The Biobehavioral Family Model: An Evidence-Based Approach to Biopsychosocial Research, Residency Training, and Patient Care.

Engel's biopsychosocial model, based in systems theory, assumes the reciprocal influence of biological, psychological, and social factors on one another and on mental and physical health. However, the model's application to scientific study is limited by its lack of specificity, thus constraining its implementation in training and healthcare environments. The Biobehavioral Family Model (BBFM) is one model that can facilitate specification and integration of biopsychosocial conceptualization and treatment of illness. The model identifies specific pathways by which family relationships (i.e., family emotional climate) impact disease activity, through psychobiological mechanisms (i.e., biobehavioral reactivity). Furthermore, it is capable of identifying positive and negative effects of family process in the same model, and can be applied across cultural contexts. The BBFM has been applied to the study of child health outcomes, including pediatric asthma, and adult health, including for underserved primary care patients, minoritized samples, and persons with chronic pain, for example. The BBFM also serves as a guide for training and clinical practice; two such applications are presented, including the use of the BBFM in family medicine residency and child and adolescent psychiatry fellowship programs. Specific teaching and clinical approaches derived from the BBFM are described in both contexts, including the use of didactic lecture, patient interview guides, assessment protocol, and family-oriented care. Future directions for the application of the BBFM include incorporating temporal dynamics and developmental trajectories in the model, extending testable theory of family and individual resilience, examining causes of health disparities, and developing family-based prevention and intervention efforts to ameliorate contributing factors to disease. Ultimately, research and successful applications of the BBFM could inform policy to improve the lives of families, and provide additional support for the value of a biopsychosocial approach to medicine.

Production of VEGF receptor 1 and 2 mRNA and protein during endochondral bone repair is differential and healing phase specific.

Physiological disturbances, including temporary hypoxia, are expected to drive angiogenesis during bone repair. Evidence suggests that the angiogenic ligand vascular endothelial growth factor (VEGF)-A plays an important role in this process. We characterized the expression of two receptors that are essential for mediating VEGF signaling, VEGFR1/Flt-1 and VEGFR2/Flk-1/KDR, in a mouse rib fracture model. Their mRNA and protein levels were assessed in four healing phases, which were characterized histologically as hemorrhage formation on postfracture day (PFD) 1, inflammatory response on PFD 3, initiation of callus development on PFD 7, and the presence of a mature callus on PFD 14. Transcript was detected for VEGFR1 and VEGFR2, as well as VEGF. While mRNA expression of VEGFR1 was monophasic throughout all healing phases, VEGFR2 showed a biphasic profile with significantly increased mRNA expression during callus formation and maturation. Expression of VEGF mRNA was characterized by a more gradual increase during callus formation. The protein level for VEGFR1 was below detection sensitivity during the initial healing phase. It was then restored to a stable level, detectable through the subsequent healing phases. Hence, the VEGFR1 protein levels partially mirrored the transcript expression profile. In comparison, the protein level of VEGFR2 increased gradually during the healing phases and peaked at callus maturation. This correlated well with the transcriptional expression of VEGFR2. Intact bone from age-matched male mice had considerable protein levels of VEGFR1 and VEGF, but no detectable VEGFR2. Together, these findings uncovered expression signatures of the VEGF-VEGFR axis in endochondral bone repair.

Cancellous bone osseointegration is enhanced by in vivo loading.

Biophysical stimuli may be an effective therapy to counteract age-related changes in bone structure that affect the primary stability of implants used in joint replacement or fracture fixation. The influence of controlled mechanical loading on osseointegration was investigated using an in vivo device implanted in the distal lateral femur of 12 male rabbits. Compressive loads (1 MPa, 1 Hz, 50 cycles/day, 4 weeks) were applied to a porous titanium foam implant and the underlying cancellous bone. The contralateral limbs served as nonloaded controls. Backscattered electron imaging indicated that the amount of bone ingrowth was significantly greater in the loaded limb than in the nonloaded control limb, whereas the amount of underlying cancellous periprosthetic bone was similar. No significant difference in the mineral apposition rate of the bone ingrowth or periprosthetic bone was measured in the loaded compared to the control limb. Histological analysis demonstrated newly formed woven bone in direct apposition to the implant coating, with a lack of fibrous tissue at the implant-periprosthetic bone interface in both loaded and nonloaded implants. The lack of fibrous tissue demonstrates that mechanical stimulation using this model significantly enhanced cancellous bone ingrowth without the detrimental effects of micromotion. These results suggest that biophysical therapy should be further investigated to augment current treatments to enhance long-term fixation of orthopedic devices. Additionally, this novel in vivo loading model can be used to further investigate the influence of biophysical stimulation on other tissue engineering approaches requiring bone ingrowth into both metallic and nonmetallic cell-seeded scaffolds.