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BDS3 - Periodontology > periodontal treatment 2 > Flashcards

periodontal treatment 2 Flashcards

1
Q

what are the different types of necrotising periodontal disease

A
  • necrotising gingivitis
  • necrotising periodontitis
  • necrotising stomatitis
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2
Q

what are the different names for necrotising periodontal disease

A
  • acute necrotising ulcerative gingivitis/periodontitis
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3
Q

what is Vincents angina

A
  • different diseae to NPD
  • occurs independently to NPD
  • spirochete microbiota in necrotic areas in tonsils during sore throat infections
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4
Q

what are the main features of NPD

A
  • painful, bleeding gums and ulceration and necrosis of the interdental papilla
  • rapidly restrictive and debilitating
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5
Q

why’s ANUG/P known to occur in epidemic type patterns

A
  • due to shared predisposing factors in a population = students during period of exams, armed forces
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6
Q

what type of infection is ANUG//P

A
  • opportunistic infection

- caused by bacteria inhabiting healthy oral cavity

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7
Q

what countries is it more common

A
  • epidemiology less 1% in developed countries, 27% in developing countries
  • quite urgent problem in developing countries
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8
Q

what is necrotising ulcerative gingivitis

A
  • acute necrotising ulcerative gingivitis, or called necrotising gingivits
  • common, non-contagious infection of the gums
  • if improperly treated NUG may become chronic and/or recurrent
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9
Q

what is necrotising ulcerative periodontitis

A
  • Necrotising periodontitis or acute necrotising ulcerative periodontitis
  • Infection leads to attachment loss
  • May be an extension of NUG into the periodontal ligaments, although this is not completely proven
  • Maybe both disease develop without connection
  • Bone involved and inflammation spread to bone
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10
Q

what is necrotising stomatitis

A
  • Progression of NUP into tissue beyond the mucogingival junction characterizes necrotizing stomatitis – mostly in malnutrition and HIV infection – may result in denudation of the bone leading to osteitis and oro-antral fistulas
  • Infection of oral mucosa
  • Not evolution of other NPD, can occur independently
  • Cancrum oris (also termed noma) is a necrotizing and destructive infection of the mouth and face, and therefore not strictly speaking a periodontal disease. In modern times, this condition usually occurs almost exclusively in malnourished children in developing countries. It may be disfiguring and is frequently fatal.
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11
Q

what does the gingiva look like

A
  • ulcerated and necrotic papillae and gingival margin result in a characteristic punched-out appearance
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12
Q

what are the ulcers covered in

A
  • yellowish, white or greyish slaim
  • termed pseudomembrane = but that is misleading, no coherence only slime made of firing, necrotic tissue, leukocytes, erythrocytes and mass of bacteria
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13
Q

what are the symptoms of ANUG/P

A
  • bleeding readily provoked
  • first lesions are most often seen IP
  • in NUP ulcerations are often associated with deep pockets formation as gingival necrosis coincides with loss of crystal alveolar bone
  • swelling of lymph nodes
  • usually no elevation of body temperature
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14
Q

why is the diagnosis not based on any test

A
  • biopsy = histopathology is not characteristic for NPD

- microbiology = not characteristics as well

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15
Q

what flora is constantly associated

A
  • treponema sp., selenomonas sp., fusobacterium sp., Prevotella intermedia
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16
Q

why is ANUG/P not a contagious infection

A
  • these bacteria are always in the mouth but there, but only when conditions allow it, they will thrive and become a problem
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17
Q

what is the difference between NPD and PHG (herpetic gingvostomatitis) aetiology

A
  • NPD = bacteria

- PHG = herpes simplex virus

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18
Q

what is the difference between NPD and PHG age

A
  • NPD = 15-30 years

- PHG = children

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19
Q

what is the difference between NPD and PHG site

A
  • NPD = interdental papilla, rarely outside gingiva

- PHG = gingiva and enture oral mucosa

20
Q

what is the difference between NPD and PHG symptoms

A
  • NPD = ulcerations and necrotic tissue and a yellowish white plaque
  • PHG = multiple vesicles which disrupt, leaving small round fibrin-covered ulcerations
21
Q

what is the difference between NPD and PHG duration

A
  • NPD = 1-2 days if treated

- PHG = 1-2 weeks

22
Q

what is the difference between NPD and PHG contagious

A
  • NPD = no

- PHG = yes

23
Q

what is the difference between NPD and PHG immunity

A
  • NPD = no

- PHG = partial

24
Q

what is the difference between NPD and PHG healing

A
  • NPD = destruction of periodontal tissue remains

- PHG = no permanent destruction

25
Q

what are the risk factors for NPD

A
  • stress, sleep deprivation, poor oral hygiene, smoking, immunosuppression
26
Q

what is the treatment for NPD

A
  • treatment of acute disease if by debridement and antibiotics, usually metronidazole
  • ultrasonic debridement
  • pain prevent patient from brushing = use 0.2% chlorohexidine most wash
  • 200mg metronidazole 3 times daily for 3 days
  • 400mg metronidazole for 3 days
  • smoking cessation, vitamin supplementation, dietary advice
  • for NP need to carry out HPT after removing acute symptoms
27
Q

what is the most important treatment for NPD

A
  • improve oral hygiene
28
Q

what must there be a balance between for healthy mouth

A
  • microbial plaque and host immune system
29
Q

how can periodontal disease be treated

A
  • mechanical disruption = reducing bacterial challenge, scaling and root surface debridement
  • systemic antibiotics or local antimicrobials
  • host modulation therapy
  • all of these aim of target biofilm
30
Q

how is biofilm mechanically disrupted

A
  • tooth-brushing technique
  • flossing
  • interdental brushes
  • supra and sub gingival plaque control
31
Q

how are systemic antibiotics used for periodontal treatment

A
  • systemic antibiotics in periodontal treatment are not he 1st line defence and if used in selected cased are only allowed once combined with mechanical disruption of biofilm
32
Q

what is a biofilm

A
  • aggregate of microorganisms in which cells adhere to each other on a surface
  • cells are embedded within a self-produced matrix of extracellular polymeric substance
  • resistant to antibiotics, antibacterial agents, hidden from immune system of the host
  • once we have mechanically disrupted biofilm, we can use antibiotics as well to kill these bacteria
33
Q

what cases do we treat with systemic antibiotics and mechanical disruption

A
  • aggressive periodontitis

- young people with grade B/C = fast progressing periodontitis

34
Q

what are contraindications for each antibiotics

A
  • amoxicillin = allergies
  • metronidazole = alcohol intake, pregnancy, increase effect of warfarin
  • doxycycline = tetracycline staining of teeth
35
Q

what is the treatment protocol for specialist treatment

A
  • OH
  • supra gingival scaling and RSD of all sites indicated in pocket chart
  • start antibiotic regimen on the morning of the first RSD visit
36
Q

what drug regimens are used for antibiotic

A
  • 500mg amoxicillin 3 times a day for 7 days
  • 200mg BSP metronidazole 3 times a day for 7 days
  • 400mg metronidazole 3 times a day for 7 days
  • use doxycycline if allergic to amoxicillin or on warfarin = 100mg one a day for 21 days
  • 500mg azithromycin one a day for 3 days
37
Q

what are advantages of local antimicrobials

A
  • reduced systemic dose
  • high local concentration
  • superinfection, such as C Dif unlikely
  • drug interactions unlikely
  • site specific
  • patient compliance not an issue as applied by healthcare provider
  • can utilise agents which can’t be utilised systemically
38
Q

what are the disadvantages of local antimicrobials

A
  • expensive
  • still require RSD or biofilm disruption
  • limited indications
39
Q

what is periochip used for

A
  • effective auxiliary aid in the local treatment of the periodontitis than studies proofing its ineffectiveness
  • benefits are visible only in certain clinical conditions
  • seems better financially and time wise – to wait until most of the pockets heal after instrumentation during HPT and use it in persisting pockets only during targeted roof surface debridement and maintenance recalls
40
Q

what are indications for using local antiseptics as periochip

A
  • bovine origin gelatine based and Piscean (fish collagen based), Chlo-site (chlorhexidine gel)
41
Q

when is periochip used

A
  • • 1 - only persisting pockets > 5 mm
    • 2 - always with RSD
    • 3 - Only in isolated pockets – (if many deep periodontal pockets in one area - OFD or systemic antibiotics combined with RSD c is more beneficial
    • 4 - in case of periodontal abscesses – after evacuation of pus and RSD.
    • Periochip recommended for 1st line instrumentation in each pocket
42
Q

what are some antibiotics

A
  • 1 – arestin  1mg minocycline HCl microspheres
  • 2 – atridox  doxycycline hyclate 10%
  • 3 – elyzol  25% metronidazole
  • Advantages of antibiotics is it is made up of microsphere which is good as it is only a specific small amount used which is good as reduces resistance to antibiotics
43
Q

what alternative therapies are used to treat

A
  • periostat

- periowave

44
Q

what is periostat

A
  • • 20 mg of doxycycline - twice a day for 3 months, systemically, as an adjunct to supra-/sub-gingival instrumentation.
    • This low dose of doxycycline is considered to be sub-antimicrobial, meaning that the dose is insufficient to inhibit the growth of bacteria, it is prescribed for its role as a collagenase inhibitor - an enzyme produced by both bacterial and human cells, is responsible for the breakdown of collagen and is implicated in periodontal tissue damage. Sub-antimicrobial dose of doxycycline was unlikely to exert a significant evolutionary pressure and therefore less likely to accelerate the development of drug resistant bacteria.
45
Q

what is periowave

A
  • 1.Irrigate: photosensitizing solution is topically applied to the gums at the treatment site. It then preferentially attaches to the harmful bacteria and toxins associated with periodontal disease.
  • 2.Illuminate: A thin, plastic light diffusing tip is painlessly placed into the treatment site. The treatment site is illuminated with a specifically calibrated laser light, activating the photosensitizing solution and destroying the harmful bacteria and toxins.
46
Q

what are some host modulation therapies (not been successful so fr)

A
  • corticosteroids
  • NSAIDs
  • anti-cytokine and biological therapies
  • lipid mediators of resolution of inflammation
  • small molecule compounds = target specific cytokines-mediated processes, inhibition of RANKL induced osteoclast
  • bisphosphonates

BDS3 - Periodontology (8 decks)

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