Dolph Houben

12 CHAPTER 1 The Clinical Problem: segmental bone and joint loss Segmental loss of bone and/or joint in the appendicular skeleton results from limb-sparing resection of primary bone tumors (3450 cases/year in 2018) [1] , metastatic tumors, severe complex trauma, infection, congenital deficiency or failed primary reconstruction. Frequent complications occur with current available reconstructive methods, including cryopreserved bone allografts, vascularized bone autografts, prosthetic replacement, reimplantation of autoclaved tumor bone, bone transport, or a combination of vascularized autografts with massive allograft as discussed below. Future reconstructive methods may use a different approach by reconstructing the defect with “like for like” living tissue while minimalizing complications. Cryopreserved bone allograft (CBA) reconstruction Reconstruction of segmental defects with a CBA provides immediate stability and bulk when combined with rigid internal fixation. They are widely used since they are easy to size and shape to match the defect. CBAs do not contain viable cells due to the process of freezing or irradiation, which diminishes the immunologic response. Therefore, bone healing occurs by creeping substitution. This is a slow and incomplete process, which is mostly seen at the host/allograft junction and periosteal surfaces. Fifty percent of the lamellar bone remains necrotic over time, with resorption of the CBA as result. Therefore, significant weakening results at 6-12 months after reconstruction [2] . Although CBAs do not contain viable cells, a host immune response occurs which includes the development of anti-HLA antibodies [3, 4] . Clinical outcomes of CBA reconstruction are often problematic with high incidences of non-union (14%), stress fractures (19%) and infection (12.8%) [5, 6] . Fracture and non-union require revision since they lack the ability to repair and remodel [7] . Infection is a catastrophic complication. Due to the avascular status neither the immune system nor antibiotics will reach the infected bone. ischemia-reperfusion requires allograft removal and has a significant risk of recurrence when revised [4, 5] . Vascularized bone autograft (VBG) reconstruction Transfer of living bone has been a reconstructive method since 1905 [8-10] . The first free vascularized fibula transfer was described in 1975 [11] . Other donor sites included rib, iliac crest, scapula, radius, femoral condyle and trochanteric bone [12] . VBGs are indicated in large segmental bone defects or can also be used in smaller bone defects where other non-vascularized options are likely to result in “biologic failure”. Examples include persistent non-union after CBA reconstruction, scarred or irradiated soft tissue beds, and the need to re-vascularize avascular bone in cases of radionecrosis [13-16] . Other indications include tissue loss requiring composite bone/soft tissue reconstruction, joint arthrodesis, congenital pseudarthrosis and need for longitudinal bone growth requiring physeal transfer possible with the inclusion of the proximal fibular epiphysis and physis [16-18] . VBG remain viable due to maintenance of its endosteal and/or periosteal circulation provided by microvascular repair of its vascular supply. Therefore, osteocytes and other cellular components remain viable. No creeping substitution occurs, obviating osteocytopenia and resulting in improved strength and healing capacity compared to other methods [15, 19] . Up to 80% of the structural VBG will show significant hypertrophy over time in response to stress loading by 24 months following reconstructive surgery [20, 21] . In many instances, VBGs require protection