Abstract

BackgroundReports showing high recurrence rates for intralesional curettage and bone grafting have made the current treatment principle for fibrous dysplasia controversial. This study aimed to report the postoperative clinical outcomes from three minimally invasive surgical strategies we use for monostotic fibrous dysplasia (MFD).Patients and methodsTwelve patients with MFD presenting with no pathologic fracture or deformity and treated with one of three surgical strategies—plain open biopsy, plain alpha-tricalcium phosphate (ATP) reconstruction, and prophylactic bridge plating—were included. There were nine men and three women, with median age of 38 years. Mean follow-up was 88 weeks. Five cases involved the proximal femur, two each involved the femoral and tibial diaphyses, and one each involved the distal humerus, radial diaphysis, and proximal tibia. All cases were reviewed for functional and radiological outcomes.ResultsMedian time to full activity was 1 day (range 1 to 3) for the plain open biopsy group, while the prophylactic bridge-plating and plain ATP reconstruction groups had longer median recovery times (59 days, range 3 to 143, and 52 days, range 11 to 192, respectively). Musculoskeletal Tumor Society scores at last follow-up were excellent for all the cases (mean 29.6, range 25 to 30). Radiological analysis using Gaski et al.’s criteria showed plain open biopsy resulted in partial resolution of proximal femoral lesions, while ATP reconstruction and prophylactic plating resulted in no change and progression in this lesion site, respectively. For femoral diaphyseal lesions, prophylactic plating resulted in partial resolution, while ATP reconstruction resulted in no change. In the tibial diaphysis, prophylactic plating resulted in partial resolution, while plain open biopsy resulted in no change. For the lesions involving the distal humerus and the proximal tibia, plain open biopsy resulted in partial resolution, while for the radial diaphyseal lesion, ATP reconstruction resulted in no change. Radiological progression was limited in 11 (92%) cases, and none had postoperative complications.ConclusionPlain open biopsies for asymptomatic lesions; prophylactic bridge plating for symptomatic, large diaphyseal lytic lesions; and plain ATP reconstructions for both small and large nondiaphyseal symptomatic lytic lesions may be acceptable alternatives to curettage-incorporating procedures for MFD.

Highlights

  • Reports showing high recurrence rates for intralesional curettage and bone grafting have made the current treatment principle for fibrous dysplasia controversial

  • Plain open biopsies for asymptomatic lesions; prophylactic bridge plating for symptomatic, large diaphyseal lytic lesions; and plain alpha-tricalcium phosphate (ATP) reconstructions for both small and large nondiaphyseal symptomatic lytic lesions may be acceptable alternatives to curettage-incorporating procedures for monostotic fibrous dysplasia (MFD)

  • Analysis of radiological outcomes per lesion site shows that plain open biopsy resulted in the partial resolution of lesions located in the proximal femur, while plain ATP reconstruction and prophylactic bridge plating resulted in no change and progression in this lesion site, respectively

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Summary

Introduction

Reports showing high recurrence rates for intralesional curettage and bone grafting have made the current treatment principle for fibrous dysplasia controversial. This study aimed to report the postoperative clinical outcomes from three minimally invasive surgical strategies we use for monostotic fibrous dysplasia (MFD). Fibrous dysplasia (FD) is a developmental, nonneoplastic disorder that is associated with mosaic somatic activating mutations in GNAS, which encodes the cAMP pathway-associated G-protein, Gsα, and affects tissues derived from the ectoderm, mesoderm, and endoderm [1]. There is a wide range of involvement and it can vary from an isolated single lesion in a single bone (monostotic) to involvement of many bones (polyostotic), if not the entire axial and appendicular skeleton [3]. Increased Gsα signaling is the underlying cause of the bone and skin lesions, accelerating both the osteogenic commitment of bone marrow stromal cells but inhibiting their further differentiation into osteoblasts [6] and the action of alphamelanocyte-stimulating hormone (alpha-MSH) to stimulate melanin production [7], respectively

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