Instructor: Prof Bill Keevil
Key Diseases Caused by Dental Plaque
Understand the major diseases: caries, gingivitis, and periodontitis.
Important Streptococci in Early Teeth Colonisation
Learn about their ability to form polysaccharides and ferment dietary sugars.
Anaerobes Associated with Gingivitis
Identify several key anaerobes involved in this disease.
Pathogens in Periodontosis
Recognize the “big 3” pathogens linked to this condition.
Types of Plaque Colonisers
Name examples of pioneer, secondary, and tertiary plaque colonisers.
H. Pylori Survival Mechanism
Explain how it survives stomach acidity and colonises epithelia.
Gut Flora in Infants
Compare the gut flora of breast-fed versus formula-fed babies.
Role of Bacteroides fragilis PSA
Describe its role in maintaining healthy flora.
Infection Statistics
CDC: 65% of infections are biofilm-related (1999).
NIH: 80% are biofilm-related (2002).
Historical Perspective
Leeuwenhoek observed polymicrobial communities- animacules - dental plaque under microscope
Pasteur and Koch focused on isolating single species.
Primary Infection Sites
Mouth (infection via bleeding gums).
Catheter entries (e.g., subvenous catheter).
Implanted devices (e.g., artificial hip joint).
Common Areas of Secondary Infection
Brain, kidneys, intervertebral spaces, bones around devices.
Teeth:
Plaque flora leads to malodour, tooth decay, gum diseases.
Stomach:
H. pylori causes gastric ulcers.
Intestine:
E. coli O157 leads to gastroenteritis.
Colon:
C. difficile causes gastroenteritis.
Upper Respiratory Tract:
Ps. aeruginosa is linked to cystic fibrosis.
Heart Valves:
Streptococci lead to endocarditis.
Urethral/Cervical Epithelium:
Infections from gonococci, Candida, Treponema.
Bone:
Infections from staphylococci and streptococci lead to osteomyelitis.
Microbial Interactions
Over 700 different bacterial groups.
Presence of fungi (Candida spp) and mycoplasma.
Interaction between microbes and the host can shift from healthy to disease microflora (dysbiosis).
Normal Microflora
Facultatives: streptococci, lactobacilli, staphylococci; Anaerobes: Bacteroides.
Health Conditions
Healthy oral flora to gingivitis to caries to periodontitis progression.
Inflammation Due to Dental Plaque
Leads to gingivitis and periodontal diseases.
Equilibrium
Balance between endogenous bacteria and oral defence systems:
Physical Barriers: Keratinized epithelium, mucin, salivary flow.
Chemical Compounds: Salivary enzymes, antibacterials.
Inflammatory Reactions: Dynamic interface between host and microbes, with quorum sensing as a communication method.
At Birth: Sterile environment.
Hours Post-Birth: Streptococcus spp. colonisation begins.
1 Year: Increase in diverse bacteria, including S. mutans and S. sanguis with tooth eruption.
Daily Bacterial Shedding: 1 x 10^8 bacteria.
Plaque Composition: 5% salivary flora; >300 species in plaque; 1 mg plaque contains 1 x 10^6 bacteria.
Healthy Gingiva Flora: Mainly aerobic and facultative anaerobes; >40% unculturable.
Caries: Linked to high sugar diet and poor hygiene; leads to holes and malodour.
Periodontal Diseases:
Gingivitis: Non-destructive, caused by poor hygiene.
Periodontitis: Destructive, often occurs with age or poor hygiene leading to gum and bone loss.
Metabolism Types:
Saccharolytic: metabolise sugars.
Acidogenic: produce acids that lower pH.
Aciduric: survive and thrive at low pH.
Veillonella:
Gram-negative anaerobic cocci, slows caries by converting lactic acid.
Lactobacillus:
Found in normal gut flora; some species linked to caries.
Infections:
Conditions such as Acute necrotizing ulcerative gingivitis caused by various anaerobic bacteria.
Treponema denticola: Key spirochete involved in tissue destruction.
Porphyromonas gingivalis: Strongly linked to chronic periodontitis with virulence factors.
Aggregatibacter actinomycetemcomitans: Associated with aggressive periodontitis; produces leukotoxin and immunosuppressive factors.
Quorum Sensing: Mediated by signaling molecules for intra- and inter-species interactions.
Preventing Biofilm Formation: Use of attachment blockers or detachment signals to hinder periodontal pathogens.
Introduction: Follows the Human Genome Project to identify the variety of species across different body sites using molecular techniques.
Attachment & Survival:
Attaches to mucus lining and neutralizes stomach acid via urease.
Produces toxins and invades the epithelial lining, causing ulcers.
Microbial Density: Approximately 100 trillion microbes in the intestine; metabolic activity comparable to an organ.
Diversity: Over 300–1000 species but dominated by a few.
Anaerobes: Represent >99% of flora; graduates to strict anaerobes.
Colonisation Post-Birth:
Influenced by maternal transfer; dominated initially by E. coli and streptococci.
Bifidobacterium dominates breast-fed infants.
Formula-fed infants show diverse flora.
Functions:
Ferment unused energy, train immune system, produce vitamins, regulate gut development.
Potentially pathogenic under certain conditions.
Associated Conditions:
Link to various diseases such as asthma, obesity, autism, and heart diseases, addressing the role of gut health in systemic conditions.
Role of Microflora:
Influences the development and function of the immune system, helping to differentiate between beneficial and harmful bacteria.
Immunological Role:
Help the intestine identify pathogens and initiate defense responses through inflammation activation.
Capsular Polysaccharides of B. fragilis:
Important for immune modulation and restoration of T cell levels.
Th1/Th2 Balance:
Restores immune balance, crucial for gut health; influences cytokine levels and immune responses.
Clinical Appearance: Visible exudative plaques that can lead to severe gastrointestinal issues due to dysbiosis.
Effectiveness:
Significant cure rates for recurrent Clostridium difficile infections highlighted by various treatment comparisons.
Common Pathogens:
Waterborne and foodborne bacteria including Salmonella, Vibrio, Campylobacter, and Listeria.
Complex Interactions: Emphasizes the importance of a healthy microbiome and the consequences of disrupting it through dietary changes or antibiotics.