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
