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Obesity
BMI >30
High waist circumference
Comorbidities of Obesity
Type II Diabetes
Hypertension
Cardiovascular disease
Cancer
Statistical associations between obesity and periodontal disease
Typically probing pocket depth
Clinical attachment loss
Bleeding on probing
Overall higher probability of perio disease in obese people compared to normal weights
Xerostomia and Obesity
Saliva is the main defense against acid in the oral cavity
Inflammation disrupts salivary acinar glands, which reduces secretions and alters the composition
Inflammation disrupts PNS salivary stimulation
Comorbid insulin resistance leads to microvascular blood flow, disrupted by AGEs
Impaired nutrient and O2 delivery to salivary glands
Comorbid sleep apnea and chronic mouth breathing
Polypharmacy
Caries and Obesity
Diet with fermentable sugars leads to acidic biofilm and microenvironment
Low bicarb content in saliva and reduced saliva in general
Inflammation and insulin sensitivity
How does saliva neutralize acid?
Bicarb
Physical clearance
Ions are buffers that bind H+
How does saliva reduce bacteria?
Mucin
Physical clearance
Antibodies and anti-microbials
Oral consequences of GERD
Dental erosion
Dental attrition
PPIs
Dental erosion
Chemical disillusion of enamel independent of bacteria
Hydroxyapatite crystals are damaged by low pH
More common on palatal surfaces of maxillary teeth
Increased tooth sensitivity and pain with dentin exposure is secondary to erosion
Dental attrition
Mechanical wear from tooth-to-tooth contact
PPIs for GERD
Most prescribed drug treatment
Many pts will take these
Xerostomia
Increased pH
Oral candidiasis
Bariatric surgeries
Re-route the GI tract to alter metabolism
Physically restrict food intake
Reduce nutrient absorption
Oral consequence of bariatric surgery
Increased vomiting and GERD leads to erosion
Increased caries from more frequent meals
Vitamin B12 deficiencies and altered nutrient absorption
Delayed wound healing
Vitamin B12 deficiency and gastric bypass
Gastric rerouting and stomach loss leads to reduced parietal cells and intrinsic factor
Glossitis (beefy red tongue)
Glossitis and vitamin B12
B12 is needed for DNA synthesis with folate in high-turnover cells like mucosa
Reduced proliferation leads to atrophy
Red, patchy, thin epithelium, painful or numb, inflamed
Delayed wound healing and bariatric surgery
Gastric rerouting reduces acid secretion, pepsin, and protein breakdown
Bile and bicarb are introduced later since the duodenum is bypassed, reducing protein breakdown and fat absorption
Effects of reduced protein breakdown
Poor proliferation, collagen synthesis, angiogenesis, and cell migration
Delayed healing
Post-procedure ulcers
Incretins
Glucose-dependent insulinotropic peptide (GIP)
Glucagon-like peptide 1 (GLP-1)
Site of GIP
Duodenal K cells
Site of GLP-1
Ileal L-cells
What does GLP-1 therapy do?
Increases insulin secretion
Slows down gastric motility
Responsible for most of the post-prandial insulin response
Oral glucose load produces a greater insulin response compared to IV
How is GLP-1 used therapeutically?
Human GLP-1 has a short half-life
Mimetic and receptor agonists prolong the GLP-1 effect
Prolonged insulin release and gastric delay
How does GLP-1 affect dentistry?
12-15% of adults reported using the therapy in 2025
Can cause hypoglycemia
Can reduce hydration
Can cause gastroparesis and vomiting
Could cause inaccurate history and reporting if pt does not admit use
Inflammatory bowel disease
Chron’s or UC
Diagnosed based on symptoms, site, and histopathology
Oral consequences of inflammatory bowel disease
Affects up to 50% of IBD pts
Enlarged lips, ulcers, cobblestoning
Caries, infection, and perio disease
Malnutrition
Immunosuppressants
Oral consequences of immunosuppressants
Increased risk of infection
Delayed wound healing
Some bleeding risks
Risk for alveolar bone loss
DNA mutations
Active oncogenes
Suppress tumor-suppressor genes
Abnormal proliferation that leads to normal stratification and barriers often involves what?
Metaplasia
Dysplasia
Carcinoma
Metaplasia
Replacement of cell type, adaption to stress
Dysplasia
Abnormal growth of abnormal cells
Carcinoma
Malignant invasion
Cancer pathophysiology
DNA mutations
Abnormal proliferation
Inflammation
Angiogenesis
What do oral tissues depend on?
Lost of epithelial turnover
Enough vascular support
Continuous protein and micronutrient availability
Oral cancer pathophysiology
DNA mutations in squamous cells (90% is oral squamous cell carcinoma)
Tongues gingiva, floor of mouth
Alcohol, tobacco, and HPV are major risks
Clinical presentation of oral cancer
Non-healing lesions
Chronic sore tongue
Red, white, or mixed patches
What do oral squamous cells normally tolerate?
Mechanical stress
Chemical exposure
Microbes
Adaptive metaplasia doesn’t usually occur, only dysplasia with chronic insults
Esophageal cancer pathophysiology
Chronic irritation of the esophageal lining
Squamous cells carcinoma in upper/mid esophagus
Adenocarcinoma in the lower esophagus
Squamous cells are replaced with gastric-like columnar cells
Clinical presentation of esophageal cancer
Difficulty/painful swallowing
Unintentional weight loss
Long term nutrient deficiencies due to weight loss and reduced intake
What can cause difficulty swallowing?
Fibrotic responses in tissues that increase stiffness
Invasive growth
Pathophysiology of stomach cancer
Mainly gastric adenocarcinoma affects gastric pits/glads
Chronic inflammation leads to gastritis, metaplasia (reduced acid, IF, and loss of normal function)
Metaplasia leads to dysplasia (breakdown of control, abnormal cell cycles, less DNA repair)
Parietal cell gastric adenocarcinoma
Acid
Intrinsic factor
Chief cell gastric adenocarcinoma
Pepsinogen
ECL gastric adenocarcinoma
Histamine for acid
Goblet cells for adenocarcinoma
Mucous
Clinical presentation of stomach cancer
Early stages may be asymptomatic or vague
Protein and micronutrient deficiencies (vit B12)
Oral consequence of GI cancer
Nutritional deficiencies
Cancer therapies (impaired mucosal renewal)
Xerostomia
Altered taste