W4: Antimicrobial Therapy and LA in Dentistry Flashcards
What are the most common odontogenic infections?
Abcess
Cellulitis
What is an abscess and what happens if the abscess is untreated?
- Localized area of inflammation with purulent exudate
- Pyogenic bacteria (e.g. Streptoccoi)
- Resists phagocytosis (capsule)
-Fibroblasts “wall it off”
Untreated abscess:
- Macrophage enzymes breakdown hard and soft tissues
- Treat surgically
* drain pus by extraction or root canal)
* incision to drain soft tissues
- Cellulitis
- inflammation of the connecitive tissue
What is maxillary sinusitis and of which origin?
Maxillary sinusitis of endodontic origin:
- spread from maxillary posterior teeth
- can be atypical infections
- often unilateral
- apical periodontitis -> periapical mucositis
What is oral candidiasis?
Oral candidiasis (thrush)
- endogenous infection
- overgrowth of the yeast *Candida albicans *
* less common C.glabrata, C. tropicalis
- opportunistic pathogen
What are the risk factors to develop oral candidiasis?
- very old or very young
- In poor health
- Overuse of antibiotics
- HIV infection or AIDs
- Chemotherapy or immunosuppressuve drugs
- Taking steriod medication
- Diabetic with high blood sugar
- Poorly fitting dentures
Define antimicrobial resistance
Antimicrobial reistance:
- the strain of microorganism that is not inhibited or killed by that antimicorbial
- Failure of a treatment to manage a patients infection
What is the relevance of antimicrobials to dentistry? What is the primary approach? When should antimicrobials be prescribed?
Significant portion of clincal work involved dealing with the impact of infection
* caries, periodontal disease, dental abscess, maxillary sinusitis of endodontic origin, candidiasis
Primary approach is surgical
* restorations, scaling and root planing, root canal therapy, properly fitting dentures
Antimicrobials are a useful ADJUNCT therapy but must be a clear need for them
* spreading infections, fever, risk groups
What are the two most common dental prescriptions?
Antibiotics
Antifungal
*from the 2021 data
Which bacteria in periodontal disease is developing antimicrobal resistance to which drug?
Prevotella resistant to Penicillin (Russia, Romania, Europe)
How can bacteria be reistant to anti-microbial drug?
Innate
Acquired
What is innate reistance?
- No mechanism to transport drug into cell
- Do not contain ore rely on the antibiotics target process or protein
- example: gram-negative bacteria are naturally resistant to beta-lactams
What is acquired resistance?
- Microorganisms develop genetic mutations that allow them to resist antibiotics
- Develops with repeated exposure
- Resistant strains can become dominant
When should antibiotics be used?
- Infection is spreading
cellulitits - Lymph node invovlement
- Signs of inflammation
- LA ineffective
- Systemic involvement (fever malaise)
- Periodontal disease
When should antibiotics be used with periodontal disease and what is the management?
- Inflammation of the gingiva and periodontal tissues
- bacteria in plaque
- Surgical approach if SRP
- Chlorhexidine mouth wash
- Moderate to severe- SRP PLUS Amoxicillin/Metronidazole
When should antibiotics be used with prophylaxis?
- Prophylaxis
- Commonly used to reduce the risk of infective endocarditis
- Side effect and risk of reistance
- Prescribe for patients with cardiac conditions and high risk of adverse outcomes
- Artificalheart valves, history of infective endocarditis, congenital heart conditions, transplant with problem in valve
- Low SES also a factor
What is infective endocarditis?
- Reapted Group A Strep infecton
- Strep throat, impetigo, scabies
- Acute rheumatic fever
- Autoimmune response, damages heart valves
- Rheumatic heart disease
- Bacteremia following dental procedures
What and when is prophylactic therapy?
- Recommended dose 2g amoxicilln orally 1 hour before procedure
- clindamycin for patients with immediate hypersensitvity to penicillin or cefalexin for non-immediate hypersensitvities
- Not all procedures
- only ones with high bacteremia (extraction, SRP)
- Oral health of patient (full mouth probing with periodontitis)
- Not restorations, LA administration or probing healthy teeth
https://tgldcdp.tg.org.au/viewTopic?topicfile=infection-prevention-endocarditis§ionId=abg16-c98-s2#toc_d1e251
What are examples narrow spectrum antibiotics?
Penicillin V
Amoxicilln
What are examples broad spectrum antibiotics?
Co-amoxylav (Augmetin)
Azithromycin
Metronidazole
Clindamycin
*metronidazole is debateable?
Which antibiotics are bacteriocidal?
Metronidazole
Penicillin
Which antibiotics are bacteriostatic?
Trimethoprim
Sulfonamides
Tetracycline
Azithromycin
Which antibiotics are used for odontogenic infections?
- First line antibiotics
- Amoxicillin or Penicillin V
- Allergies (Clindamycin)
*Second line if necessary - Allergy (?)
- Unresponsive infection
- Cellulitis
Which type of antibiotics contributes to resistance?
Broad spectrum
Which antibiotics should be used for unresponsive infections?
- Metronidazole plus Amoxicillin or Penicillin V
- Co-AmonyClav
Which antibitoics should be used for:
Maxilliary Sinusitis?
Periocoronitis?
Candidiasis?
Patients on bicillin?
Maxilliary Sinusitis: Augmentin
Periocoronitis: Metronidazole or Amoxicillin
Candidiasi: Ampgotericin B
Patients on bicillin: Amoxicillin
What is selective toxicity?
- Drug work by disrupting metabolic processes
- Need drugs that kill or inhibit the microorganism without damaging the host cells
- side effects
- Exploit the differences
- Bacteria (prokaryotes)
- Fungi, protozoa, helminths (eukaryotes)
- Viruses (obligaet intracellular)
What are adverse reactions?
- Unexpected or unintended effect
- range from headaches, comiting to liver or kidney injury
- Dose-related
- Extension effects or side effects
- Allergic reaction
- requires sensitization
- penicillin
- Idiosyncratic
- Not really understood, but may have genetic causes
What are the risks and side effects with antibiotics?
- GI upsets are common
-Nausea, vomitting, diarrhoea - Colitis
- Clostridium dificile infections
-Broad spectrum antibiotic use (Clindamycin, Co-Amoxyclav)
-Health-care associated infection
-Vulnerable people (elderly, history of GI disease) - Other infections
-Fungal infections (on increase) -
Hypersensitivity reactions
*Known issue with beta-lactams and sulphonamides *
-medical history is important
-immediate hypersensitivity reactions
anaphylaxis (trouble breathing, low BP, swelling of tongue, swelling of throat- ADRENALINE INJECTION NEEDED)
-Delayed
rashes (antihistamines)
Which medications do antibiotics interact with?
- Warfarin (clotting factors)
- Oral contraceptives (enterohepatic cycling)
What are risk and side effects of Tetracyclines?
Dental staining, enamel hypoplasia, bone deformation
NOT FOR CHILDREN UNDER 12, PREGNANT WOMEN
What are the risks and side effects of Metronidazole?
- “Dislfirum-like” reactions- nausea, vomiting, flushing of the skin, tachycardia, shortness of breath
* AVOID ALCOHOL
What are the target sites of antibacterial drugs?
- Cell wall synthesis
- Protein synthesis
- Nucleic acid synthesis
- Cell membrane function
Which antibiotics affect cell wall synthesis?
- Beta lactams and Cephalosporins
-Example: Penicillin and Flucloxacillin - Glycopeptides
-Exampl: Vancomycin (Gram-positive bacteria only) - Target peptidoglycan
- Allergies
Which antibiotics affect protein synthesis?
- Aminoglycosides
- Tetracyclines
- Macrolides
- Chloraphenicol
*Clindamycin
-Prokaryote ribosomes are 70S
-These drugs interfere with the binding of mRNA to ribosome or translation
What antibiotics affect nucleic acid synthesis?
- Sulfonamides
- Trimethoprim
-Structure of DNA is the same in prokaryotes and Eukaryotes
-Target process
*both of these drugs are BACTERIOSTATIC
Which antibiotics target cell membrane function?
- Polymixins
-Example: Colistin
-bind to LPS and interact with phospholipids in outer and inner membranes (catinic detergents)
-Effective against MDR Gram-Negatives (Pseudomonas aeruginosa)
What is the target of anti-fungal drugs?
- Cell membrane: β-glucan synthesis
- Amohotericin B
- Azoles: Ergosterol
What are the genetic aspects of antibiotics resistance?
Antibiotic resistance may arise by:
* Spontaneous chormosomal mutation
-alterged protein
-selective advantage
* Horizontal gene transfer
-acquire pieces of DNA from other bacteria
What are the mechanisms antibiotic resistance?
- Altered target
-target enzyme may change sufficiently (by mutation to cause lowered affinity for the antimicrobial drug)
-Example: mutations in DNA Gyrase and Quinilones - Alteration in access to the target site (altered reuptake)
-Decreased permeability (Vancomycin and Gram-negative bacteria)
-Active transport (E.Coli and Tetracycline, P.falciparum and Chloroquine, C.albicans and azoles) - Drug inactivation
-production of enzymes that inactive the anti-nacterial agent
-Example: Beta-lactamases inactivate beta lactams - Horizontal gene transfer
-Plasmids containig reistance genes
What is the mechanisms of reistance for Fungi?
Similar to bacteria
* efflux pumps
* Decreased permeabilty
* Altered drug targets
* Degradtive enzymes
* Overproduction of target
What are local anaethetics sometimes described as?
“Membrane stablizers”
What do local anaesthetics block?
Local anaesthetics are essentially voltage-gated sodium channel blockers
What are commonly used local anaesthetics in dentistry and what are local anaesthetics typically delievered with?
Commonly used local anaesthetics in dentistry are aminoamides to be metabolized in the liver. These include lignocaine, mepivacaine, articaine, prilocaine. Typically local anaesthetics are delievered with a vasoconstrictor like adrenalne or fenylpressin.
What is local anaesthetic ionization?
Ionization:
Most local anaesethics are weak bases and mostly ionized at physiological pH. Local anaesthetics usually exist as salts. Terminal amine can exist as tertiary (lipid soluble) or quaternary (ionized/water soluble forms). The degree of ionization changes as molecules cross the axon membrane. Non-ionized (tertiary amine) have a weak channel blocking activity. The local anaesthetics **act on cystosolic side on S6 transmembrane domain. The time of onset is dependent on the solubility. ** Those molecules that are highly lipid soluble cross the interstitial spaces slowly and may be sequestered in myelin and adipose tissues. Inflamed tissues have a lower pH and may therefore be more difficult in achieveing effective local anaesthesia.
