Drugs and fracture repair

Aspenberg, Per

doi:10.1080/17453670510045318

Cited by 89 publications

(61 citation statements)

References 63 publications

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“…Relatively speaking, Cox2 produces huge amounts of prostaglandins, so when Cox2 is turned on, the production from Cox1 becomes neglible. Thus, in fracture repair, both unspecific and specific Cox2 inhibitors dramatically reduce prostaglandin production and should therefore be expected to have similar effects 11 . There is a substantial amount of literature on the effects of Cox inhibitors on bone repair in experimental animals.…”

Section: Discussionmentioning

confidence: 99%

“…In those studies where Cox inhibitors appear harmless, the dosing of the Cox inhibitor may be inadequate. In male rats, the selective Cox2 inhibitors celecoxib and rofecoxib are metabolized so quickly by the liver that also a high dose given once daily will yield too low a serum concentration to be relevant 11 . In this work, the dense formation of bony trabeculae in the animals of the group III seems to be related with the use of salmon calcitonin right after the surgical procedure.…”

Section: Discussionmentioning

confidence: 99%

“…Some drugs can have effects on the proliferation of early callus tissue, others on the differentiation of chondrocytes or osteoblasts, capillary formation, sensitivity to mechanical input etc. If the repair of long bones is not optimized, it should be quite possible to enhance it by pharmacological or other means 11,12 . We chose the rat as an animal model because it is easy to obtain a homogenous sample, and it is simple to handle.…”

Section: Discussionmentioning

confidence: 99%

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Bone repair in rats treated with sodic diclofenac and calcitonin<A NAME="volta1"></A>

Sassioto¹,

Inouye²,

Aydos³

et al. 2006

Acta Cir. Bras.

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Purpose:To investigate clinical and histologically the bone repair in treated animals with calcitonin and sodic diclofenac. Methods: Ninety-six femoral defects were created in forty-eight animals distributed in four groups (n=24): either left untreated, treated with the sodic diclofenac or calcitonin or both. Follow-up was 7, 14 and 21 days. Histological sections stained by haematoxylin-eosin was observed under light microscopy (100X) and quantitatively scored for their trabecular formation. The groups and subgroups were compared being used the Kruskall-Wallis test. Results: Smaller trabecular formation was observed in the animals of the group II and larger trabecular formation in the animals of the group III. Was found significant differences in the comparison between all the groups (Kruskall-Wallis, p <0.05). Conclusion: The obtained data suggest that the bone repair is a time-dependent process, which can be delayed by the sodic diclofenac and accelerated by the calcitonina, when used separately. The associated use of calcitonina and sodic diclofenac didn't show to be the best therapeutic option in the treatment of bone defects surgically created. Key words: Osteogenesis. Anti-inflammatory agents. Calcitonin. Rats. RESUMO Objetivo:Investigar clínica e histologicamente o reparo ósseo em animais tratados com calcitonina e diclofenaco sódico. Métodos: Foram criados 96 defeitos femorais, em 48 animais distribuídos em quatro grupos (n = 24): não tratados, tratados com diclofenaco sódico ou calcitonina ou ambos. O período de seguimento foi 7, 14 e 21 dias. As secções coradas por hematoxilina e eosina foram observadas sob microscopia óptica (100x) e analisadas quantitativamente em relação à neoformação trabecular. Os grupos e subgrupos foram comparados utilizando-se o teste de Kruskall-Wallis. Resultados: Foi observada menor formação de trabéculas ósseas nos animais do grupo II e maior formação de trabéculas ósseo nos animais do grupo III. Foram encontradas diferenças significantes na comparação entre todos os grupos (Kruskall-Wallis, p <0.05). Conclusão: Os dados obtidos sugerem que o reparo ósseo é um processo tempo-dependente, que pode ser retardado pelo diclofenaco e acelerado pela calcitonina, quando utilizados isoladamente. O uso associado de calcitonina e diclofenaco sódico não mostrou ser a melhor opção terapêutica no tratamento de defeitos ósseos criados operatoriamente.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Bone repair in rats treated with sodic diclofenac and calcitonin<A NAME="volta1"></A>

Sassioto¹,

Inouye²,

Aydos³

et al. 2006

Acta Cir. Bras.

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“…Complications in bone healing including delayed fracture healing are experienced during systemic inflammation (2,(4)(5)(6). Therapeutic agents such as cyclooxygenase (COX) inhibitors and corticosteroids are factors involved in delayed fracture healing and could partly explain the delayed fracture healing observed in patients with chronic inflammation (7)(8)(9). Mechanical loading enhances endochondral ossification and fracture healing (10).…”

Section: Introductionmentioning

confidence: 99%

Serum of patients with active rheumatoid arthritis inhibits differentiation of osteochondrogenic precursor cells

Pathak

Verschueren

Lems

et al. 2016

Connective Tissue Research

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Delayed fracture healing is frequently experienced in patients with systemic inflammation such as during rheumatoid arthritis (RA). The reasons for this are diverse, but could also be caused by inflammatory cytokines and/or growth factors in serum from patients with active disease. We hypothesized that serum from patients with active RA contains circulating inflammatory factors that inhibit differentiation of osteochondrogenic precursors. Serum was obtained from 15 patients with active RA (active RA-sera) and from the same patients in clinical remission 1 year later (remission RA-sera; controls). The effect of active RA-sera on osteochondrogenic differentiation of chondrogenic ATDC5 cells and primary human periosteum-derived progenitor cells (HPDC) was determined in micromass culture. In ATDC5 cells, active RA-sera reduced Ki67 transcription levels by 40% and cartilage matrix accumulation by 14% at day 14, and Alp transcription levels by 16%, and matrix mineralization by 17% at day 21 compared with remission RA-sera. In HPDCs, active RA-sera inhibited metabolic activity by 8%, SOX9 transcription levels by 14%, and cartilage matrix accumulation by 7% at day 7 compared with remission RA-sera. In conclusion, sera from patients with active RA negatively affect differentiation of osteochondrogenic precursors, and as a consequence may contribute to delayed fracture healing in these patients. ARTICLE HISTORY

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“…Many new therapeutic strategies have been developed to accelerate fracture-healing or to diminish the complication rate during the course of fracture-healing 16,17 . Existing treatment protocols have provided evidence that some approaches can influence fracture-healing 18 . However, widely accepted guidelines are needed to demonstrate the positive or negative interactions of the bioactive substances, drugs, and other agents that are being used to promote fracture-healing in clinical trials.…”

mentioning

confidence: 99%

Critical Issues in Translational and Clinical Research for the Study of New Technologies to Enhance Bone Repair

Goldhahn

Mitlak²,

Aspenberg³

et al. 2008

Journal of Bone and Joint Surgery

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Drugs and fracture repair

Cited by 89 publications

References 63 publications

Bone repair in rats treated with sodic diclofenac and calcitonin<A NAME="volta1"></A>

Bone repair in rats treated with sodic diclofenac and calcitonin<A NAME="volta1"></A>

Serum of patients with active rheumatoid arthritis inhibits differentiation of osteochondrogenic precursor cells

Critical Issues in Translational and Clinical Research for the Study of New Technologies to Enhance Bone Repair

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