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Aspenberg, Per
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Publications (10 of 203) Show all publications
Aspenberg, P. (2017). Apropå! En arrogant organisation [Letter to the editor]. Läkartidningen, 114
Open this publication in new window or tab >>Apropå! En arrogant organisation
2017 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 114Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Stockholm, Sweden: Läkartidningen Förlag AB, 2017
National Category
Health Sciences Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-146347 (URN)29292934 (PubMedID)
Available from: 2018-04-07 Created: 2018-04-07 Last updated: 2018-04-20Bibliographically approved
Aspenberg, P. (2017). Beslut att operera kopplat till ortopeders attityder till kirurgi. Läkartidningen, 114(41)
Open this publication in new window or tab >>Beslut att operera kopplat till ortopeders attityder till kirurgi
2017 (English)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 114, no 41Article in journal, Editorial material (Refereed) Published
Abstract [en]

[No abstract available]

Place, publisher, year, edition, pages
Läkartidningen Förlag, 2017
National Category
Orthopaedics
Identifiers
urn:nbn:se:liu:diva-147019 (URN)2-s2.0-85031295393 (Scopus ID)
Available from: 2018-04-09 Created: 2018-04-09 Last updated: 2018-04-24
Blomgran, P., Blomgran, R., Ernerudh, J. & Aspenberg, P. (2017). Cox-2 inhibition and the composition of inflammatory cell populations during early and mid-time tendon healing. Muscles, ligaments and Tendons journal, 7(2), 223-229
Open this publication in new window or tab >>Cox-2 inhibition and the composition of inflammatory cell populations during early and mid-time tendon healing
2017 (English)In: Muscles, ligaments and Tendons journal, ISSN 2240-4554, Vol. 7, no 2, p. 223-229Article in journal (Refereed) Published
Abstract [en]

Background: During early tendon healing, the cells within the regenerating tissue are, to a large part, inflammatory leukocytes (CD45+). In a rat Achilles tendon healing model, the inflammation resolves between 5 and 10 days. In the same model, Cox inhibitors (NSAIDs) impair healing when given during the first 5 days, but have a positive effect if given later. We tested the hypothesis that a Cox inhibitor would exert these effects by influencing inflammation, and thereby the composition of the inflammatory cell subpopulations.Methods: Achilles tendon transection was performed in 44 animals. Animals were randomized to either parecoxib or saline injections. Healing was evaluated by mechanical testing day 7 after surgery and by flow cytometry day 3 and 10.Results: Cross-sectional area, peak force and stiffness were reduced by parecoxib 31, 33, and 25% respectively (p=0.005, p=0.002, and p=0.005). By flow cytometry, there was a strong effect of time (p<0.001) on virtually all inflammatory cell subpopulations (CD45, CD11b, CD68, CCR7, CD163, CD206, CD3, CD4), but no significant effect of parecoxib at any time point.Conclusion: The results suggest that the negative effects of Cox inhibitors on tendon healing might be exerted mainly via mechanisms not directly related to inflammatory cells.

Place, publisher, year, edition, pages
Rome, Italy: CIC Edizioni Internazionali, 2017
Keyword
tendon healing; NSAID; inflammation; rat model; flow cytometry
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:liu:diva-142352 (URN)10.11138/mltj/2017.7.2.223 (DOI)
Available from: 2017-10-27 Created: 2017-10-27 Last updated: 2018-04-17
Sandberg, O., Bernhardsson, M. & Aspenberg, P. (2017). Earlier effect of alendronate in mouse metaphyseal versus diaphyseal bone healing. Journal of Orthopaedic Research, 35(4), 793-799
Open this publication in new window or tab >>Earlier effect of alendronate in mouse metaphyseal versus diaphyseal bone healing
2017 (English)In: Journal of Orthopaedic Research, ISSN 0736-0266, E-ISSN 1554-527X, Vol. 35, no 4, p. 793-799Article in journal (Refereed) Published
Abstract [en]

Healing of injured cancellous bone is characterized by a transient stage of rapid bone formation throughout the traumatized bone volume, often followed by similarly rapid resorption. This is different from the slower diaphyseal healing via an external callus. We, therefore, hypothesized that antiresorptive treatment might have an earlier positive effect in cancellous bone healing than in diaphyseal fractures. One hundred and twenty-three male C57bl6 mice received either an internally stabilized diaphyseal osteotomy of the femur or a screw inserted into the tibial metaphysis. The mice were randomized to daily alendronate injections (200 μg/kg/day), or control injections, and killed for mechanical testing after 14, 21, or 28 days. The hypothesis was tested by a three-way Anova (time, site, and drug). The ultimate force was increased by bisphosphonate treatment in both models. There was a significant interaction between time, site, and drug (p < 0.001) so that the full positive effect of alendronate was evident in the metaphysis at 14 days, but first after 28 days in the diaphysis. While the early effect in the metaphysis might be translated into earlier healing, the late effect in the diaphysis was due to delayed remodeling of the callus, which might have less clinical importance. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res

Place, publisher, year, edition, pages
John Wiley & Sons, 2017
Keyword
fracture, bisphosphonate, metaphysis, cancellous bone, trabecular bone, alendronate
National Category
Clinical Medicine Orthopaedics Nursing
Identifiers
urn:nbn:se:liu:diva-130921 (URN)10.1002/jor.23316 (DOI)000399728400008 ()27233101 (PubMedID)
Funder
Swedish Research CouncilLinköpings universitetÖstergötland County CouncilEU, FP7, Seventh Framework Programme
Note

Funding agencies: Swedish Research Council [VR 02031-47-5]; Linkoping University; Ostergotland County Council; European Communitys Seventh Framework Programme [FP7/2007-2013]

Available from: 2016-08-31 Created: 2016-08-31 Last updated: 2018-05-03Bibliographically approved
Amirhosseini, M., Andersson, G., Aspenberg, P. & Fahlgren, A. (2017). Mechanical instability and titanium particles induce similar transcriptomic changes in a rat model for periprosthetic osteolysis and aseptic loosening. Bone Reports, 7, 17-25
Open this publication in new window or tab >>Mechanical instability and titanium particles induce similar transcriptomic changes in a rat model for periprosthetic osteolysis and aseptic loosening
2017 (English)In: Bone Reports, ISSN 2352-1872, Vol. 7, p. 17-25Article in journal (Refereed) Published
Abstract [en]

Wear debris particles released from prosthetic bearing surfaces and mechanical instability of implants are two main causes of periprosthetic osteolysis. While particle-induced loosening has been studied extensively, mechanisms through which mechanical factors lead to implant loosening have been less investigated. This study compares the transcriptional profiles associated with osteolysis in a rat model for aseptic loosening, induced by either mechanical instability or titanium particles. Rats were exposed to mechanical instability or titanium particles. After 15 min, 3, 48 or 120 h from start of the stimulation, gene expression changes in periprosthetic bone tissue was determined by microarray analysis. Microarray data were analyzed by PANTHER Gene List Analysis tool and Ingenuity Pathway Analysis (IPA). Both types of osteolytic stimulation led to gene regulation in comparison to unstimulated controls after 3, 48 or 120 h. However, when mechanical instability was compared to titanium particles, no gene showed a statistically significant difference (fold change = ± 1.5 and adjusted p-value = 0.05) at any time point. There was a remarkable similarity in numbers and functional classification of regulated genes. Pathway analysis showed several inflammatory pathways activated by both stimuli, including Acute Phase Response signaling, IL-6 signaling and Oncostatin M signaling. Quantitative PCR confirmed the changes in expression of key genes involved in osteolysis observed by global transcriptomics. Inflammatory mediators including interleukin (IL)-6, IL-1ß, chemokine (C-C motif) ligand (CCL)2, prostaglandin-endoperoxide synthase (Ptgs)2 and leukemia inhibitory factor (LIF) showed strong upregulation, as assessed by both microarray and qPCR. By investigating genome-wide expression changes we show that, despite the different nature of mechanical implant instability and titanium particles, osteolysis seems to be induced through similar biological and signaling pathways in this rat model for aseptic loosening. Pathways associated to the innate inflammatory response appear to be a major driver for osteolysis. Our findings implicate early restriction of inflammation to be critical to prevent or mitigate osteolysis and aseptic loosening of orthopedic implants.

Place, publisher, year, edition, pages
Elsevier, 2017
Keyword
Aseptic loosening; Implant; Instability; Microarray; Wear debris
National Category
Cell and Molecular Biology Orthopaedics
Identifiers
urn:nbn:se:liu:diva-146297 (URN)10.1016/j.bonr.2017.07.003 (DOI)28795083 (PubMedID)
Available from: 2018-04-07 Created: 2018-04-07 Last updated: 2018-04-07
Aspenberg, P. (2017). Placeboeffekten är övervärderad: »Återgång till medelvärdet« kan förklara förbättring efter skenbehandling – men misstolkas ofta. Läkartidningen, 114
Open this publication in new window or tab >>Placeboeffekten är övervärderad: »Återgång till medelvärdet« kan förklara förbättring efter skenbehandling – men misstolkas ofta
2017 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 114Article in journal, Editorial material (Refereed) Published
Place, publisher, year, edition, pages
Stockholm, Sweden: Läkartidningen Förlag AB, 2017
National Category
Other Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-146362 (URN)29292961 (PubMedID)
Available from: 2018-04-07 Created: 2018-04-07 Last updated: 2018-05-05Bibliographically approved
Blomgran, P., Blomgran, R., Ernerudh, J. & Aspenberg, P. (2016). A possible link between loading, inflammation and healing: Immune cell populations during tendon healing in the rat. Scientific Reports, 6(29824)
Open this publication in new window or tab >>A possible link between loading, inflammation and healing: Immune cell populations during tendon healing in the rat
2016 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 6, no 29824Article in journal (Refereed) Published
Abstract [en]

Loading influences tendon healing, and so does inflammation. We hypothesized that the two are connected. 48 rats underwent Achilles tendon transection. Half of the rats received Botox injections into calf muscles to reduce mechanical loading. Cells from the regenerating tissue were analyzed by flow cytometry. In the loaded group, the regenerating tissue contained 83% leukocytes (CD45(+)) day 1, and 23% day 10. The M1/M2 macrophage ratio (CCR7/CD206) peaked at day 3, while T helper (CD3(+)CD4(+)) and T-reg cells (CD25(+) Foxp3(+)) increased over time. With Botox, markers associated with down-regulation of inflammation were more common day 5 (CD163, CD206, CD25, Foxp3), and M1 or M2 macrophages and T-reg cells were virtually absent day 10, while still present with full loading. The primary variable, CCR7/CD206 ratio day 5, was higher with full loading (p = 0.001) and the T-reg cell fraction was lower (p amp;lt; 0.001). Free cage activity loading is known to increase size and strength of the tendon in this model compared to Botox. Loading now appeared to delay the switch to an M2 type of inflammation with more T-reg cells. It seems a prolonged M1 phase due to loading might make the tendon regenerate bigger.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2016
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-130383 (URN)10.1038/srep29824 (DOI)000379584000001 ()27405922 (PubMedID)
Note

Funding Agencies|Swedish Research Council [K2013-52X-02031-47-5]; Swedish National Centre for Research in Sports; King Gustaf V and Queen Victoria Free Mason Foundation

Available from: 2016-08-15 Created: 2016-08-05 Last updated: 2018-01-10
Aspenberg, P. (2016). Atypical fractures, a biased perspective. Injury, 47(1), S28-S30
Open this publication in new window or tab >>Atypical fractures, a biased perspective
2016 (English)In: Injury, ISSN 0020-1383, E-ISSN 1879-0267, Vol. 47, no 1, p. S28-S30Article in journal (Refereed) Published
Abstract [en]

When stress fractures started to show up in the femurs of elderly ladies, it was soon evident that bisphosphonate use lay behind, and the absolute risk increase due to bisphosphonate use was reasonably well estimated already in 2008. Thereafter followed a period of confusion: the term atypical fracture was introduced, with a definition so vague that the true stress fractures tended to disappear in a cloud of ambiguity. This cast doubt on the association with bisphosphonates. The association was then re-established by large epidemiological studies based on radiographic adjudication. Atypical fractures are largely caused by bisphosphonates. With a correct indication, bisphosphonates prevent many more fractures than they cause, at least during the first years of use. With an incorrect indication they are likely to cause more harm than good. (C) 2016 Elsevier Ltd. All rights reserved.

Place, publisher, year, edition, pages
ELSEVIER SCI LTD, 2016
Keyword
atypical fractures; bisphosphonates; proximal femoral fractures; osteoporosis
National Category
Orthopaedics
Identifiers
urn:nbn:se:liu:diva-124476 (URN)10.1016/S0020-1383(16)30007-9 (DOI)000367533000007 ()26768286 (PubMedID)
Note

Funding Agencies|Eli Lilly; Amgen

Available from: 2016-02-02 Created: 2016-02-01 Last updated: 2018-01-10
Kharazmi, M., Hallberg, P., Schilcher, J., Aspenberg, P. & Michaelsson, K. (2016). Mortality After Atypical Femoral Fractures: A Cohort Study. Journal of Bone and Mineral Research, 31(3), 491-497
Open this publication in new window or tab >>Mortality After Atypical Femoral Fractures: A Cohort Study
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2016 (English)In: Journal of Bone and Mineral Research, ISSN 0884-0431, E-ISSN 1523-4681, Vol. 31, no 3, p. 491-497Article in journal (Refereed) Published
Abstract [en]

Although osteoporotic fracture rates can be reduced by bisphosphonates, prolonged therapy is associated with higher risk of atypical femoral fractures. Ordinary fragility fractures are linked to high mortality rates. We aimed to determine whether atypical femoral fractures also confer excess mortality. Radiographs were reviewed for all patients aged 55 years who had experienced a subtrochanteric or femoral shaft fracture in Sweden in 2008 to 2010. The fractures were classified as either atypical or ordinary. Data on medication use, coexisting conditions, and date of death were obtained from national registers. We estimated multivariable-adjusted relative risks of death after atypical femoral fractures compared with ordinary subtrochanteric or femoral shaft fractures and calculated age- and sex-standardized mortality ratios (SMRs) for atypical and ordinary fractures compared with the population average. During a mean of 4 years of follow-up, 39 of 172 (23%) patients with an atypical fracture had died compared with 588 of 952 (62%) with an ordinary fracture, corresponding to a relative risk of 0.51 (95% confidence interval [CI] 0.38-0.68). The lower risk was evident in both users and nonusers of bisphosphonates. No patient with atypical fracture died in the first year after fracture. Individuals with an ordinary fracture had a higher mortality risk than the general population (SMR=1.82; 95% CI 1.69-1.99), but no excess risk was found in patients with atypical fracture (SMR=0.92; 95% CI 0.65-1.26). We conclude that in contrast to ordinary subtrochanteric and femoral shaft fractures, atypical femoral fractures are not associated with excess mortality. (c) 2015 American Society for Bone and Mineral Research.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2016
Keyword
ATYPICAL FRACTURE; OSTEOPOROSIS; FEMORAL FRACTURE; BISPHOSPHONATES; MORTALITY
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-127577 (URN)10.1002/jbmr.2767 (DOI)000373596800003 ()26676878 (PubMedID)
Note

Funding Agencies|Swedish Research Council

Available from: 2016-05-03 Created: 2016-05-03 Last updated: 2017-11-30
Michaelsson, K. & Aspenberg, P. (2016). Postmenopausal Osteoporosis [Letter to the editor]. New England Journal of Medicine, 374(21), 2095-2097
Open this publication in new window or tab >>Postmenopausal Osteoporosis
2016 (English)In: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 374, no 21, p. 2095-2097Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Massachusetts Medical Society, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-129152 (URN)10.1056/NEJMc1602599 (DOI)000376443500020 ()27223158 (PubMedID)
Available from: 2016-06-13 Created: 2016-06-13 Last updated: 2017-11-28Bibliographically approved
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