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  • thank you for the slides sir. makes it easier for us.
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  • thanks for uploading the slides=) looking fwd for more in the future on other topics.
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  • thank you dr bashir for the wonderful and awesome slides , very informative and helpful also it helped us students to understand better and the pictures in the slides were very helpful and entertaining , thank you very very much dr. bashir
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  • Its a very well prepared slides..definitely help in my understanding of the complications of diabetes on oral health. Terima Kasih:)
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  • thank you for preparing the slides Dr. Bashir! very informative slides with the help of diagrams.
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      By Dr Bashir Ahmed Dar
      Associate 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
    • My Home in Kashmir
    • MY HOME S
    • Complications of Diabetes
      Short term Complications
      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
    • Cutaneous complications of Diabetes
      Fungal Infections
      Tinea pedis (athlete’s foot)
      Tinea cruris (jock itch)
    • Cutaneous complications of Diabetes
      Vaginal yeast infections
      Onychomycosis (fungal infection of the nails)
    • Cutaneous complications of Diabetes
      Yellow Nails
    • Cutaneous complications of Diabetes
      Often a result of yeast infection, dry skin, and/or poor circulation
    • Cutaneous complications of Diabetes
      Digital Sclerosis
      Tight, thick, waxy skin most commonly on the back of the hand
      Finger joints can become stiff
    • Cutaneous complications of Diabetes
      Acanthosis Nigricans
      Hyperpigmented plaques.
      Most commonly found in armpits, neck, and groin
    • Cutaneous complications of Diabetes
      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
    • Diabetic Dermopathy
      Diabetic Dermopathy
    • Cutaneous complications of Diabetes
      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
    • Cutaneous complications of Diabetes (Granuloma Annulare)
    • Cutaneous complications of Diabetes
      Pigmented Purpura
      Brown to red macules and patches often coexists with diabetic dermopathy.
    • Cutaneous complications of Diabetes
      Diabetic blisters Bullosis Diabeticorum
      Most commonly on the backs of fingers, hands, toes, feet, and sometimes on legs or forearms
      Look like burn blisters
    • Cutaneous complications of Diabetes
      Eruptive Xanthomatosis
      Firm, yellow, pea-like enlargements in the skin
      Most often on backs of hands, feet, arms, legs, and buttocks.
    • Cutaneous complications of Diabetes
      Diabetic Foot Ulcers
    • Cutaneous complications of Diabetes
      Peripheral Vascular Disease
      Diabetics are more prone to develop atherosclerosis, which can result in peripheral vascular disease
      Delayed healing
      Cold, pale, hairless legs and feet
      Thick nails
    • Cutaneous complications of Diabetes
    • 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.)
    • Necrobiosis Lipoidica Diabeticorum(cont.)
    • Bullosis Diabeticorum
      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
    • Bullosis Diabeticorum (cont.)
    • 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
    • Granuloma Annulare(cont.)
    • Granuloma Annulare(cont.)
    • 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
    • Acanthosis Nigricans
    • Acanthosis Nigricans
    • Acanthosis Nigricans
      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%
      Duration of diabetes
      Poor control of Diabetes
      Obesity and hyperlipidemia
    • 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 microaneurysmswhich 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)
      Proliferative DR (PDR)
      III. Clinically significant macular oedema (CSME)
      - May exist by itself or along with NPDRand PDR
    • Mild NPDR
      At least one microaneurysm - earliest clinically detectable lesion
      • Retinal hemorrhages
      • Hard or soft exudates
    • 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
    • Proliferative DR
      Vitreous hemorrhage
      Tractional retinal detachment
      Rubeosis Iridis
    • Vitreous Hemorrhage
    • Tractional retinal detachment
    • Rubeosis Iridis
    • 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
      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
      • Proliferative DR
      • Retinal laser photocoagulation as per the judgment of ophthalmologist (in high risk eyes)
      • It converts hypoxic retina (which produces ANGIOGENIC factors) into anoxic retina
    • Screening protocol for Diabetic retinopathy
      Screening once in a 1 year
      Diabetics with normal fundus
      Mild NPDR
      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
      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
    • NPDR
    • Mild NPDR – Microaneurysms, Dot and Blot hemorrhages
    • Moderate NPDR
    • Moderate NPDR with CSME
    • Circinate retinopathy – Hard exudates in a ring around leaking aneurysms
    • Moderate – Severe NPDRCotton wool patches Hemorrhages - 4 quadrants
    • Moderate – Severe NPDRCotton 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
    • CSME in different stages of NPDR
    • Proliferative DR – New vessels elsewhere on the retina along the superior-temporal vessels
    • PDR – New vessels on disc
    • PDR –New vessels on disc and New vessels elsewhere on retina
    • PDR – with vitreous hemorrhage
      Vitreous bleed
    • Vitreous Hemorrhage
    • Tractional retinal detachment
      Fibro-vascular proliferation
      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.
      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.
      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.
      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.
      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
      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.
      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
      urinary urgency—the sudden, strong need to urinate immediately
      urge incontinence—leakage of urine that follows a sudden, strong urge to urinate.
      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.
      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
      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
      are physically inactive
    • Diabetic Muscle Infarction
      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
      “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.
    • Autonomic neuropathy
      Diabetic neuropathy can lead to
      muscular weakness,
      Loss of feeling or sensation,
      and loss of autonomic functions such as
      Bladder control, and sweating
    • Autonomic neuropathy
      Impaired urination and sexual function
      Bladder infections
      Stomach disorders, due to the impaired ability of the stomach to empty (gastric stasis)
      and bloating
    • Autonomic neuropathy
      and fainting spells
      Loss of appetite
      Abdominal swelling,
      Heat intolerance,
    • Autonomic neuropathy
      Dizziness with standing,
      Difficulty urinating and urinary incontinence.
      Exercise intolerance,
      Orthostatic hypotension,
      Erectile dysfunction,
    • Autonomic neuropathy
      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
      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
      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
    • Diabetic Neuropathic ulcer
    • Neuropathic ulcer
      • peripheral sensory neuropathy, Trauma & deformity.
      • Ischemia, callus formation, and edema.
    • Neuropathic ulcers
      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
      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.
    • 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
      Theglomerular 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.
    • (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 mesangiumthat 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.
      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.
      GBM thickening occurs.
      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).
    • Summary Pathological lesions in DM
      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.
    • Summary Pathological lesions in DM
      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 .
    • Summary Pathological lesions in DM
      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.
    • Summary Pathological lesions in DM
      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.
    • Summary Pathological lesions in DM
      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.
    • Summary Pathological lesions in DM
      In short
      Diffuse glomerulosclerosis
      or nodular diabetic glomerulosclerosis (Kimmelstiel Wilson nodules)
      Tubulointerstitial fibrosis
    • Nodular Glomerulosclerosis – KW lesion.
    • Summary Pathological lesions in DM
      Arteriosclerosis and hyalinosis of afferent and efferent arterioles .
      Necrotizing renal papillitis.
      Infections &Pyelonephritis.
      Nephrotic syndrome
      End stage kidney
    • Summary Pathological lesions in DM
      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
      Nephrotic syndrome
      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.
    • Treatment of nephropathy
      Early screening
      Spot urine albumin : creatinine ratio
      24 hour urine collection
      Tight glycemic control
    • Treatment of nephropathy
      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
    • Treatment of nephropathy
      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
    • Treatment of nephropathy
      0.8g/kg/day proteins
      Thiazide diruritics
      Vit E
    • Treatment of nephropathy
      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
      Nephrotic syndrome
    • Complications of nephropathy
      severe hypertension
      complications of hemodialysis
      complications of kidney transplant
      coexistence of other diabetes complications
      peritonitis (if peritoneal dialysis used)
      increased ifections
    • Normal Retina
    • Diabetic Retinopathy
      Neovascularization Cotton wool spots
    • Diabetic Retinopathy
      Dot blot – Hemorrhages (Microaneurysms)
    • Diabetic Retinopathy
      Pre retinal Hemorrhage - detachment
    • Diabetic Retinopathy
      Advanced fibrous plaques
    • Label the diagram.
      Hard dep.
      Optic disc
      Blot hem
      Cotton wool
    • Diabetic Gangrene
    • Blood vessel calcification:
      Amputated thumb
    • Cataract
    • Acanthosis Nigricans
      • Insulin resistance…
    • Acanthosis Nigricans
      • Insulin resistance…
    • Label the diagram.
      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.
      2h postprandial
      Not diabetic
      < 145mg/ dl.
      <100 mg/dl
      >200 mg/ dl.
      >125 mg/ dl
      Border line indicates glucose tolerance test.
      125-200 mg/dl.
      100-125 mg/dl
    • 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
      - 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.
    • 3 hour Oral glucose tolerance test
      Giving 75 gm (100 gm by other authors) glucose in 250 ml water orally
    • 3 hour Oral glucose tolerance test
      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.
    • Affects of diabetes on pregnancy
      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).
    • Affects of diabetes on pregnancy
      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
    • Affects of diabetes on pregnancy
      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
    • Diabetes and Dental health
    • 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
      Increased susceptibility to bacterial, viral and fungal (that is, oral candidiasis) infections
      Periapical abscesses
      Periodontitis and loss of teeth
      Lichen planus
      Burning Mouth Syndrome
    • 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.
    • Tooth decay & cavities
      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. 
    • Tooth decay & cavities
      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.
    • 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.
    • Periapical abcess
    • Periapical Abscess
    • 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.
    • Oral Lichen Planus
    • 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
    • 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
      Vitamin deficiency anemia
      Certain medications
    • 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.
    • Gingivitis and Diabetes
      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.
    • Gingivitis and Diabetes
      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.
    • Gingivitis
    • 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.
    • Best time to receive dental care
    • Best time to receive dental care
      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.
    • Best time to receive dental care