is
irreversible and a steady decline in glomerular
filtration occurs at a rate of 1 ml/minute per month.
the stage of macroalbuminuria may progress to
nephrotic syndrome.
• If proteins are more than 3gm/24 hours then it
results in nephrotic syndrome.

Stage 3 (overt, or dipstick-positive diabetes)
• Hypertension (high blood pressure)
typically develops during stage 3.
• Basement membrane thickening occurs
due to deposition of AGEP

Stage 4 (late-stage diabetes)
• Glomerular damage continues, with
increasing amounts of protein albumin in
the urine.
• The kidneys’ filtering ability has begun to
decline steadily, and blood urea nitrogen
(BUN) and creatinine (Cr) has begun to
increase.

Stage 4 (late-stage diabetes)
• With further progression the azotaemia
develops and progression to renal failure
and uraemia is inevitable.
• The glomerular filtration rate (GFR)
decreases about 10% annually. Almost all
patients have hypertension at stage 4.

Stage 5 (end-stage renal disease, ESRD)
• GFR has fallen to <10 ml/min and renal
replacement therapy (i.e., haemodialysis,
peritoneal dialysis, kidney transplantation)
is needed.

Glomerular Histology:
• The glomerular capillary wall is composed of an
endothelial cell layer (blood side), a thick basement
membrane, and epithelial cell layer (urine side).
(i) Glomerular Endothelium
• The glomerular endothelium is fenestrated. The
fenestrae (0.07 to 0.1 mm-micrometers- in maximal
diameter) allow the passage of electrolytes, proteins,
and globulin.
• However, platelets (3 mm), red cells (7 mm) and
neutrophils (15 mm) can't pass through the endothelial
layer.

CAPILLARY ENDOTHELIUM
BASEMENT MEMBRANE
FOOT PROCESSES OF PODOCYTES
FILTRATION SLIT
FENESTRATION

(ii) Glomerular Basement Membrane (GBM):
• The GBM is a tri-laminar structure, 0.3 microns in
thickness, composed of collagen, proteoglycans and
laminin.
• It is product of the fusion of the endothelial and
epithelial basement laminae.
• The dense central GBM area, or lamina densa, is due
to the overlapping of the two laminae.
• Around 50% of the GBM is collagen IV.

NORMAL GBM. LEFT - a single glomerulus. There are one
million of these in each kidney. RIGHT - a close up of the GBM
(G) around part of one tiny blood vessel in a glomerulus (red
circle in left hand diagram)

• The negative charge of the GBM has been attributed to
the presence of the heparan sulphate proteoglycan
(HSPG) called perlecan.
• These negatively charged molecules are geometrically
arranged in clusters separated by about 0.003 µm from
each other.
• This anionic molecular sieve restricts the passage of
molecules according to size and charge.
• Water, salts, glucose, amino acids and neutral, or
cationic, molecules with radii less that 0.0035 µm are
filtered with relative ease.
• The albumin molecule measures 0.0035 µm and is
negatively charged. Therefore its filtration is restricted.

• Presence of protein in the urine is a sign that either the
charge or the distance between the anionic clusters, or
both, are pathologically altered.
• The presence of red cells in the glomerular urine, is
certain indication of GBM ruptures.
• Other classical constituents of the basement membrane
are type IV collagen, laminin, and entactin.

Mesangium
• Mesangium a cellular network membrane like
and in the inner layer of basement membrane
surrounding the glomerular capillaries that
helps support the capillary loops.

• The intra-capsular glomerular capillary network is kept
together by the mesangium that is composed of
mesangial cells type I and II, and other tissue matrix.
• Mesangial type I cells are monocytes with phagocytic
functions. These cells can extend cytoplasmic
projections into the glomerular capillary.
• They also "clean" the mesangium of materials that leak
from the capillary lumen into the matrix. These cells are
stimulated by cytokines to produce free radicals and
cytotoxic peptides.

• Mesangial type II cells are myofibroblasts with the
ability to contract upon ADH and angiotensin
stimulation.
• Their contraction causes a reduction of the effective
glomerular filtration area.
• Mesangial Matrix is a tissue mesh composed of
different types of collagens (I, III, IV), laminin and
proteoglycans.

Three major histological changes occur in the
glomeruli of persons with diabetic nephropathy.
1. Mesangial expansion is directly induced by
hyperglycemia, perhaps via increased matrix
production or glycosylation of matrix proteins. the
cells mesangical that surrounds to glomerular
vessels increases as a result of depot similar
material to basement membrane.
2. GBM thickening occurs.
3. Glomerular sclerosis is caused by intraglomerular
hypertension (induced by renal vasodilatation or from
ischemic injury induced by hyaline narrowing of the
vessels supplying the glomeruli).

Glomerular Hyper filtration
• Glucose provides an osmotic diuretic effect
• Result is increased renal filtration, leading to
glomerular hypertrophy
• Glomerular pressure increases
• Kidney responds with hypertrophy of epithelium and
endothelium
• Accelerates glomerular cell failure
• Result is premature glomerulosclerosis

Metabolic Perturbations
• Oxidant Stress - related to glomerular hypertrophy
and abnormal metabolism
• Non-enzymatic glycosylation of macromolecules -
particularly basement membrane (BM)
• Activation of glucose metabolizing enzymes
• Cytokine and other humoral imbalances

Non enzymatic Glycosylation
• Biochemical studies have shown that basement
membranes in diabetes include excess amounts of
type IV collagen, the main component of basement
membranes, and decreased amounts of
proteoglycans
• Both changes decrease the permeability of
capillaries and disturb leukocyte diapedesis, oxygen
diffusion, nutrition and metabolic waste removal.
• Altered charge on BM may explain albuminuria
• Macrophage receptor activation leads to IL1, TNF
production which stimulates matrix
• AGEP formation leads to abnormal collagen,
increased toxic oxygen species

Humoral Imbalances in DM Nephropathy
• Insulin Deficiency
• Elevated Glucagon Concentrations
• Increased Transforming Growth Factor (TGF)-ß
• Increased angiotensin II
• Abnormally regulated thromboxanes and endothelins
• Abnormal insulin like growth factor (IGF)-1
• Elevated platelet derived growth factor (PGDF)

Role of TGF-ß
• Stimulates extracellular matrix synthesis
• Inhibits extracellular matrix degradation
• Up regulates protease inhibitors; down regulates
matrix degrading enzymes
• Stimulates synthesis of integrins (matrix receptors)
• Key role in glomerular and tubuloepithelial
hypertrophy, basement membrane thickening, and
mesangial matrix expansion
• TGF-ß has been implicated in a number of chronic,
scaring diseases

• Angiotensin II and Thrombospondin (TSP1) can both
stimulate the production of transforming growth factor-β
(TGF-β) by tubuloepithelial cells and fibroblasts.
• TGF-β, in turn, causes proliferation of fibroblasts and
tubuloepithelial cells.
• TGF-β ultimately increases extracellular matrix proteins,
likely by several mechanisms.
• TGF-β stimulates production of several growth factors
including basis fibroblast growth factor (bFGF) and
platelet derived growth factor (PDGF) that stimulate the
formation of extracellular matrix (ECM) proteins.

Ultrastructural changes of the glomerular
basement membrane in diabetic nephropathy
revealed by newly devised tissue negative
staining method.
• The normal human GBM showed a fine meshwork
structure consisting of fibrils forming the small pores.
• The diameter of these pores was slightly smaller than
that of human albumin molecules.
• The GBM in patients with diabetic nephropathy
showed irregular thickening.
• At higher magnification, unknown cavities and tunnel
structures, which were not seen in normal controls,
were observed in the thickened GBM.

• In some portions, these cavities presented a
honeycomb-like appearance.
• The diameters of the cavities and tunnels were far
larger than the dimensions of albumin molecules.
• These enlarged structures are believed to allow serum
protein molecules to pass through the GBM from the
capillary lumen to the urinary space.
• These results suggest that the cause of massive
proteinuria in diabetic nephropathy is the disruption of
the size barrier of the GBM.

Glomerular and vascular pathology is linked to
hyperglycemia.
• Changes in glomerular basement membrane structure
occur very early in diabetic nephropathy, before even
microalbuminuria is apparent.
• Collagen IV deposition is directly stimulated by
hyperglycaemia and increased urinary levels indicate
changes in the glomerular basement membrane.
• Contributing factors include the formation of advanced
glycosylation end products (AGEs) due to non-
enzymatic glycosylation of capillary basement
membranes, as a consequence of long-term
hyperglycaemia.

• Non-enzymatic glycosylation has recently attracted
increasing interest as a crucial pathophysiologic event
behind all these hyperglycaemia-related alterations and
in the pathophysiology of the development of diabetic
complications.
• Proteins and lipids exposed to aldose sugars go
through reactions which are not enzyme-dependent,
and generation of reversible Schiff bases or Amadori
products take place.
• Later, through further molecular rearrangements,
irreversible advanced glycosylation end products
(AGEs) are formed.
• This process also takes place during normal ageing, but
in diabetes their formation is accelerated to an extent
related to the level and duration of hyperglycaemia.

• Hence large studies have shown a delay in onset or
slowing of the progression of these complications if
near normo-glycaemia can be maintained.
• The glycated proteins cross-link, contributing to
basement membrane (and mesangial) thickening,
(culminating in the kidney in nodular
glomerulosclerosis), as well as loss of the normal
selective permeability (leading to proteinuria, retinal
hard exudates and microhaemorrhages).

• The potential pathophysiological significance of AGEs is
associated with their accumulation in plasma, cells and
tissues and their contribution to the formation of cross-
links, generation of reactive oxygen intermediates and
interactions with particular receptors on cellular surfaces
• AGEs have direct effects on the host response by
affecting tissue structures, e.g. by increasing collagen
cross-links, which is followed by changes in collagen
solubility and turnover.
• Thickening of basement membranes is partly due to
glycosylation of membrane proteins or entrapment of
glycosylated serum proteins into basement membrane
• It is evident that AGEs can interact with cell functions,
tissue remodelling and inflammatory reactions in several
different ways.

• When Ang II is increased, greater AT1 receptor-
mediated constriction of efferent than afferent arterioles
increases single nephron glomerular filtration rate and
raises intraglomerular pressure, causing glomerular
hypertension.
• Sustained or severe increases in intraglomerular
pressure can lead to GBM damage, glomerular
endothelial dysfunction, and ultimately, extravasation of
protein into Bowman’s capsule.
• In addition to hypertension, conditions like diabetes that
are associated with increased oxidative stress
(increased formation of reactive oxygen species)
independent of hypertension and glyco-oxidative
modification of proteins (AGEs) comprising the
glomerular basement membrane can lead to
extravasation of protein.

• Glomerular hypertension can lead to injury to the
glomerular basement membrane causing it to leak
plasma proteins into the urine.
• Attempts by the proximal tubules to reabsorb this filtered
protein causes injury to the tubular cells, activates an
inflammatory response, and is associated with the
development of lipid metabolic abnormalities that create
further oxidative stress on the already compromised
glomerulus.
• The resultant tubular inflammatory response and renal
microvascular injury activate pathways that lead to
fibrosis and scarring of both glomerular and tubular
elements of the nephron ultimately leading to contracted
kidneys.

• An additional consequence of glomerular hypertension
and resultant reduction in glomerular filtration rate
(GFR) activates growth factors and cytokines that
promote an influx of monocytes and macrophages into
the vessel wall and into the renal interstitium, and also
causes the differentiation of renal cells into fibroblasts.
• Monocytes, macrophages and fibroblasts are capable of
producing those growth factors and cytokines that
activate pathways leading to expansion of extracellular
matrix, fibrosis and loss of both tubular and glomerular
structures.

• Collagen IV is the principal component of the
glomerular basement membrane and it is released into
the urine during its turnover.
• Increased urinary levels of collagen IV are found in
several conditions where glomerular injury is found,
particularly in diabetic nephropathy.
• Collagen IV is too large to cross the glomerular
membrane (MW 540 000) and so urinary collagen IV is
a specific sensitive indicator of changes to the structure
of extracellular matrix of the kidney.
• Unlike serum creatinine, that measures changes in
glomerular function, increased levels of urinary collagen
IV indicate that damage is occurring to the renal tissue.
• Urinary collagen IV is a very early and specific
biomarker for pathological changes to the glomerular
membrane, particularly in diabetic nephropathy.

Summary Pathological lesions in DM
• The Armani-Ebstein change (or Armani-
Ebstein cells) consists of deposits of glycogen
in the tubular epithelial cells (pars straight of
proximal convoluted tubule and loop of
Henle).

• Because most diabetics are treated before this
stage, it is very rare to see it at the present
time. It appears in decompensated diabetics
with glycemia higher than 500 mg/dL and in
the presence of severe glycosuria; it is a
reversible alteration without functional
manifestations.

• Diabetic neuropathy involves two distinct
pathological patterns that may or may not
coexist.
• In the diffuse form which is more common
there is widening of the glomerular basement
membrane together with generalised
mesangial thickening .

• the basement of glomerular capillaries thicken
and can obliterate the blood vessels. The
glomerular sclerosis is diffuse, but in 50% of
cases it is accompanied with nodular sclerosis.
The nodular component denominated
Kimmelstiel-Wilson nodules is pathognomic of
diabetes.

• In the nodular form large accumulations of
PAS positive material Glycosylation End-
products are deposited at the periphery of
glomerular tufts , the Kimmelsteil-wilson
leision.

• In addition there may be hyalinization of
afferent and efferent arterioles, drops in
bowman's capsule, fibrin caps, and occlusion
of glomeruli and interstitial fibrosis.
Deposition of albumin and other proteins
occurs in both glomeruli and tubules.

• In short
• Microangiopathy
• Atherosclerosis
• Diffuse glomerulosclerosis
• or nodular diabetic glomerulosclerosis
(Kimmelstiel Wilson nodules)
• Tubulointerstitial fibrosis

Nodular Glomerulosclerosis – KW
lesion.

• Arteriosclerosis and hyalinosis of afferent and
efferent arterioles .
• Necrotizing renal papillitis.
• Infections &Pyelonephritis.
• Nephrotic syndrome
• End stage kidney

• A kidney biopsy confirms the diagnosis. However,
your doctor can diagnose the condition without a
biopsy if you meet the following three conditions:
• 1.Persistent protein in the urine
• 2.Diabetic retinopathy
• 3.No other kidney or renal tract disease
• A biopsy may be done, however, if there is any
doubt in the diagnosis

Nephropathy
• Nephropathy leads to
• Pyelonephritis
• End stage renal failure

Treatment of nephropathy
• Factors that favor the regression of
microalbuminuria include better blood sugar
control, lower blood pressure, lower serum
cholesterol and triglycerides, recent onset and
lower levels of microalbuminuria, and less
glomerular hyperfiltration.

• Early screening
• Spot urine albumin : creatinine ratio
• 24 hour urine collection
• dipstick
• Tight glycemic control

• ACE inhibitors if creatinine less than 3mg/dl
• Use ACEI as first line, if not tolerated, use ARB.
Use the maximum dose as tolerated
• If still hypertensive or proteinuric, consider
using combination ACEI and ARB, or ACEI and
diuretics

• ACE inhibitors or ARB have a strong
antiproteinuric effect apart from their
antihypertensive actions
• Increasing the dose of the ACEI or ARB beyond
the optimum antihypertensive doses further
reduces proteinuria
• Antiproteinuric effect is enhanced by a low Na
diet or diuretic

• 0.8g/kg/day proteins
• Antilipids
• Thiazide diruritics
• Vit E

• Keep BP slightly less than 130/85 mmHg
• Patients with CKD and > 1g proteinuria, BP
goal should be < 125-130/75-80 mmHg

Complications of nephropathy
• Possible complications of diabetic nephropathy
include:
• hypoglycemia (from decreased excretion of
insulin)(insulin isn't secreted by the kidneys)
• rapidly progressing chronic kidney failure
• end-stage kidney disease
• Hyperkalemia

Complications of nephropathy
• severe hypertension
• complications of hemodialysis
• complications of kidney transplant
• coexistence of other diabetes complications
• peritonitis (if peritoneal dialysis used)
• increased ifections

Diabetic Retinopathy
Neovascularization Cotton wool spots

Dot blot – Hemorrhages (Microaneurysms)

Pre retinal Hemorrhage - detachment

Advanced fibrous plaques

Label the diagram.
1.
2.
3.
4.
5.
Hard dep.
Optic disc
Macula
Blot hem
Cotton wool

Blood vessel calcification:
Amputated thumb

Acanthosis Nigricans
Insulin resistance…

Label the diagram.
1.
2.
3.
4.
Capillary
Nodule – AGE
Bowman caps
Hyaline
arteriolo
sclerosis in
arteriole.

Infections in Diabetes:
• Decreased metabolism – low immunity.
• Decreased function of lymphocytes & neutrophils –
glycosylation.
• Glycosylation of immune mediators. Ab
• Capillary thickening – impaired inflammation.
• Ischemia & infarctions.
• Increased glucose (alone is not the cause*)
• Diabetes  State of immunosuppression.

Laboratory Diagnosis:
• Urine glucose - dip-stick –Screening
• Random or fasting blood glucose (<11)
• Fasting > 7mmol, Random >11mmol
• If Fasting level is between 7-11 then OGTT
• HbA1c - for follow-up, not for diagnosis
• Fructosamine - for long term maintenance.

Gestational diabetes
• Gestational diabetes and impaired glucose
tolerance (IGT) in pregnancy affects between
of all pregnancies and both have been
associated with pregnancy complications.

Fasting and 2 hours postprandial venous
plasma sugar during pregnancy.
Border line indicates
glucose tolerance test.
125-200 mg/dl.100-125 mg/dl
Diabetic>200 mg/ dl.>125 mg/ dl
Not diabetic< 145mg/ dl.<100 mg/dl
Result2h postprandialFasting

50-g oral glucose challenge
The screening test for GDM, a 50-g oral glucose
challenge, may be performed in the fasting or fed
state. Sensitivity is improved if the test is performed
in the fasting state .
A plasma value above one hour after is
commonly used as a threshold for performing a 3-
hour OGTT.
If initial screening is negative, repeat testing is
performed at 24 to 28 weeks.
130 - 140 mg/dl

3 hour Oral glucose tolerance test
• Prerequisites:
• - Normal diet for 3 days before the test.
• - No diuretics 10 days before.
• - At least 10 hours fast.
• - Test is done in the morning at rest.

• Giving 75 gm (100 gm by other authors)
glucose in 250 ml water orally

• Criteria for glucose tolerance test:
• The maximum blood glucose values during pregnancy:
• - fasting 90 mg/ dl,
• - one hour 165 mg/dl,
• - 2 hours 145 mg/dl,
• - 3 hours 125 mg/dl.
• If any 2 or more of these values are elevated, the patient is
considered to have an impaired glucose tolerance test.

Affects of diabetes on pregnancy
• birth defects or be stillborn.
• Infants of mothers with preexisting diabetes
experience double the risk of serious injury at
birth, triple the likelihood of cesarean delivery,
and quadruple the incidence of newborn
intensive care unit (NICU) admission.

• Infants born to mothers with GDM are at risk
of being both large for gestational age
(macrosomic)[63] and small for gestational
age. Macrosomia in turn increases the risk of
instrumental deliveries (e.g. forceps, ventouse
and caesarean section) or problems during
vaginal delivery (such as shoulder dystocia).

• Neonates are also at an increased risk of low blood
glucose (hypoglycemia), jaundice, high red blood cell
mass (polycythemia) and low blood calcium
(hypocalcemia) and magnesium
(hypomagnesemia).[66] GDM also interferes with
maturation, causing dysmature babies prone to
respiratory distress syndrome due to incomplete lung
maturation and impaired surfactant synthesis

• Studies have shown that the offspring of
women with GDM are at a higher risk for
congenital malformations.
• women with GDM have a higher risk of
preeclampsia
• spontaneous abortion and congenital
malformations in infants

Indications for detection of diabetes in pregnant
women
• Family history of Diabetes
• Glucose in urine sample
• History of unexplained prenatal loss
• History of large baby

Indications for detection of diabetes in pregnant
women
• History of congenitally malformation infant
• Maternal obesity
• Maternal age more than 25 years
• Members of ethnic/racial group with high
prevalence of Diabetes Mellitus

Management during pregnancy
• Quit smoking/alcohol
• Home blood glucose monitoring
• Diet control/Folate supplementation
• Regular exercise
• Fetal monitoring by ultrasound scan
• Accurate insulin regimen

The Importance of Dental Care With
Diabetes
• Diabetes is a disease that can affect the whole body,
including your mouth.
• Dental care is particularly important for people with
diabetes because they face a higher than normal risk
of oral health problems due to poorly controlled
blood sugars. The less well controlled the blood
sugar, the more likely oral health problems will arise.
This is because uncontrolled diabetes impairs white
blood cells, which are the body's main defense
against bacterial infections that can occur in the
mouth.

What Dental Problems are You at a higher
risk for?
• Dry mouth, xerostomia and
salivary gland dysfunction
• Caries
• Increased susceptibility to
bacterial, viral and fungal (that is,
oral candidiasis) infections
• Periapical abscesses
• Periodontitis and loss of teeth
• Lichen planus
• Burning Mouth Syndrome
• Gingivitis

Dry Mouth
• Uncontrolled diabetes can decrease saliva flow,
resulting in dry mouth. Dry mouth can further lead to
sores, ulcers, infections, and tooth decay.

Dry Mouth Leads to Ulcers and Sores

Dry Mouth Can…
• Cause difficulties in tasting, chewing,
swallowing, and speaking
• Increase your chance of developing dental
decay and other infections in the mouth
• Be a sign of certain diseases and conditions
• Be caused by certain medications or medical
treatments

Symptoms Include…
• A sticky, dry feeling in
the mouth
• Trouble chewing,
swallowing, tasting, or
speaking
• A burning feeling in the
mouth
• A dry feeling in the
throat
• Cracked lips
• A dry, tough tongue
• Mouth sores
• An infection in the
mouth
• Decay, when there is
not an adequate supply
of saliva, the rate of
tooth decay increases
rapidly

Symptoms Include…
• The average person creates around 1 Liter of
saliva a day.
• If saliva production is reduced, an individual's
oral bacteria levels can increase 10 times over
normal levels.

Salivary gland dysfunction and
Xerostomia
• There are reports of dry mouth complaints, which is
known as xerostomia, as well as salivary
hypofunction in patients with diabetes, which may
be due to polyuria, or an underlying metabolic or
endocrine problem.
• When the normal environment of the oral cavity is
altered because of a decrease in salivary flow or
alteration in salivary composition, a healthy mouth
can become susceptible to dental caries and tooth
deterioration.

Treatment of Dry Mouth:
• a high-fluoride toothpaste like Colgate’s Prevident
5000+ to help reduce decay
• Biotene, an oral rinse found over the counter which
relieves of dry mouth.
• Salagen ( Pilocarpine). Salagen pills have been shown
to provide significantly increased saliva flow and
relief of dry mouth. Since Salagen may cause
fluctuations in blood pressure or heart rate, you
should be closely supervised by an M.D.

Treatment of Dry Mouth:
• Chew gum or sour candy. Look for sugarless
gum or candy with Xylitol.
• If you chew this gum for five minutes after
every meal, studies show that you can reduce
the incidence of tooth decay up to 62%.

Dental Caries & Cavities
• It occurs when your teeth are frequently exposed to foods
containing carbohydrates such as starches and sugars like
soda pop, candy, cake and even sticky fruits.
• Cavities have been identified
as a bacterial infection.
• Bacteria inhabit the plaque and form up to 500 different

How Cavities Form
• Plaque interacts with food deposits on your teeth to produce
acid that will slowly dissolve the calcium in your teeth. The
surface of the tooth..."enamel" is 97% calcium, causing tooth
decay and some of the other products cause gum disease and
bad breath.
• When enough calcium dissolves from the tooth surfaces, the
surface breaks and forms a hole. That is how cavities form. An
active lesion demineralizes the tooth and can be diagnosed
based upon color, surface texture and x-rays.
• White spots can be active lesions if they are not glossy, and
feel rough to the explorer.

Cavities
• An area of decay may take
as long as 6-8 years or as
short as 6 months to
dissolve the outer layer
(enamel) of the tooth. If
you have a "cavity" this
outer layer has collapsed
producing a hole that
cannot repair itself.

Tooth decay & cavities
• Root cavities:
• As you age, your gums can recede, leaving
parts of your tooth root exposed. Since there
is no enamel covering your tooth roots, these
exposed areas easily decay. Most people over
60 have root cavities as a result of gum
disease.

• Gum recession has been found to occur more
frequently and more extensively in moderate-
and poorly-controlled diabetic patients
because plaque responds differently, creating
more harmful proteins in the gums.

• Repeated decay around existing fillings:
• Decay can form around existing fillings and
crowns. This is because these areas are not as
smooth as a natural tooth surface and can
decay easier.

Bacterial, Viral and Fungal Infections
• Thrush, or oral candidiasis, is an infection caused by
a fungus that grows in the mouth. People with
diabetes are at risk for thrush because the fungus
thrives on high glucose levels in saliva.
• Smoking, taking antibiotics often, or wearing
dentures, (especially when they are worn
constantly), can also lead to this fungal infection.
Medication is available to treat this infection.
• Good diabetic control, not smoking, and removing
and cleaning dentures daily can help prevent thrush.

Periapical Abscesses
• A dental abscess is an infection of the mouth, face, jaw, or
throat that begins as a tooth infection or cavity.
• Although these infections can be caused by poor dental
health and can result from lack of proper and timely dental
care, they may also occur in people with underlying
autoimmune disorders and people who have other conditions
that weaken the immune system (diabetes, post-
radiation/chemotherapy cancer care & diabetes).
• Dental abscesses can also be triggered by minor trauma in the
oral cavity.

Periodontitis
• Diabetics are more
prone to the
development of gum
disease, (periodontal
disease), from gingivitis
that is caused by the
presence of bacteria in
plaque

Periodontitis
• Plaque is the white
sticky film that
accumulates on teeth
both above and below
the gum line that can
harden into a rough
yellow or brown deposit
called tartar or calculus.

Any periodontal disease you may develop can be more
severe and harder to control
• Without regular dental checkups, periodontal
disease may result if gingivitis is left untreated. It
can also cause inflammation and destruction of
tissues surrounding and supporting teeth, gums,
bone and fibers which hold the gums to the
teeth. Gum infections can make it hard to control
blood sugar.
• Once a gum infection starts, it can take a long
time to heal. If the infection is severe, teeth can
loosen or even fall out.

Periodontitis Facts
• It has been shown that patients with type 2 diabetes
are three times more likely to develop periodontal
disease than are people without diabetes.
• When people with diabetes smoke, they are 20 times
more likely to develop periodontitis with loss of
supporting bone than are those without diabetes.
• One-third of people with DM have severe
periodontal disease

Diabetes and Periodontitis
• Periodontal disease has been proposed as the
sixth complication of DM; the other five
complications are retinopathy, neuropathy,
nephropathy, cardiovascular disease and
peripheral vascular disease

Lichen Planus
• Lichen planus is a relatively common, chronic
mucocutaneous disease of unknown cause. It
generally is considered to be an immunologically
mediated process that involves a hypersensitivity
reaction on the microscopic level.
• In the mouth, it looks like lacy white patches on the
inside of the cheeks or on the tongue.

Causes of Lichen Planus
The common causes and risk factor's of Lichen planus include
the following:
The exact cause is unknown, but the disorder is likely to be
related to an allergic or immune reaction.
Medical conditions: Medical conditions associated with oral
lichen planus include lichen planus of the skin, hypertension,
diabetes and peptic ulcers.
The disorder has been known to develop after exposure to
potential allergens such as medications, dyes, and other
chemical substances.

Causes of Lichen Planus
The link with diabetes and oral lichen
planus is more than likely an adverse
affect of the drug therapy used to
treat diabetes mellitus.

Burning Mouth Syndrome
• Patients with burning mouth or burning tongue
syndrome usually exhibit no clinically detectable
lesions, although the symptoms of pain and burning
can be intense. The etiology of burning mouth is
varied and often difficult to decipher clinically.
• Burning mouth syndrome (BMS) is a complex, vexing
condition in which a burning pain occurs on your
tongue or lips, or over widespread areas involving
your whole mouth, without any obvious reason.

BMS
• The main symptom of burning mouth syndrome is a burning
sensation in your tongue, lips, gums, palate or throat. People
with the syndrome may describe the sensation in the affected
areas as hot or scalded, as if they had been burned with a hot
liquid.
• Other symptoms may include:
• Dry mouth
• Sore mouth
• A tingling or numb sensation in the mouth or on the tip of the
tongue
• A bitter or metallic taste

Causes of BMS
• Dry mouth
• Oral thrush
• Geographic tongue
• Depression
• Vitamin deficiency anemia
• Heartburn/GERD
• Bruxism
• Diabetes
• Hypothyroidism
• Menopause
• Certain medications
• Allergies

Gingivitis and Diabetes
Gingivitis, a reversible condition, is characterized by
inflamed and bleeding gums. Since it can be a
precursor to chronic periodontitis, gingivitis requires
treatment.
In gingivitis, periodontal disease is confined to the
gingiva with no loss of junctional epithelial
attachment. Gingivitis results from bacterial plaque
accumulation at the gum margin and in the sulcus
between the margin and the tooth.

• Thickening of blood vessels is a complication
of diabetes that may increase risk for gum
disease. Diabetes causes blood vessels to
thicken, which slow the flow of nutrients to
the mouth and slows the removal of harmful
wastes away from the mouth.

• When diabetes is poorly controlled, high
glucose levels in mouth fluids may help germs
grow and set the stage for gum disease.
• Smoking increases the risk for gum disease. If
you are a smoker with diabetes, age 45 or
older, you are 20 times more likely than a
person without these risk factors to get severe
gum disease, bone loss and tooth loss.

You can do these simple things to help reverse gingivitis and
prevent periodontal disease:
• Diet and exercise may be the most important changes that
you can make to improve your quality of life and oral health.
• Brush your teeth after each meal.
• Floss daily.
• Get regular dental cleanings and check-ups.
• Scrape your tongue with a tongue scraper.
• Be sure both their medical and dental care providers are
aware of your medical history and periodontal status.
• Be aware of your blood sugar levels, triglycerides and
cholesterol levels and have them checked on a regular
basis. If your gums bleed while you are brushing your teeth
or eating, or a bad taste stays in your mouth, go to the
dentist. Tell the dentist about any other changes you see,
such as white patches, in your mouth.

When is the best time to receive
dental care if you are a diabetic?

Best time to receive dental care
• Dental procedures should be as short and as stress free
as possible.Make morning
• appointments because blood glucose levels tend to be
under better control at this time of day.
• If you have a scheduled appointment, eat and take
your medications as directed.
• Test your blood sugar level and take your blood
pressure and bring these results with you to our office.
• Be prepared to update your health/dental history at
each visit so we can provide you with the best possible
care for your condition.

• Postpone non-emergency dental procedures if
your blood sugar is not in good control. However,
abscesses should be treated right away.
• See your dentist on a regular basis, every 3 to 4
months, for exams and cleanings. Keep the
dentist informed of your health status and if you
have any problems controlling your blood sugar.
• Know that healing time will take longer due to
your diabetic condition.

THANK YOU SO MUCH
• Trust the physician and the teacher, and drink
his remedy in silence and tranquility. For his
hand though heavy and hard is guided by
tender hand of unseen. And the cup he brings,
though it burn your lips has been fashioned of
the clay which the potter have moistened with
his tears and sacred feelings.

COMPLICATIONS OF DIABETES

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