Removal of patient-specific reconstruction plates after mandible reconstruction with a fibula free flap: is the plate the problem?

Computer-aided microvascular mandible reconstruction is an increasingly common procedure in oral and maxillofacial surgery. The aim of this retrospective single-centre study was to evaluate the rate and specifics of hardware removal after fibula free flap (FFF) fixation with a patient-specific reconstruction plate. The study included patients who underwent hardware removal between April 2017 and October 2019. Statistical analyses were performed regarding the different indications for plate removal (dental implantation versus complication) and the surgical approach (intraoral versus extraoral). Plate removal was performed in 29 of 98 patients (29.6%) after FFF fixation with a patient-specific reconstruction plate. Plate removal was done prior to dental implantation in 58.6% of cases and due to complications in 41.4%. Complications seen between reconstructive surgery and plate removal were less frequent in the dental rehabilitation group (8/17 vs 12/12; P=0.002). Within this group, 35.3% of plates were removed intraorally, and the majority of partial plate removals were performed in the patients with plate removal for dental rehabilitation (72.7% vs 27.3%). Hospitalization was shorter with an intraoral approach (1.7 days vs 4.0 days, P=0.052). The removal of patient-specific reconstruction plates prior to dental implantation is often partial and can be performed intraorally. The use of patient-specific miniplates for fixation of FFF might facilitate later dental rehabilitation.

Biomechanical comparison of polylactide-based versus titanium miniplates in mandible reconstruction in vitro.

OBJECTIVES: Evaluation of the mechanical integrity and reliability of polylactide-based miniplates for osseous free flap fixation at the mandible in an experimental study setup of a mandible reconstruction model. MATERIAL AND METHODS: 1.0mm titanium miniplates (group TI) (MatrixMandible, DePuy Synthes, Umkirch, Germany) and 1.5mm polylactide miniplates (group PL) (Inion CPS, Inion Oy, Tampere, Finland) were used to fix a polyurethane (PU) fibula segment to a PU mandible reconstruction model using monocortical non-locking screws. Mastication was simulated via unilateral cyclic dynamic loading at 1Hz with increasing loads (+ 0.15N/cycle, Bionix, MTS, USA). A 3D optical tracking system (Aramis, GOM, Braunschweig, Germany) was used to determine interosteotomy movements (IOM). RESULTS: IOM were higher in the polylactide group (distal: P=0.001, mesial: P=0.001). Differences in mean stiffness (titanium: 478±68N/mm; polylactide: 425±38N/mm, P=0.240) and mean force at a vertical displacement of 1.0mm (titanium: 201.6±87.1N; polylactide: 141.3±29.9N, P=0.159) were not significant. CONCLUSIONS: The results of this study suggest that polylactide-based miniplates provide reduced mechanical integrity and higher interosteotomy movements in comparison to titanium miniplates in vitro. Indications for clinical use of polylactide-based miniplates in mandible reconstruction have to be placed critically. Future studies will focus on clinical complications of polylactide-based plates in risk patients.

Complication rates and clinical outcomes of osseous free flaps: a retrospective comparison of CAD/CAM versus conventional fixation in 128 patients.

Studies evaluating plate-related complications in patient-specific versus conventional fixation systems in free flap surgery are lacking. This was a retrospective study of 128 osseous free flaps with a minimum follow-up of 12 months. Wound healing disorders, plate exposure, fixation failure, and subtotal osseous union were recorded and evaluated statistically by univariate and regression analysis. Complication rates were as follows: wound healing disorders 33.6% (computer-aided design and computer-aided manufacturing (CAD/CAM) vs. conventional: 35.1% vs. 33.0%); plate exposure 21.9% (29.7% vs. 18.7%); fixation failure 7.0% (8.1% vs. 6.6%); subtotal osseous union 36.7% (45.9% vs. 33.0%). Radiotherapy (P<0.001) and more than two segments (P=0.026) were independent variables for the overall complication rate and were negatively correlated with the dental implantation rate. The time between diagnosis and ablative surgery was increased by 11.0days in the CAD/CAM group (34.2±16.2days vs. 23.2±12.0 days; P=0.002). Rates of dental rehabilitation were not significantly different (35.1% vs. 44.0%, P=0.358). On average, 3.2±1.7 dental implants were placed into flap segments. Plate-related complications were increased with radiotherapy and multisegment flaps. There was a non-significant trend towards increased complications with patient-specific plates in comparison to conventional reconstruction plates.

Free flap surgery in Europe: an interdisciplinary survey.

Free flap surgery is essential for the aesthetic and functional reconstruction of various parts of the body. The aim of this study was to compare current concepts of perioperative flap management between ENT, craniomaxillofacial, and plastic surgeons. A European survey was conducted among 570 surgical departments, covering all aspects of free flap surgery. Focus was placed on antibiotic and antithrombotic drug use, aspects of osseous reconstruction, and flap monitoring strategies. One hundred and seventy-two medical units participated. A broad spectrum of anticoagulant regimens and a trend towards prolonged antibiotic prophylaxis were found. Fixation with (CAD/CAM) reconstruction plates was more popular than monocortical locking with miniplates in the mandible. Visual assessment and Doppler systems were reported to be the most common monitoring modalities. The flap loss rate was stated to be higher after osseous reconstruction. Only a few differences in perioperative flap management were identified between the different surgical fields, and osseous reconstruction appears to be the most challenging.

Effects of extracellular phosphate on gene expression in murine osteoblasts.

That phosphate homeostasis is tightly linked to skeletal mineralization is probably best underscored by the fact that the phosphaturic hormone FGF23 is primarily expressed by terminally differentiated osteoblasts/osteocytes and that increased circulating FGF23 levels are causative for different types of hypophosphatemic rickets. In contrast, FGF23 inactivation results in hyperphosphatemia, and unexpectedly this phenotype is associated with severe osteomalacia in Fgf23-deficient mice. In this context it is interesting that different cell types have been shown to respond to extracellular phosphate, thereby raising the concept that phosphate can act as a signaling molecule. To identify phosphate-responsive genes in primary murine osteoblasts we performed genome wide expression analysis with cells maintained in medium containing either 1 or 4 mM sodium phosphate for 6 h. As confirmed by qRT-PCR, this analysis revealed that several known osteoblast differentiation markers (Bglap, Ibsp, and Phex) were unaffected by raising extracellular phosphate levels. In contrast, we found that the expression of Enpp1 and Ank, two genes encoding inhibitors of matrix mineralization, was induced by extracellular phosphate, while the expression of Sost and Dkk1, two genes encoding inhibitors of bone formation, was negatively regulated. The ability of osteoblasts to respond to extracellular phosphate was dependent on their differentiation state, and shRNA-dependent repression of the phosphate transporter Slc20a1 in MC3T3-E1 cells partially abolished their molecular response to phosphate. Taken together, our results provide further evidence for a role of extracellular phosphate as a signaling molecule and raise the possibility that severe hyperphosphatemia can negatively affect skeletal mineralization.

Increased expression of transthyretin in leptin-deficient ob/ob mice is not causative for their major phenotypic abnormalities.

The hormone leptin is a critical regulator of adipogenesis and energy metabolism. Similarly, leptin-deficient ob/ob mice display various metabolic abnormalities, including not only obesity and insulin resistance, but also hypogonadism and high bone mass. By genome-wide expression analysis using hypothalamus RNA from wild-type and ob/ob mice, we observed the increased expression of the gene for transthyretin (Ttr) in the latter, as confirmed by quantitative real-time-polymerase chain reaction. Because Ttr encodes a carrier protein for retinol transport, and because we further found increased retinol levels in the serum of ob/ob mice, we investigated whether the additional absence of Ttr would influence the ob/ob phenotype. It was found that Ttr-deficient ob/ob mice were indistinguishable from ob/ob littermates in terms of body weight, as well as serum glucose, insulin and cholesterol levels. Although all of these parameters were identical to wild-type controls in Ttr-deficient mice, we found that the sole deletion of Ttr caused a significant increase of trabecular bone mass, bone marrow adiposity and mean adipocyte area in white adipose tissue. Interestingly, all these latter parameters were highest in Ttr-deficient ob/ob mice, and only in these mice did we observe a full penetrance of liver steatosis at 24 weeks of age. Taken together, our data demonstrate that the increased expression of Ttr in ob/ob mice does not cause (but rather attenuates) their phenotypic abnormalities.