Exam 3 Flashcards
Cortelini 2018
Thin tissue biotype associated with recession
Biotype includes gingial thickness, bone morphotype, and tooth dimension
Menta 2010
We need to consider both width and thickness of attached gingiva in determining risk to create an overall risk factor. The overall volume of KT is what is predictive of inflammation and recession rather than width alone
Ercoli 2018
2018 review paper of teh role of tooth morphology and dental prosthesis on gingivitis
crown margins in the JE and CT are assocaited with recession, crestal CT remodeling occurs histologically resulting in higher BOP .
direct restorations iwth an overhang greater than 0.2mm and inditect with 0.5-1mm overhangs are assocated with crestal bone loss, deeper PD and inflammation.
Jeffcoat 1980
Study on amalgam restoration overhangs and bone loss.
Retrospective study without standardized radiographs
Different materials have different effects, likely due to surface roughness.
Jernberg 1983
Open contacts had similar PD, GI, Crevicular bleeding, debris index, calculus index compared to contralateral teeth
the majority were anterior teeth, more accessible and smaller contacts
Masters 1964
cervical enamel projections in mandibular molars of 28% and maxillary molars of 17%.
Study on extracted teeth
numbers may be biased, but indicates that it is likely a significant factor in our practices
Hammerle 2018
hard and soft tissue deficiencies around dental implants
deficiencies can be related prior to implant placement due to trauma, periodontitis/peri-implantitis, expansion of the sinus floor, anatomical pre-conditions.
After implant placement some evidence of mechanical overload, thin soft tissues, lack of KT, malpositioning of implants, migration of teeth, lifelong growth, and systemic diseases
Ravida 2022
Systematic review
lack of 2mm KT had a significant difference in plaque index, but not BOP, PD, recession, or marginal bone loss.
This difference is very small, but presumably could contribute to peri-implant mucositis, and therefore peri-implantitis
Dhalen 2019
Review paper, infection occurs when virulence factors exceed host defense, resulting in invasion
intercellular by motile microbes (spirochetes)
intracellular by invasion (Pg, Tf, Pi, Cr) - Fimbrae related to this ability
Rodrigues 2020
Pg strains with FimA II were more prevalent in Stage II and IV periodontitis patients (80-90%)
Fimbrae are related to adherence to cells and salivary components
Pg more prevalent in Grade C than B, and in deeper PD, higher CAL, more BOP.
cross sectional study, so can’t prove FimA II causes disease, and no healthy controls in the community to compare rates to, but it is suggestive that this virulence factor may contribute to overall virulence of the bacteria
Darveau 2012
germ free mice colonized with Pg did not have bone loss, but mice with other bacteria colonized with Pg did.
Indicates that Pg facilitates invasion of other bacteria but does not necessarily invade itself.
Pg increased total microbial load, and altered the composition of the bacteria.
Virulence effect of Pg could be blocked by pharmacologic blockage of the compliment receptors, indicating that this virulence factor has a very important effect on the host.
Zheng 2021
Review. Main effect of Pg is gingipains, proteases that degrade inflammatory mediators
Pg induces autophagy in different cells, including epithelial/endothelial cells, fibroblasts, macrophages, and dendritic cells, potentially evading host immunity
compliment protein levels were higher in gingivitis than periodontitis, and similar in periodontitis to health
compliment involved in the phagocytosis of microbes
may be how Pg facilitates infection of other microbes
endotoxin release, increases macrophages capture of antigen, but decreases antigen presentation to T cells
Bueno 1998
JP2 strain of Aa for disease progression
prospective study, african patients in different locations
JP2 has a 530 BP deletion in promoter leukotoxin gene, producing more leukotoxin.
54% of hosts with JP2 converted to disease vs 15% with other Aa strains
Damgaard 2021
cohort study measuring host antibodies to Aa and LtxA with periodontitis
Found antibodies to Aa significantly correlated with Grade C and LtxA antibodies associated with Grade B and C
(may indirectly measure JP2 as it produces 20X the LtxA
Loe and colleagues 1965
non-specific plaque hypothesis
more plaque equals more disease
Did not work for the aggressive periodontitis group, or the non-progression group
Slotts 1976
Correlated Aa with juvenile periodontitis
Socransky 1998
Red, orange, yellow, green, purple, and blue complex
general trend from gram positive aerobes to gram negative anaerobes
general trends identified, but no clear initiator of disease
as plaque accumulation occurs for longer there is a more distinct shift in strains
the strains tend to be observed sequentially, with orange preceeding red, and red unlikely to be seen without orange
Haffagee 1986
systematic review, periodontal disease occurs in bursts of periods of activity and inactivity
may indicate why the specific plaque hypothesis is unproven
Ecological plaque hypothesis
disease is a relationship betwen bacteria and the host genetic/immunological factors and diseases such as diabetes, RA, or environmental factors such as smoking or nutrition
proposed in the 90’s
Barthold 2013
review paper on plaque theories. Differnetiates specific plaque and ecological plaque theories due to the host response, but individual plaque still play a role, as well as their byproducts and virulence factors interacting with the host
Yamamoto 2021
review paper summarizing the tissue response to peridoontal disease
JE begins to detatch from the tooth and becomes pocket epithelium, reducing the height of JE
micro-ulceration occurs as well
chronic periodontitis patients tend to have a significant antibody response, vs aggressive patients that do not
There is little evidence of invasion of the bacteria through the connective tissue itself
Farrugia 2022
Zebrafish showing toxicity of periodontal pathogens when they are introduced systemically
Berglundh 2011
Review paper
different proportions of immune cells around peri-implantitis
peri-implantitis had granulocytes and macrophages more frequently
This results in a slower reduction of immune markers, as well as clinical signs of inflammation
Salvi 2012
3 weeks of plaque accumulation aroudn implants and natural teeth causes similar increases in gingival index, but gingival index remains elevatedaround implants over the 6 week observation period, vs teeth that resolved after 3 weeks
Ivanovski 2018
The periodontum is a very vascular wide fan shaped collagen network, vs peri-implant tissue is a wound healing zone with relatively avascular parallel collagen fibers.
supracrestal attachment is shorter around teeth at 2.04mm (0.97JE and 1.07CT) vs implants at 3-3.5mm (2mmJE, 1-1.5mm CT)
Local factors
18 tortelini with 10 meta broccoli 18’s, crouching under 80 jeffcoats. 83 Jernbergs were playing in the 64 masters, hammered 18 rivers 22 feet wide
18 tortelini with 10 meta broccoli 18’s, crouching under 80 jeffcoats. 83 Jernbergs were playing in the 64 masters, hammered 18 rivers 22 feet wide
Cortelini 2018
Mehta 2010
Ercoli 2018
Jeffcoat 1980
Jernberg 1983
Masters 1964
Hammerle 2018
Ravida 2022
Virulence factors
19 dull rod guys with 20 dark flow 12’s. 21 sengers found 98 no-bueno dam guards in 21 feet
19 dull rod guys with 20 dark flow 12’s. 21 sengers found 98 no-bueno dam guards in 21 feet
Dhalen 2019
Rodrigues 2020
Darveau 2012
Zheng 2021
Bueno 1998
Damgaard 2021
Pathogenesis of periodontal disease
65 low slots found 76 to 98 cranky begees in 86 bars with 13 areas. 21 motos forged 22 burgelers with 11 saved 12 ivans to 18
65 low slots found 76 to 98 cranky begees in 86 bars with 13 areas. 21 motos forged 22 burgelers with 11 saved 12 ivans to 18
Loe and colleagues 1965
Slots 1976
Socransky 1998
Haffajee 1986
Bartold 2013
Yamamoto 2021
Farrugia 2022
Berglundh 2011
Salvi 2012
Ivanovski 2018
