Periosteal response to transient ischemia: Histological studies on the rat tibia

Svindland, Aud; Nordsletten, Lars; Reikerås, Olav; Skjeldal, Sigmund

doi:10.3109/17453679508995589

Cited by 18 publications

(10 citation statements)

References 13 publications

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“…Hsieh et al [31] reported that reperfusion injury in bone the mechanism spreading ischemia to more vessels was supported by a decrease in reperfusion and caliber of vessels, and an increase in vascular permeability, leukocyte adherence, and net bone resorption after 24 h of reperfusion phase. Svindland et al [21] showed that there was marked hypertrophy and hyperplasia of the cells at periost, similar to the initial formation of external callus during fracture healing, without fracture after ischemia-reperfusion. But Kase et al [22] reported that ischemia-reperfusion did not affect to tibia fracture healing, although bone mineral turnover was found to be lower in the ischemic-reperfusion group.…”

Section: Discussionmentioning

confidence: 94%

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Effect of Preconditioned Hyperbaric Oxygen and Ozone on Ischemia-Reperfusion Induced Tourniquet in Skeletal Bone of Rats

Koca

Yurttaş

Bïlgïç

et al. 2010

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 94%

“…However, some studies showed that fracture resulted in oxidative stress by increasing MDA both animals [19] and humans [20]. In addition, one study [21] reported that IR increased bone formation, while another study [22] indicated IR did not influence fracture healing. We wondered whether IR affects the bone like other tissues or not.…”

Section: Introductionmentioning

confidence: 99%

Effect of Preconditioned Hyperbaric Oxygen and Ozone on Ischemia-Reperfusion Induced Tourniquet in Skeletal Bone of Rats

Koca

Yurttaş

Bïlgïç

et al. 2010

Journal of Surgical Research

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“…Otero-Cagide et al 9 speculated that the bone formation after an FGG may be the result of a combination of periosteal trauma during site preparation and the activation of osteoprecursor cells contained in the connective tissue of the graft. Svindland et al 10 suggested vascular disruption as a consequence of the surgical trauma results in transient ischaemia in the periosteum, which would produce hypertrophy and hyperplasia of the periosteal cells, with an osteogen differentiation. Among the related reports, all the authors suggest that the periosteal trauma seemed to be the main aetiological agent associated with the exostosis development 3–5.…”

Section: Discussionmentioning

confidence: 99%

Alveolar bone exostoses subsequent to orthodontic implant placement

et al. 2013

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Alveolar bone exostoses (ABE), also known as a buttress bone formation, are not uncommon to the literature. Although, exostoses in response to the trauma from occlusion are a popular concept proposed more than 45 years ago, still the aetiological factors behind this development are unclear. Various risks and complications associated with orthodontic implants have been published, but buttress bone formation subsequent to this procedure has not been reported till date. This article describes a case of ABE, subsequent to the placement of orthodontic mini implants, where after careful evaluation, resective osseous surgery was performed.

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“…For this reason, only a few methods are available for investigating the microcirculation of the periosteum of the calvaria in vivo. Previous studies of the periosteum have therefore been based on acute examinations especially of histological specimens [23,24]. The chamber model presented here allowed us to evaluate the periosteum in vivo repeatedly over several days [19].…”

Section: Discussionmentioning

confidence: 99%

Increase in periosteal angiogenesis through heat shock conditioning

et al. 2011

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ObjectiveIt is widely known that stress conditioning can protect microcirculation and induce the release of vasoactive factors for a period of several hours. Little, however, is known about the long-term effects of stress conditioning on microcirculation, especially on the microcirculation of the periosteum of the calvaria. For this reason, we used intravital fluorescence microscopy to investigate the effects of heat shock priming on the microcirculation of the periosteum over a period of several days.MethodsFifty-two Lewis rats were randomized into eight groups. Six groups underwent heat shock priming of the periosteum of the calvaria at 42.5°C, two of them (n = 8) for 15 minutes, two (n = 8) for 25 minutes and two (n = 8) for 35 minutes. After 24 hours, a periosteal chamber was implanted into the heads of the animals of one of each of the two groups mentioned above. Microcirculation and inflammatory responses were studied repeatedly over a period of 14 days using intravital fluorescence microscopy. The expression of heat shock protein (HSP) 70 was examined by immunohistochemistry in three further groups 24 hours after a 15-minute (n = 5), a 25-minute (n = 5) or a 35-minute (n = 5) heat shock treatment. Two groups that did not undergo priming were used as controls. One control group (n = 8) was investigated by intravital microscopy and the other (n = 5) by immunohistochemistry.ResultsDuring the entire observation period of 14 days, the periosteal chambers revealed physiological microcirculation of the periosteum of the calvaria without perfusion failures. A significant (p < 0.05) and continuous increase in functional capillary density was noted from day 5 to day 14 after 25-minute heat shock priming. Whereas a 15-minute exposure did not lead to an increase in functional capillary density, 35-minute priming caused a significant but reversible perfusion failure in capillaries. Non-perfused capillaries in the 35-minute treatment group were reperfused by day 10. Immunohistochemistry demonstrated an increase in cytoprotective HSP70 expression in the periosteum after a 15-minute and a 35-minute heat shock pretreatment when compared with the control group. The level of HSP70 expression that was measured in the periosteum after 25 minutes of treatment was significantly higher than the levels observed after 15 or 35 minutes of heat shock exposure.ConclusionA few days after heat shock priming over an appropriate period of time, a continuous increase in functional capillary density is seen in the periosteum of the calvaria. This increase in perfusion appears to be the result of the induction of angiogenesis.

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Periosteal response to transient ischemia: Histological studies on the rat tibia

Cited by 18 publications

References 13 publications

Effect of Preconditioned Hyperbaric Oxygen and Ozone on Ischemia-Reperfusion Induced Tourniquet in Skeletal Bone of Rats

Effect of Preconditioned Hyperbaric Oxygen and Ozone on Ischemia-Reperfusion Induced Tourniquet in Skeletal Bone of Rats

Alveolar bone exostoses subsequent to orthodontic implant placement

Increase in periosteal angiogenesis through heat shock conditioning

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