Pain and negative mood during rehabilitation after anterior cruciate ligament reconstruction: a daily process analysis.

Daily diary methods were used to examine changes in pain and negative mood over the first 6 weeks of rehabilitation after surgical reconstruction of the anterior cruciate ligament (ACL). Participants (58 men and 33 women) completed measures of personal factors (i.e., age, athletic identity, neuroticism, optimism) before surgery and indices of daily pain, negative mood, and stress for 42 days after surgery. Multilevel modeling revealed that, as would be expected, daily pain ratings decreased significantly over the course of the study and that the rate of decline in pain ratings decreased over time. Age and daily negative mood were positively associated with daily pain ratings. Daily negative mood also decreased significantly over the course of the study and was positively associated with neuroticism, daily pain, and daily stress. Athletic identity and optimism interacted with time since surgery in predicting daily negative mood such that participants with high levels of athletic identity and low levels of optimism reported greater decreases in daily negative mood over time. Overall, the findings reveal a pattern of improved psychological functioning over the early stages of post-operative ACL rehabilitation.

Biochemical pathway mediating the response of bone cells to capacitive coupling.

Rat calvarial bone cells or mouse MC3T3-E1 bone cells subjected to a capacitively coupled electric field of 20 mV/cm consistently showed significant increases in cellular proliferation as determined by deoxyribonucleic acid content. Verapamil, a membrane calcium channel blocker; W-7, a calmodulin antagonist; indocin, a prostaglandin synthesis inhibitor; or bromophenacyl bromide, a phospholipase A2 inhibitor, each at a concentration that did not interfere with cell proliferation in control cultures, inhibited proliferation in those cultures subjected to the electric field. In contrast, neomycin, an inhibitor of the inositol phosphate cascade, did not inhibit this electrically induced cellular proliferation. Prostaglandin E2 production also was increased significantly with electrical stimulation, and this increase was inhibited by verapamil or indocin but not by neomycin. Thus, the data suggest that the signal transduction mediating the proliferative response of cultured bone cells to a capacitively coupled field involved transmembrane calcium translocation via voltage gated calcium channels, activation of phospholipase A2, and a subsequent increase in prostaglandin E2. Increases in cytosolic calcium and activated calmodulin are implied. The inositol phosphate pathway, unlike its dominant role in signal transduction in mechanically stimulated bone cells, does not appear to play a role in signal transduction in the proliferative response of bone cells to electrical stimulation.

The biochemical pathway mediating the proliferative response of bone cells to a mechanical stimulus.

Calvarial bone cells of rats were subjected to either a cyclic biaxial strain of 0.17 per cent (1700 microstrain) or a hydrostatic pressure of 2.5, five, or ten pounds per square inch (17.2, 34.5, or sixty-nine kilopascals). The frequency was held constant at one hertz for both types of mechanical stimulation. When cultured bone cells that had been subjected to a cyclic biaxial strain for two hours were harvested twenty-two hours later, it was found that the level of prostaglandin E2 had increased significantly (p < 0.01) as had cellular proliferation (p < 0.01), as indicated by the incorporation of [3H]-thymidine. The addition to the medium of indomethacin, an inhibitor of prostaglandin synthesis, at a ten-micromolar concentration significantly inhibited (p < 0.01) the increase in prostaglandin E2 synthesis but had no effect on the strain-induced increase in cellular proliferation, as indicated by the incorporation of [3H]-thymidine. Twenty-four hours after exposure to the same cyclic biaxial strain for thirty seconds, other cultured bone cells showed a significant increase in the level of cytoskeletal calmodulin (p < 0.05) and in the DNA content (p < 0.05). N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7), a calmodulin antagonist, was added to the medium at a one-micromolar concentration, which had been shown to have no effect on the increase in the DNA content of control cells; W-7 completely blocked the increase in the level of cytoskeletal calmodulin and in the DNA content in the cells that were subjected to a cyclic biaxial strain. The bone cells subjected to a hydrostatic pressure showed a dose-dependent increase in the concentration of cytosolic Ca2+, as measured with Fura 2-AM, a fluorescent indicator of intracellular calcium. With a pressure of ten pounds per square inch (sixty-nine kilopascals), the increase in the concentration of cytosolic Ca2+ was nearly eight times greater than that at 2.5 pounds per square inch (17.2 kilopascals) (126 +/- 15.2 compared with 16 +/- 8.0 nanomolar, mean and standard deviation). The addition to the medium of neomycin, an inhibitor of the inositol phosphate cascade, at a ten-millimolar concentration completely blocked the increase in the concentration of cytosolic Ca2+ in these cells; this concentration of neomycin had been shown to have no effect on proliferation in control bone cells. There was also a dose-dependent relationship between the duration of the stimulus and the cellular proliferation. Remarkably, one cycle of pressure at ten pounds per square inch (sixty-nine kilopascals) and a frequency of approximately one hertz produced a 57 per cent increase in the incorporation of [3H]-thymidine at twenty-four hours (p < 0.001). From these findings, we hypothesized that the inositol phosphate cascade-cytosolic Ca(2+)-cytoskeletal calmodulin system plays a dominant role in the signal transduction of a mechanical stimulus into increased proliferation of bone cells, at least under the conditions reported here.

Failure of anterior cruciate ligament reconstruction: the biologic basis.

The replacement tissue used for anterior cruciate ligament reconstruction undergoes extensive biologic remodeling and incorporation after implantation. Successful biologic incorporation of the graft is dependent on a number of factors including graft placement, tensioning, and the nature of the tissue (allograft versus autograft). Failure of an anterior cruciate ligament reconstruction may occur on the basis of either technical, mechanical, or biological factors. Biologic factors include cellular repopulation, matrix remodeling, the ultimate small diameter collagen fibril orientation, the final cross sectional area of the graft, a favorable vascularization, and not overloading the graft during the remodeling process. The fully incorporated graft never duplicates the native anterior cruciate ligament but works as a check reign that makes the knee more functional.