Theme II: Part 2 (20-35) Flashcards
In health, what types of bacteria make up plaque. And how does this change in disease (gingivitis and periodontitis)
- In health, it is usually made of aerobic, gram-positive streptococci.
- In gingivitis, environment changes and there is increased heterogeneity/ diversity of species, mainly consisting of gram-positive rods (Actinomyces).
- Eventually there will be a shift towards pathogenic anaerobic, proteolytic gram-negative motile rods which cause periodontitis (P gingivalis, T. forsythia, T denticola)
How is periodontitis caused (mention biofilm, specific bacteria, changes, immune response, consequence)
- Pellicle on tooth attracts early colonizers, usually streptococci.
- Biofilm builds up sub gingivally as bacteria bind to each other.
- Environment changes in pocket, leading to changes in homeostasis of subgingival microbiota, altered gene expression, change in microbial population = DYSBIOSIS
- Bridging organisms (fusobacterium nucleatum) bridge early colonisers and the pathogenic late colonisers.
- Interaction between micro-organisms in plaque, host tissues and inflammatory cells.
- Exaggerated immune response causes breakdown of alveolar bone, loss of attachment of tooth to periodontium, loss of support, tooth loss.
What environmental changes occur during periodontitis, and why these occur
- Flow of gingival cervical fluid increases (this triggers inflammatory response)
- Increased temperature (due to changes in the composition, and increased blood flow)
- Pathogenic bacteria species selected for and increase -Proteolytic bacteria as they metabolize proteins in the pockets/ GCF
- Increased alkali production due to proteolytic metabolism into ammonia
- Less oxygen, so anaerobic bacteria selected for due to less oxidation.
What are keystone pathogens
- manipulate and change the environment and composition of biofilms, driving dysbiosis.
- Low abundance in health
- They don’t cause disease themselves, but they allow pathogen to cause disease
What are fusobacterium nucleatum (role and shape etc.)
- bridge early and late colonisers in periodontal disease
- gram negative, proteolytic, anaerobic, long thin rods
Virulence factors of p gingivalis (5)
- Fimbriae for adhesion and invasion
- capsule to resit phagocytosis
- LPS to trigger inflammatory response
- Haemagluttinins to bind to epithelial cells
- proteases to break down proteins (collagen, fibrinogen)
Aggregatibacter actinomytemcomitans. Its role and virulence factors. Shape
- involved in severe periodontitis. Also causes endocarditis
- anaerobic, non-motile, capnophilic (CO2), haemolytic, coccobacillus
- Adhesion and invasion due to fimbriae
- LPS which triggers bone resorption
- Leukotoxin: kills WBCs
- Proteases
[star shapes]
How periodontitis can cause systemic infection. What diseases is associated with it
-Periodontium is highly vascular so immune cells, bacteria, metabolites can enter the systemic circulation and go to distal sites.
- Diabetes mellitus (type 2) as pathogens could affect glycemic control.
- Rheaumatoid arthritis
- CVD: P gingivalis, A.a detected in atherosclerosis. Endocarditis associated with A.a.
- Obesity
- Stroke
- Colon cancer
Candida is a dimorphic fungi. What does this mean. And why it is dimorphic
- Transitions between yeast and filamentous hyphae form
- hyphae form allows it to invade tissue and spread between host cells
Explain the 4 forms of fungi (yeast, moulds, hyphae, mycelium)
- Yeasts – unicellular with spherical or ovoid bodies
- Moulds – multicellular with a variety of specialised structures that perform specific functions
- Hyphae – structural units of a mould. Thread-like tubes containing the fungal cytoplasm and its organelles.
- Mycelium – mass of hyphae that forms the mould colony
Important structure of candida’s cell wall
-thick 2-layered cell wall surrounding the plasma membrane, provides rigidity & strength to resist osmotic lysis due to the high internal water pressure.
-Cell wall important for antigenicity & adherence to host cells.
1-Inner wall – polysaccharides eg. Chitin & glucans to provide strength.
2-Outer wall - glycoproteins, carbohydrates, and mamans which make it a porous structure
Diseases caused by candida albicans
- Oropharyngeal candidiases
- Intra-abdominal candidiases (causes abscesses)
- Denture stomatitis, acute erythematous etc.
- GI candidiasis
- Vulvovaginal candidiases
Why is hyphae form so important. When transition happens
-Hyphal forms invade oral epithelium, have phagocytosis resistance, helps with adhesion, drug susceptibility, antigenicity.
- Switching is under a complex regulatory circuit, controlled in response to changing environment: temp, pH, osmotic shock, nutrients, cell density salivary factors (statherin), oral bacteria.
- Bacteria either compete or cooperate with candida species. Streptococci help them switch to hyphal form, while lactobacillus species tend to inhibit them.
What type of agar allows you to identify different types of candida. How is c albicans and c glabrata identified on this agar.
- CHROM agar used, as they grow as different colours (unlike on normal agar where they all look like creamy white colonies)
- C albicans= turquoise
- C glabrata= red colonies
Virulent factors of candida. (and what does aspartyl proteinase, phospholipase, and candidalysin do)
1-Adherence: specific adhesins to oral epithelium or prosthetic devices.
2-hyphae formation- facilitate epithelial cell penetration & invasion.
3-Hydrolytic enzymes: cause direct damage to cells:
eg. Aspartyl proteinases adapt cell morphology, break down tissue barriers, facilitate adherence & damage host cell.
eg. Phospholipases hydrolyse phospholipids, promoting cell lysis.
4. Candidalysin: a peptide toxin which helps c.albicans penetrate epithelial cells. Causes cell damage and triggers immune response. Forms biofilms, resistant to saliva flow, growth rate at least equal to rate of loss (sloughing)
Risk factors for oral candidosis (local and systemic factors)
LOCAL:
- Denture wearing (reservoir for infection)
- Inhaled corticosteroids (for asthma)
- Reduced saliva
- Carbohydrate rich diet
- Medication – corticosteroids, immunosuppressants, cytotoxins, broad-spectrum antibiotics
SYSTEMIC:
- Immunosupression: leukaemia, malignancy, HIV
- Endocrine disorders – diabetes melitus
- Anaemia
- nutritional deficiencies
- Extremes of age
Diagnosis of Candida albicans
- Clinical appearance: where it is found, shape and size, can white plaques be scraped off
- Blood test: To look for deficiencies in vitamins & minerals
- Microbiology: Oral rinse or oral swab if quite difficult to access
- Biopsy. To identify/ quantify the fungi, or assess the fungi sensitivity of the patient
How do azoles, polyenes, DNA analogues and echinocandins treat candida
- Azoles: blocks CYP450 involved in ergosterol synthesis
- Polyenes: binds to ergosterol to increase permeability and force membrane apart causing death
- DNA analogues: inhibits DNA and protein synthesis
- Echinocandins: Inhibits B1,3 D-glucan synthesis involved in cell wall formation
What is acute pseudomembranous candidosis (what it looks like, where, usual cause)
-most common. Aka oral candidosis/ oral thrush
-White oval or irregular shaped white patches over the entire oral mucosa (Hard and soft palate and potentially the tongue)
Can be scraped off to reveal an inflamed layer underneath
-Usually associated with inhaled steroid therapy
What is acute erythematous candidosis (what it looks like, where, usual cause)
- Covers dorsal surface of tongue as red patches. Soreness and loss of finely formed papillae
- usually develops due to taking broad-spectrum antibiotics, which reduces levels of bacteria in oral microflora which allows candida to increase.
- [ Aka antibiotic sore mouth/stomatitis]
What is chronic erythematous candidosis (what it looks like, where, usual cause, treatment)
- aka denture stomatitis
- associated with denture use, due to inadequate cleaning of dentures or poorly fitting dentures.
- Reddening of the mucosa beneath the fitting surface of the denture, usually on palate
- Treatment initially via local measures: mechanically clean dentures thoroughly & soak them in chlorhexidine mouthwash or sodium hypochlorite for 15 mins twice daily. Leave dentures out as often as possible. Denture replacement or adjustment
- Antifungal therapy if it persists if local management fails
What is chronic hyperplastic candidosis (what it looks like, where, usual cause, diagnosis, treatment, consequence)
- Appear as thickened white plaque in corners of mouth or dorsum of the tongue
- Smoking and alcohol risk factors
- PAS staining method to detect hyphal invasion of C. albicans
- Treatment: antifungal treatment, advised to stop smoking
- Could develop into oral cancer. It is a premalignant condition.-Would usually refer patient to oral surgery department to take a biopsy.
What is angular cheilitis (where, causes/ risk factors, treatment)
- secondary form of candidosis
- affects angles of mouth, soreness.
- Seen in patients with B12 or iron deficiency, Crohn’s, down’s syndrome, immunosuppression
- Caused by infection with candida or streptococcus/ staphylococcus
- if it appears in a denture wearer, them the likely cause is candida, so treat with Miconazole cream
- If caused by strep or staph, treat with sodium fusidate ointment
Median rhomboid glossitis (where, what it looks like, causes)
- a secondary form of candidosis
- symmetrical shaped area in midline of tongue
- Chronic infection
- Atrophy of the filiform papillae
- Associated with smoking & inhaled steroids
How do abscess form. Name the 2 types of dental abscesses. What types of bacteria are involved
-Pus (bacteria and neutrophils) can form if tartar builds up or if food gets trapped in pockets for example. Pus is walled off by a barrier due to an inflammatory response to invasion. If the pus can’t drain it forms an abscess.
1-Periapical/ dentoalveolar abscesses
2-periodontal abscesses
-Anaerobic and proteolytic bacteria
