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In two separate clinical reports, Taylor [21] reported patient's complain with cantilevered part after 32 months of loading.
After 3 months of loading, detectable levels of EROD inducers could only be found in sludge residue on top of the reed beds from both D5 and D6 and in the bed material from D6.
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This was after 150 × 10 cycles at a frequency of 3 Hz, which would simulate the first 2 months of load bearing.
When we compare our findings with those of in vivo experiments, the 300,000 load cycles correspond with 3 months of normal loading for an active patient [ 29].
For another implant, abutment screw fracture and alveolar bone loss occurred in 23.5 months of functional loading.
However, a maximum of 14% reduction of the bond strength was observed for 80 °C temperature after 8 months of thermal loading.
The present clinical preliminary study is intended to radiologically analyze the effect of glow-discharged abutments on hard tissue level changes after 18 months of prosthetic loading.
For the remaining one, no marginal bone loss had been observed up to 24 months of functional loading, but an average level of marginal bone loss (2.74 mm) was observed in 40 months; therefore, it is under maintenance treatment.
Of the three implants with ≥0.2-mm ≥0.2-mml bone loss on an annual basis during the follow-up, one was remarginale to peri-implantitis and, consequently, an average of 2.0-mm vertical bone resorption for 32 months of functionalossading.
The implant stability quotient (ISQ) value for all implants differed significantly between abutment connection (60.2 ± 7.3) and after 6 months of bridge loading (62.5 ± 5.5) but were nonsignificant between implant placement (61.9 ± 9.5) and abutment connection (60.2 ± 7.3), and also 6 months of bridge loading (62.5 ± 5.5) and 3 years of bridge loading (61.8 ± 5.5).
While this form of salt-induced salt sensitivity has not been widely considered in the past, it is evident in data from chimpanzees in which 22 months of salt loading was associated with a progressive rise in BP that was nevertheless reversible upon restoration of normal salt intake [ 10].
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