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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
IN MY YOUTH
Complications of Diabetes
Short term Complications Hypoglycemia Diabetic Ketoacidosis Non Ketotic hyperosmolar diabetic coma Lactic acidosis
Yellow Nails
Diabetic Dermopathy
Diabetic Dermopathy
Diabetic Dermopathy
Diabetic Dermopathy
Gangrene
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
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
Acanthosis Nigricans
Acanthosis Nigricans
Acanthosis Nigricans
DIABETIC RETINOPATHY
Epidemiology of DR
RISK of developing DR: Type I or IDDM 70% Type II or NIDDM - 39%
RISK FACTORS:
1. 2. 3. 4. 5. 6. 7. Duration of diabetes Poor control of Diabetes Pregnancy Hypertension Nephropathy Obesity and hyperlipidemia 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
Non-proliferative DR (NPDR) Mild Moderate Severe
I.
II.
Proliferative DR (PDR)
III. Clinically significant macular oedema (CSME) - May exist by itself or along with NPDR and PDR
Mild NPDR
At least one microaneurysm earliest clinically detectable lesion
Moderate NPDR
Microaneurysms and/or dot and blot hemorrhages in at least 1 quadrant
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
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
NVD
Vitreous Hemorrhage
SUBHYALOID HEMORRHAGE
Rubeosis Iridis
Neovascular Glaucoma
Complication of rubeosis iridis
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
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
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
NPDR
Moderate NPDR
Severe NPDR
Cotton-wool patches, venous segmentation
Proliferative DR New vessels elsewhere on the retina along the superior-temporal vessels
Vitreous bleed
Vitreous Hemorrhage
Fibro-vascular proliferation
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
Hand Abnormalities
Carpal Tunnel Syndrome Dupuytrens contracture Flexor tenosynovitis Limited joint mobility
Each condition present in ~ 20% patients with diabetes
Dupuytrens 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
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, Raynauds, 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. Focalor 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 Digestion, Erection, 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) Nausea, Vomiting and bloating Dizziness,
Autonomic neuropathy
Lightheadedness, and fainting spells Loss of appetite Abdominal swelling, Heat intolerance, Impotence, Diarrhea,
Autonomic neuropathy
Constipation, Dizziness with standing, Difficulty urinating and urinary incontinence. Tachycardia, Exercise intolerance, Orthostatic hypotension, Gastroparesis, 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 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.
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
Nephropathy
The syndrome was discovered by British physician Clifford Wilson (19061997) and German-born American physician Paul Kimmelstiel (19001970) and was published for the first time in 1936.
Nephropathy
Usually manifests 1525 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).
Significant microalbuminuria will progress to endstage renal disease (ESRD). Therefore, all diabetes patients should be screened for microalbuminuria on a routine basis.
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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.
Hypertension (high blood pressure) typically develops during stage 3. Basement membrane thickening occurs due to deposition of AGEP
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.
FENESTRATION
FILTRATION SLIT
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 m 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 m are filtered with relative ease. The albumin molecule measures 0.0035 m 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. 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).
2. 3.
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
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
Role of TGF-
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- has been implicated in a number of chronic, scaring diseases
Angiotensin II and Thrombospondin (TSP1) can both stimulate the production of transforming growth factor- (TGF-) by tubuloepithelial cells and fibroblasts. TGF-, in turn, causes proliferation of fibroblasts and tubuloepithelial cells.
TGF- ultimately increases extracellular matrix proteins, likely by several mechanisms. TGF- 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.
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 crosslinks, 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 receptormediated 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 Bowmans 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.
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 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.
Treatment of nephropathy
Early screening Spot urine albumin : creatinine ratio 24 hour urine collection dipstick 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 Antilipids 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 Hyperkalemia 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
Diabetic Retinopathy
Dot blot Hemorrhages (Microaneurysms)
Diabetic Retinopathy
Pre retinal Hemorrhage - detachment
Diabetic Retinopathy
Advanced fibrous plaques
Diabetic Gangrene
Cataract
Acanthosis Nigricans
Insulin resistance
Acanthosis Nigricans
Insulin resistance
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.
2h postprandial
< 145mg/ dl. >200 mg/ dl. 125-200 mg/dl.
Result
Not diabetic
Diabetic
Border line indicates glucose tolerance test.
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
Lichen planus
Increased susceptibility to bacterial, viral and fungal (that is, oral candidiasis) infections
Periapical abscesses
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.
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.
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.
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, postradiation/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.
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.
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.
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 Depression Vitamin deficiency anemia Heartburn/GERD Bruxism Diabetes Hypothyroidism Menopause Certain medications Allergies
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?