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IBICL - Case 4 (My Wobbly Teeth), Background/Patient History, Chief…
IBICL - Case 4 (My Wobbly Teeth)
Diabetes Mellitus
9.4% adults
Diagnosed with Type
TWO
Diabetes
Asymptomatic until on holiday and went suddenly
BLIND
Diabetic Retinopathy
is the LEADING cause of blindness.
No
attempts to change lifestyle until post-diagnosis
Risk factors - Polygenetic disease
Non-Modifiable
Pre-diabetesPre-diabetes
Genetics, increased age, male, low socioeconomic status
Previous History of Gestational Diabetes
Modifiable
Low activity levels, increased alcohol consumption, excessive refined sugar consumption
Obesity/High Visceral Fat
Pathogenesis
Glucotoxicity (type I & II)
PKC
Synthesis of DAG in response to an increase in intracellular glucose thereby blocking the intake of glucose into the cell.
This will activate PKC causing:
Altered enzyme activities
Cell proliferation and turnover
Production of inflammatory cytokines
Abnormalities in the Polyol Pathway
AGE (advanced glycation end products)
Excess glucose in the blood can attach to amino acid groups via
a ketoamine bond
This causes the production of Amadori products and advanced glycation end products
Amadori products cause
◊ Impaired enzyme activity
◊ Conformational changes
◊ Ligand bondig
◊ Glycated LDLs are not recognized by receptors and are therefore trapped in ECM and arteries
◊ Amadori produces are able to be oxidised
AGE causes
◊ Stiffening, thickening, decreased digestibility and decreased extracellular matrix turnover in diabetes
◊ Act as recognition signals for uptake and degradation of proteins by macrophages which can contributed to release of cytokines and oxidative stress causing disease
◊ Leads to increased protein cross linking
Bind to specific receptor (RAGE) on macrophages, t cells, endothelial cells and vascular smooth muscles cells
Lipotoxicity (type II)
○ increase in obesity decreases sensitivity of peripheral tissues to insulin
○ this occurs when there is an increase in Non-esterified fatty acids in combination with insulin sensitivity and a decrease in glucose utilisation
○ Adipokines which were once predisposed to release anto-inflammatory cytokines, will no release inflammatory cytokines instead.
Teeth are "wobbly"
Can assume connection between Diabetes and PERIODONTITIS.
Perio disease & DM are two of the most common chronic diseases and are LINKED.
Periodontitis - 42.2% dentate adults
Diabetes can raise glucose in Saliva. Leads to more bacterial growth and plaque build-up.
Diabetes also increases the risk of tooth loss, which interferes with diet, often resulting in poor glycemic control.
Our patient had LONG-term Diabetes, studies indicate that DM is a RISK FACTOR for Periodontitis and that it PRECEDES Periodontitis.
CYCLIC interaction that worsens both conditions. Also note the risk factors are higher age and male gender, which our patient checks off.
IF our patient is on medication, these often cause dry mouth, a STRONG risk factor for both Periodontitis and Caries
.
Biological Systems:
Matrix Metalloproteinases 8/9
BOTH very valuable diagnostic tools to treat PERIODONTITIS.
MMP-8 can degrade type 1, 2, and 3 Collagens
MMP-8 is the main collagenase in periodontitis
90% to 95% of collagenolytic activity in gingival crevicular fluid originated from MMP-8.
MMP-9 can degrade type 4 and 5 Collagens.
Also more apoptosis of matrix-producing cells like fibroblasts and osteoblasts that LIMIT repair. Further limited in diabetic perio tissues by reduced anabolic activities linked to diminished growth factor expression.
Prostaglandin E2
IL-1Beta, IL-6, Interferon-gamma, IL-8, TNF-alpha, IL-17, IL4, IL-10
Medication(s)
Breakdown based on mechanisms/targets
Pramlintide
(1+2) and
alpha-glucosidase inhibitors
(3+4) targets
GI tract
: Delay of gastric emptying (1), inhibitions of glucagon release (2) & glucose absorption (3), and stimulation of GLP-1 release (4)
Sulfonylureas, Meglitinides, and Incretin mimetics DPP-4 Inhibitors
target
Pancreatic B-cells
Acute stimulation of insulin release (1,2,3), Stim of insulin biosynthesis (3), Inhib. of B-cell apoptosis (3), and Stim. of B-cell differentiation (3)
Metformin
works in the
LIVER
for Inhibition of glucose production and raising hepatic insulin sensitivity
Thiazolidinediones
ALSO work in Liver, but mainly in Adipose tissue. Work to suppress NEGA release, redistribute fat (visc. to subcut) and modulate adipokine release
Background/Patient History
Signs & Symptoms
Osmotic imbalance
Thirst, frequent urination
Weight loss
Microvascular complications
Blurred vision, loss of vision, cataracts, glaucoma
Numb/tingling extremities -> nerve damage
Kidney disease
Fatigue
Frequent infections -> can lead to amputation
Macrovascular complications
Stroke
Heart disease
Peripheral vascular disease e.g. gangrene, ulcers
Poor wound healing
Chief Complaint