Seigniorage and the International Payments

The α-defensins, human neutrophil peptides (HNPs) are the predominant antimicrobial peptides of neutrophil granules. They are synthesized in promyelocytes and myelocytes as proHNPs, but only processed in promyelocytes and stored as mature HNPs in azurophil granules. Despite decades of search, the mechanisms underlying the posttranslational processing of neutrophil defensins remain unidentified. Thus, neither the enzyme that processes proHNPs nor the localization of processing has been identified. It has been hypothesized that proHNPs are processed by the serine proteases highly expressed in promyelocytes: Neutrophil elastase (NE), cathepsin G (CG), and proteinase 3 (PR3), all of which are able to process recombinant proHNP into HNP in vitro. We investigated whether serine proteases are in fact responsible for processing of proHNP in human bone marrow cells and in human and murine myeloid cell lines. Subcellular fractionation of the human promyelocytic cell line PLB-985 demonstrated proHNP processing to commence in fractions containing endoplasmic reticulum. Processing of 35S-proHNP was insensitive to serine protease inhibitors. Simultaneous knockdown of NE, CG, and PR3 did not decrease proHNP processing in primary human bone marrow cells. Furthermore, introduction of NE, CG, and PR3 into murine promyelocytic cells did not enhance the proHNP processing capability. Finally, two patients suffering from Papillon-Lefèvre syndrome, who lack active neutrophil serine proteases, demonstrated normal levels of fully processed HNP in peripheral neutrophils. Contradicting earlier assumptions, our study found serine proteases dispensable for processing of proHNPs in vivo. This calls for study of other protease classes in the search for the proHNP processing protease(s)

Is gingival bleeding a symptom of type 2 and 3 von Willebrand disease?

Background: Von Willebrand disease (VWD) is the most common inherent bleeding disorder. Gingival bleeding is a frequently reported symptom of VWD. However, gingival bleeding is also a leading symptom of plaque-induced gingivitis and untreated periodontal disease. In type 1 VWD gingival bleeding was not increased compared to controls. Thus, this study evaluated whether type 2 and 3 VWD determines an increased susceptibility to gingival bleeding in response to the oral biofilm. Methods: Twenty-four cases and 24 controls matched for age, sex, periodontal diagnosis, number of teeth and smoking were examined hematologically (VWF antigen, VWF activity, factor VIII activity) and periodontally (Gingival Bleeding Index [GBI]), bleeding on probing [BOP], Plaque Control Record [PCR], periodontal inflamed surface area [PISA], vertical probing attachment level). Results: BOP (VWD: 14.5±10.1%; controls: 12.3±5.3%; p = 0.542) and GBI (VWD: 10.5±9.9%; controls: 8.8±4.8%; p = 0.852) were similar for VWD and controls. Multiple regressions identified female sex, HbA1c, PCR and PISA to be associated with BOP. HbA1c and PCR were associated with GBI. Number of remaining teeth was negatively correlated with BOP and GBI. Conclusion: Type 2 and 3 VWD are not associated with a more pronounced inflammatory response to the oral biofilm in terms of BOP and GBI

Comparison of two different periodontal risk assessment methods with regard to their agreement: Periodontal risk assessment versus periodontal risk calculator

Aim: To evaluate the level of agreement between the periodontal risk assessment (PRA) and the periodontal risk calculator (PRC). Materials and methods: Periodontal risk was retrospectively assessed among 50 patients using PRA and PRC. Both methods were modified. PRA by assessing probing pocket depths and bleeding on probing at four (PRA4) and six (PRA6) sites per tooth, PRC by permanently marking or unmarking the dichotomously selectable factors “irregular recall,” “oral hygiene in need of improvement” and “completed scaling and root planing” for PRC. Agreement between PRA and PRCred (summarized risk categories) was determined using weighted kappa. Results: Fifty patients enrolled in periodontal maintenance (48% female, age: 63.8 ± 11.2 years) participated. PRA4 and PRA6 matched in 32 (64%) patients (κ‐coefficient = 0.48, p < .001). There was 100% agreement between both PRC versions. There was minimal agreement of PRA6 and PRCred (66%, 28% one different category, 6% two different categories; κ‐coefficient = 0.34; p = .001). PRA4 and PRCred did not match (60% agreement, 34% one different category, 6% two different categories; κ‐coefficient = 0.23; p = .13). For the SPT diagnosis of severe periodontitis, PRA6 and PRCred agreed weakly (κ‐coefficient = 0.44; p = .004). Conclusion: PRA and PRC showed a minimal agreement. Specific disease severity may result in improved agreement

Long-term results after placing dental implants in patients with Papillon-Lefèvre syndrome: results 2.5–20 years after implant insertion

Aim: A retrospective evaluation of patients with Papillon-Lefèvre syndrome (PLS) treated with dental implants to identify factors that may influence treatment outcomes. Methods: All PLS patients with dental implants currently registered at the Department of Periodontology, Goethe-University Frankfurt (20–38 years; mean: 29.6 years), were recruited. Five patients from three families (two pairs of siblings) with a total of 48 dental implants (inserted in different dental institutions) were included with a follow-up time of 2.5–20 years (mean: 10.4 years). Results: Implant failure occurred in three patients (at least 15 implants). Nearly all patients demonstrated peri-implantitis in more or less advanced stages; 60% of patients demonstrated bone loss ≥50% around the implants. Two patients did not follow any supportive therapy. Conclusions: Implants in PLS patients who did not follow any maintenance programme had a high risk of peri-implantitis and implant loss

Discomfort/pain due to periodontal and peri‐implant probing with/without platform switching

Objective: To compare discomfort/pain following periodontal probing around teeth and peri‐implant probing around implants with or without platform switching. Methods: Two dentists recruited and examined 65 patients, each of them exhibiting a dental implant with a contralateral tooth. Only two types of implants were included: one with and one without platform switching. Periodontal and peri‐implant probing depths (PPD) and probing attachment level (PAL) were assessed. Whether implant or tooth was measured first was randomly assigned. Immediately after probing, patients scored discomfort/pain using a visual analogue scale (VAS). The emergence profiles of implant crowns were assessed as angles between interproximal surfaces on radiographs. Results: Sixty‐five patients (age 69; 63/76 years [median; lower/upper quartile]; 38 females, 11 smokers) were examined. With the exception of mean PPD and PAL (p < .05) clinical parameters (PPD, PAL, bleeding on probing, suppuration) were well balanced between implants and teeth. Peri‐implant probing (VAS: 10; 0.75/16.25) caused significantly (p < .001) more discomfort/pain than periodontal probing (4; 0/10). Logistic regression analysis identified a larger difference between discomfort/pain for peri‐implant and periodontal probing in the maxilla than the mandible (p = .003). Comparing discomfort/pain between implants maxilla (p = .006) and emergence profile (p = .015) were associated with discomfort/pain. Type of implant (with/without platform switching) had no significant effect on discomfort/pain. Conclusions: Peri‐implant probing caused significantly more discomfort/pain than periodontal probing. Implant design with/without platform switching failed to have a significant effect on discomfort/pain

Patient characteristic (chronic periodontitis: ChP).

<p>Patient characteristic (chronic periodontitis: ChP).</p

Discomfort/pain due to periodontal and peri‐implant probing with/without platform switching

Objective: To compare discomfort/pain following periodontal probing around teeth and peri‐implant probing around implants with or without platform switching. Methods: Two dentists recruited and examined 65 patients, each of them exhibiting a dental implant with a contralateral tooth. Only two types of implants were included: one with and one without platform switching. Periodontal and peri‐implant probing depths (PPD) and probing attachment level (PAL) were assessed. Whether implant or tooth was measured first was randomly assigned. Immediately after probing, patients scored discomfort/pain using a visual analogue scale (VAS). The emergence profiles of implant crowns were assessed as angles between interproximal surfaces on radiographs. Results: Sixty‐five patients (age 69; 63/76 years [median; lower/upper quartile]; 38 females, 11 smokers) were examined. With the exception of mean PPD and PAL (p < .05) clinical parameters (PPD, PAL, bleeding on probing, suppuration) were well balanced between implants and teeth. Peri‐implant probing (VAS: 10; 0.75/16.25) caused significantly (p < .001) more discomfort/pain than periodontal probing (4; 0/10). Logistic regression analysis identified a larger difference between discomfort/pain for peri‐implant and periodontal probing in the maxilla than the mandible (p = .003). Comparing discomfort/pain between implants maxilla (p = .006) and emergence profile (p = .015) were associated with discomfort/pain. Type of implant (with/without platform switching) had no significant effect on discomfort/pain. Conclusions: Peri‐implant probing caused significantly more discomfort/pain than periodontal probing. Implant design with/without platform switching failed to have a significant effect on discomfort/pain

Is gingival bleeding a symptom of type 2 and 3 von Willebrand disease?

<div><p>Background</p><p>Von Willebrand disease (VWD) is the most common inherent bleeding disorder. Gingival bleeding is a frequently reported symptom of VWD. However, gingival bleeding is also a leading symptom of plaque-induced gingivitis and untreated periodontal disease. In type 1 VWD gingival bleeding was not increased compared to controls. Thus, this study evaluated whether type 2 and 3 VWD determines an increased susceptibility to gingival bleeding in response to the oral biofilm.</p><p>Methods</p><p>Twenty-four cases and 24 controls matched for age, sex, periodontal diagnosis, number of teeth and smoking were examined hematologically (VWF antigen, VWF activity, factor VIII activity) and periodontally (Gingival Bleeding Index [GBI]), bleeding on probing [BOP], Plaque Control Record [PCR], periodontal inflamed surface area [PISA], vertical probing attachment level).</p><p>Results</p><p>BOP (VWD: 14.5±10.1%; controls: 12.3±5.3%; <i>p</i> = 0.542) and GBI (VWD: 10.5±9.9%; controls: 8.8±4.8%; <i>p</i> = 0.852) were similar for VWD and controls. Multiple regressions identified female sex, HbA1c, PCR and PISA to be associated with BOP. HbA1c and PCR were associated with GBI. Number of remaining teeth was negatively correlated with BOP and GBI.</p><p>Conclusion</p><p>Type 2 and 3 VWD are not associated with a more pronounced inflammatory response to the oral biofilm in terms of BOP and GBI.</p></div

Papillon-Lefévre patients.

<p>Mutations of the Papillon-Lefévre patients. Nucleotides are numbered according to the coding DNA sequence (CDS).</p><p>Papillon-Lefévre patients.</p

Structure of preproHNP-1-3.

<p>Arrows indicate major sites of proteolytic cleavage. Positively and negatively charged amino acids are indicated in red and green, respectively. Lines indicate the disulphide linkage of cysteines (C; orange). HNP-3 is identical to HNP-1 except for having substituted alanine (A) at position 65 for aspartic acids (D).</p