Biomedical subjects

P S Landry

Publications and source records attributed to P S Landry.

5 recordsLinked to original sources

PubMed2000

Effect of soft-tissue trauma on the early periosteal response of bone to injury.

OBJECTIVE: To determine whether the periosteal response to skeletal trauma is impaired when muscle is also injured, thereby providing a possible explanation for why fractures with extensive soft-tissue damage may take longer to heal. METHODS: A bone defect was made in the tibia of male Fisher rats, and the proliferative response, osteoblast concentration, and callus formation that occurred within 7 days were measured in the presence and absence of simultaneously administered model soft-tissue injury (removal of 10% of the anterior tibialis muscle from a region within 2 to 3 mm of the bone defect). Measurements were made by using autoradiography, quantitative histology, and morphometry. RESULTS: Addition of the muscle injury increased proliferation in the cambium and in the fibrous periosteum on day 1, but had no effect thereafter; proliferation of fibroblasts in the loose connective tissue above the periosteum was not affected. Addition of the muscle injury resulted in increased osteoblast levels 2 to 5 days after injury but had no effect on the amount of callus produced. CONCLUSION: The inflammatory milieu created by the muscle injury unexpectedly resulted in an increased periosteal response to skeletal trauma, suggesting that inflammatory mediators generated in response to wounding of soft tissues are unlikely to account for delayed fracture healing. These findings may indicate that surgical trauma associated with internal fixation by using plates and screws may not be as deleterious to the fracture-healing response as previously thought.

Animals↗

PubMed2000

Programmed cell death in post-traumatic bone callus.

Some osteoblasts in the expanded population of periosteal cells that occurs following bone injury are removed from the callus by apoptosis. Our objective was to study whether the consequences of activation of the death program could include feedback control of the healing response. Transforming growth factor beta and interleukin-1beta were delivered together continuously to a standardized tibial defect in rats for 3 days using implanted micro-osmotic pumps. The bones were recovered at 1, 2, 3, 5, 7, 10 and 14 days after injury (n = 6 in each treated and control group) and concentrations of proliferating cells, osteoblasts and apoptotic bodies were determined. The injury-induced apoptotic component of the healing response was shifted in time due to the combined cytokines, compared with vehicle only, with the result that the peak in the concentration of apoptotic bodies occurred 2-3 days earlier in the treated animals. Neither osteoprogenitor proliferation nor osteoblast concentration was affected by addition of the cytokines. The results suggested that activation of apoptosis during injury repair was not necessarily a passive consequence of the cellular response to injury. Programmed cell death could therefore have an active role in modulating bone repair.

Animals↗

PubMed1997

Electromagnetic fields can affect osteogenesis by increasing the rate of differentiation.

Electromagnetic fields of various kinds can alter osteogenesis in animals with osteotomies and patients with nonunions, but the underlying cellular mechanisms are unknown. The aims of this study were to determine whether I gauss at 60 Hz affected periosteal proliferation and differentiation in either the normal rat tibia or 1 to 14 days after a surgically induced defect. In the injured rats, using histologic study, autoradiography, and morphometry, it was found that exposure for 1 or 3 days had no effect on proliferation but that it produced an increase in osteoblasts 3 days after the injury. Proliferation and differentiation were unaffected by exposure in the absence of injury. The results suggest that the primary effect of the fields was to promote differentiation but not proliferation. Because fields can stimulate proliferation of osteoblastlike cells in vitro, the results of this study may indicate the presence of an in vivo factor that antagonizes the tendency of fields to increase mitotic activity.

Animals↗

PubMed1996

Bone injury response. An animal model for testing theories of regulation.

Therapeutic treatment of bone disease and attempts to accelerate normal healing require knowledge of the soluble factors that control bone repair and the specific effects that they produce. To facilitate study of this regulatory system, an animal model involving creation of a hole in the cortex of the rat tibia was developed. Proliferation, differentiation, and callus formation at the injury site were measured more precisely than in previous animal models by means of autoradiographic, histologic, histochemical, and morphometric methods. Several novel features of bone healing were observed, including the following: (1) synthesis of bone matrix in the defect occurred only after a cambial compartment was established by regeneration of the fibrous periosteum and (2) at least 3 kinds of osteoblasts could be distinguished depending on when and where they deposited calcifiable matrix. The model is well suited to evaluating the use of interventional strategies that involve chemical or electrical agents because the cellular parameters of interest can be measured precisely.

Animals↗

PubMedDate not supplied

Regulation of osteoblast levels during bone healing.

OBJECTIVE: To confirm the occurrence of programmed cell death of osteoblasts during bone healing and to evaluate the role of interleukin-1beta (IL-1beta) in regulating osteoblast concentration. STUDY DESIGN: Electron microscopic study of the response of rats to a controlled bone injury, and a randomized controlled study of the effect of IL-1beta administered continuously for three days. METHODS: A standardized defect (1.1 millimeter in diameter, 0.5 millimeter deep) was created unilaterally on the anteromedial surface of the tibia. In some animals, the injury site was recovered five days after operation and processed for ultrastructural evaluation of osteoblasts in the callus. In another group, IL-1beta was delivered to the bone defect using micro-osmotic pumps (0.5 nanograms/hour); control rats received vehicle only. The bones were recovered one to fourteen days after injury, and concentrations of proliferating cells, osteoblasts, and apoptotic bodies were determined. The amount of callus that formed in the defect was measured. RESULTS: Osteoblasts in the callus exhibited ultrastructural changes characteristic of cells undergoing apoptosis, including condensation of chromatin, membrane blebbing, formation of apoptotic bodies, and phagocytosis by nearby osteoblasts. Addition of IL-1beta significantly increased the number of osteoblasts at the injury site and significantly decreased the number of apoptotic bodies in relation to the number of osteoblasts. The amount of callus in the bone defect was not affected by IL-1beta treatment. CONCLUSION: The role of programmed cell death of osteoblasts as a normal concomitant of bone healing was confirmed. Evidence was found suggesting that IL-1beta mediated the appearance and disappearance of osteoblasts, possibly by affecting the rates of differentiation and apoptosis, respectively. Understanding these mechanisms conceivably could lead to the ability to control osteoblast levels at an injury site.

Animals↗