Identification of novel genetic loci for bone size and mechanosensitivity in an ENU mutant exhibiting decreased bone size.

Using a dominant ENU mutagenesis screen in C57BL/6J (B6) mice to reveal gene function, we identified a mutant, 917M, with a reduced bone size phenotype, which is expressed only in males. We show that mutation results in osteoblasts with reduced proliferation, increased apoptosis, and an impaired response to in vitro mechanical load. The mutation is mapped to a novel locus (LOD score of 7.9 at 10.5 cM) on chromosome 4. INTRODUCTION: Using a dominant ENU mutagenesis screen in C57BL/6J (B6) mice to reveal gene function, we identified a mutant, 917M, with a reduced bone size phenotype, which is expressed only in males. In this report, we show the chromosomal location of this mutation using linkage analysis and cellular characterization of the mutant phenotype. MATERIALS AND METHODS: The mutant mouse was bred to wildtype B6 to produce progeny for characterization of the bone size phenotype. Periosteal osteoblasts isolated from the tibia and femur of mutant and wildtype mice were studied for proliferation, differentiation, and apoptosis potential. To determine the chromosomal location of the mutation, a low-resolution linkage map was established by completing a genome-wide scan in B6C3H F2 male mice generated from intercross breeding of mutant mice. RESULTS AND CONCLUSIONS: Mutant progeny (16 weeks old) displayed a total body bone area that was 10-13% lower and a periosteal circumference that was 5-8% lower at the femur and tibia midshaft compared with wildtype B6 mice. Periosteal osteoblasts from mutant mice showed 17-27% reduced cell proliferation and 23% increased apoptosis compared with wildtype controls. In addition, osteoblasts from mutant mice showed an impaired response to shear stress-induced proliferation rate, an in vitro model for mechanical loading. Interval mapping in B6C3H F2 males (n = 69) indicated two major loci affecting bone size on chromosome 1 at 45 cM (LOD 4.9) and chromosome 4 at 10.5 cM (LOD 7.9, genome-wide p < 0.01). Interval mapping using body weight as covariate revealed only one significant interval at chromosome 4 (LOD 6.8). Alleles of the chromosome 4 interval inherited from the B6 mutant strain contributed to a significantly lower bone size than those inherited from C3H. A pairwise interaction analysis showed evidence for a significant interaction between loci on chromosome 1 with the chromosome 4 quantitative trait loci. The 917M locus on chromosome 4 seems to be novel because it does not correspond with those loci previously associated with bone size on chromosome 4 in B6 and C3H/HeJ mice or other crosses.     

Detecting Novel Bone Density and Bone Size Quantitative Trait Loci Using a Cross of MRL/MpJ and CAST/EiJ Inbred Mice

Most previous studies to identify loci involved in bone mineral density (BMD) regulation have used inbred strains with high and low BMD in generating F₂ mice. However, differences in BMD may not be a requirement in selecting parental strains for BMD quantitative trait loci (QTL) studies. In this study, we intended to identify novel QTL using a cross of two strains, MRL/MpJ (MRL) and CAST/EiJ (CAST), both of which exhibit relatively high BMD when compared to previously used strains. In addition, CAST was genetically distinct. We generated 328 MRL × CAST F₂ mice of both sexes and measured femur BMD and periosteal circumference (PC) using peripheral quantitative computed tomography. Whole-genome genotyping was performed with 86 microsatellite markers. A new BMD QTL on chromosome 10 and another suggestive one on chromosome 15 were identified. A significant femur PC QTL identified on chromosome 9 and a suggestive one on chromosome 2 were similar to those detected in MRL × SJL. QTL were also identified for other femur and forearm bone density and bone size phenotypes, some of which were colocalized within the same chromosomal positions as those for femur BMD and femur PC. This study demonstrates the utility of crosses involving inbred strains of mice which exhibit a similar phenotype in QTL identification.     

Skeletal metastases in 102 patients evaluated before surgery for renal cell carcinoma.

During a 3-year period a consecutive series of 102 patients were treated for renal cell carcinoma at one urological unit. Thirty-three patients (32.4%) had metastatic spread, but bone metastases were found in six patients only, i.e. 5.9% of the whole series and 18.2% of the patients with metastases preoperatively. The bone metastases had in all six patients given local symptoms first indicating radiography, and thereafter radionuclide scintigraphy of the entire skeleton. Bone scintigraphy performed merely by routine in 70 patients did not reveal one single case of bone metastasis. Only one patient had a solitary bone metastasis, and this metastasis was considered inoperable because of its location and size and the patient's age. The decision about nephrectomy was not in any case altered by the finding of bone metastases. Solitary bone metastasis must be diagnosed early since they may be radically removed. Routine scintigraphy of the skeleton in symptomless patients, however, has a low yield. Screening for skeletal metastases may therefore be best performed by careful physical examination and history-taking.     

Subtalar fusion with iliac bone free flap after a recalcitrant nonunion: Report of two cases

Fractures of the calcaneus are associated with secondary osteoarthritis of the subtalar joint. In a persistent nonunion, vascularized bone flaps offer superior biologic and mechanical properties as well as accelerates joint fusion and decreases morbidity. In this report, we present results of the use of vascularized iliac bone free flap for treating subtalar failed fusions in two patients. Two patients sustained calcaneal fractures due to foot trauma, which were initially or subsequently treated with subtalar arthrodesis. Case one developed septic subtalar nonunion during treatment and case two failed three attempts at subtalar arthrodeses. The iliac crest bone flap harvested measured 4 × 4 cm (case one) and 3 × 3 cm (case two). The flap was pedicled by the deep circumflex iliac artery, which was anastomosed to the anterior tibial artery at the recipient site. No flap donor or recipient site complications occurred. Fusion was confirmed on CT scan and weight bearing was initiated at 5–6 months. At latest follow up (1–2 years), no complications occurred. Our results show that subtalar nonunion treatment with a vascularized iliac bone flap may be feasible and such a reconstruction could be clinically successful. © 2015 Wiley Periodicals, Inc. Microsurgery 36:501–506, 2016.     

Minocycline-induced Periarticular Black Bones in Inflamed Joints Which Underwent Arthroplastic Reconstruction

Background

Minocycline-induced pigmentation of bone (black bone) is well described in tooth-bearing intra-oral bone, but is less known in periarticular bone in patients who have undergone total joint arthroplasty. On a retrospective basis, we investigated the short-term clinico-radiological results of total joint arthroplasties in which the patient developed minocycline-induced periarticular black bone.

Methods

We found 5 cases (0.08%), in 4 patients, of periarticular bone pigmentation revealed during total joint arthroplasties (2 hips, 2 knees, and 1 ankle) in our series of total joint surgeries (6,548 cases) over a 10-year time period in our 3 institutes. Their mean age was 56 years at surgery. All patients had received long-term minocycline treatment. Mean dosage and duration of minocycline was 160 mg/day and 2.2 years, respectively. Minocycline had been prescribed for reactive arthritis (one), rheumatoid arthritis (two) and late infection after total joint arthroplasty (two patients). Mean follow-up period was 3.4 years after the surgeries.

Results

All cases had black or brown pigmentation in the periarticular bones during the surgery. There was no pigmentation in the cartilage or soft tissues of the joints. The mean Japanese Orthopaedic Association (JOA) score or Japanese Society for Surgery of the Foot (JSSF) scale for rheumatoid arthritis foot and ankle joints at latest follow-up (case 1, 66; case 2, 87; case 3, 77; case 4, 77; case 5, 80) improved compared to those of pre-surgery (case 1, 47; case 2, 45; case 3, 55; case 4, 34; case 5, 55). No implant loosening was noted on radiographic examination during the follow-up period. No abnormal bone formation, bone necrosis, hemosiderin deposition, malignancy or metallic debris was found on histological examination.

Conclusions

No clinico-radiological symptoms of total joint arthroplasties showed in the patients with minocycline-induced periariticular black bone in the short-term. Systemic minocycline treatment has the potential to induce significant black pigmentation of many tissues. In particular, minocycline-induced pigmentation of periarticular bone may be accelerated by inflammation due to rheumatic or pyogenic arthritis. Surgeons should recognize the risk of bone pigmentation in inflamed joints due to the systemic treatment of minocycline and explore its influence on periarticular bone and total joint arthroplasty in the long-term.     

Genome screen for quantitative trait loci underlying normal variation in femoral structure.

Femoral structure contributes to bone strength at the proximal femur and predicts hip fracture risk independently of bone mass. Quantitative components of femoral structure are highly heritable traits. To identify genetic loci underlying variation in these structural phenotypes, we conducted an autosomal genome screen in 309 white sister pairs. Seven structural variables were measured from femoral radiographs and used in multipoint sib-pair linkage analyses. Three chromosomal regions were identified with significant evidence of linkage (log10 of the odds ratio [LOD] > 3.6) to at least one femoral structure phenotype. The maximum LOD score of 4.3 was obtained for femur neck axis length on chromosome 5q. Evidence of linkage to chromosome 4q was found with both femur neck axis length (LOD = 3.9) and midfemur width (LOD = 3.5). Significant evidence of linkage also was found to chromosome 17q, with a LOD score of 3.6 for femur head width. Two additional chromosomal regions 3q and 19p gave suggestive (LOD > 2.2) evidence of linkage with at least two of the structure phenotypes. Chromosome 3 showed evidence of linkage with pelvic axis length (LOD = 3.1), midfemur width (LOD = 2.8), and femur head width (LOD = 2.3), spanning a broad (60 cm) region of chromosome 3q. Linkage to chromosome 19 was supported by two phenotypes, femur neck axis length (LOD = 2.8) and femur head width (LOD = 2.8). This study is the first genome screen for loci underlying variation in femoral structure and represents an important step toward identifying genes contributing to the risk of osteoporotic hip fracture in the general population.     

Chromosome 18 suppresses prostate cancer metastases

Loss of heterozygosity and allelic imbalance data has shown that there are two distinct regions of loss on chromosome 18q associated with the progression of prostate cancer (CaP). To investigate the functional significance of chromosome 18q loci in CaP, we utilized the technique of microcell-mediated chromosome transfer to introduce an intact chromosome 18 into the human prostate cancer cell line, PC-3. Three of the resulting hybrid lines were compared to the PC-3 cells in vitro and in vivo. The hybrid cell lines, containing an intact copy of the introduced chromosome 18, exhibited a substantial reduction in anchorage-dependent and independent growth in vitro. These hybrid cell lines also made smaller tumors in nude mice following subcutaneous injection compared to PC-3 cells. Because tumor growth was not completely eliminated by introduction of chromosome 18, we assessed the ability of the hybrids to metastasize to bone after intra-cardiac inoculation in a nude mouse model. Mice inoculated with PC-3 hybrids containing intact copies of chromosome 18 had significantly fewer bone metastases and dramatically improved survival compared to PC-3 cells. In addition, the introduction of chromosome 18 significantly reduced tumor burden in extraskeletal sites. This was not because of differences in growth rates because mice bearing hybrids were monitored for metastases over twice as long as mice bearing PC-3 cells. Taken together, these data suggest that chromosome 18 has a functional role in CaP to suppress growth and metastases. Identification of the responsible gene(s) may lead to molecular targets for drug discovery.     

Analysis of Hurthle cell neoplasms of the thyroid by interphase fluorescence in situ hybridization.

Recent studies have indicated that numerical chromosomal abnormalities including changes in p53 and cyclin D1 may be involved in Hurthle cell tumorigenesis. We analyzed a series of Hurthle cell neoplasms of the thyroid to evaluate the diagnostic and prognostic utility of numerical anomalies by DNA fluorescent probes for cyclin D1 and p53 gene loci and chromosomes 5, 7, 11, 12, 17, and 22. Interphase fluorescence in situ hybridization (FISH) analysis was performed on paraffin-embedded tissue sections from 10 Hurthle cell adenomas, 19 Hurthle cell carcinomas, and 7 normal thyroid tissues used as controls. Directly labeled fluorescent DNA probes for the centromere region of chromosomes 7, 11, 12, and 17 and locus-specific probes for chromosomes 5 and 22, cyclin D1, and p53 were utilized for dual-probe hybridizations. Sixty percent (6 of 10) Hurthle cell adenomas and 63% (12 of 19) Hurthle cell carcinomas showed chromosome gains. Twenty percent (2 of 10) Hurthle cell adenomas and 26% (5 of 19) Hurthle cell carcinomas showed chromosome losses. Normal thyroid tissues used as controls showed no chromosomal abnormalities. Among Hurthle cell tumors with chromosomal abnormalities, adenomas averaged 2.7 gains and 0.3 losses per case, and carcinomas averaged 3.3 gains and 0.6 losses per case. The two adenomas with chromosome losses each showed loss of one chromosome, whereas the five carcinomas with losses averaged 1.8 losses per case. Chromosome 22 was the most common loss identified, occurring in three of the 11 patients who died of disease. These results indicate that chromosomal imbalances as gains are common in both benign and malignant Hurthle cell neoplasms, but Hurthle cell carcinomas tend to have more chromosome losses than adenomas. Among Hurthle cell carcinomas in this study, chromosome losses were identified only from patients who died of disease. The loss of chromosome 22 may have prognostic value in Hurthle cell carcinoma of the thyroid.     

Chromosome analysis of renal cell carcinoma

Of 8 tumors surgically extirpated from 8 patients with renal cell carcinoma, 7 were successfully processed in short-term culture by collagenase method, and 130 metaphases were extracted from these 7 tumors and were subjected to chromosomal analysis according to the G banding technique. As for karyotype, 4, 2 and 1 cases were mainly diploid, hypodiploid and aneuploid, respectively. The highest incidence of chromosome aberration was marked by #3 chromosome (5 of 7 cases of which 4 and 1 showed monosomy as clonal aberration and trisomy as non-clonal aberration, respectively). The commonest gain of chromosome was noted for #7 trisomy (4 of 7 cases). Two cases had already had metastases at the time of surgery, each showing #7 trisomy. Marker chromosome was noted in 6 of 7 cases. Structural chromosome aberration had a lesser incidence compared with numerical aberration; only clonal aberrations were long-arm aberrations (2q+, 6q+) of #2 and #6 chromosomes. Short-arm aberrations (3p-, 8p-) of #3 and #8 chromosomes were noted in one case each. 3p deletion, which is reported to be predominant in the literature, was noted only in one case. This was observed in triploid cells. However, all of metaphases showing 2q+ and 6q+ had concomitant #3 monosomy, and excess portions of #2 and #6 chromosomes were in good agreement with the band pattern of #3 chromosomal long-arm. Therefore, translocation of 3q12-qter in #2 and #6 chromosomes is supposed to lead to 3p deletion. A similar mechanism seems to be involved in the formation of marker chromosomes, suggesting the involvement of deleted #3 chromosome in marker chromosomes.     

Sex-specific quantitative trait loci contribute to normal variation in bone structure at the proximal femur in men

Bone structure is an important determinant of osteoporotic fracture. In women, bone structure is highly heritable, and several quantitative trait loci (QTL) have been reported. There are few comparable data in men. This study in men aimed at establishing the heritability of bone structure at the proximal femur, identifying QTL contributing to normal variation in bone structure, and determining which QTL might be sex-specific. Bone structure at the proximal femur was measured in 205 pairs of brothers age 18-61. Heritability was calculated, and linkage analysis performed on phenotypes at the proximal femur. Heritability estimates ranged from 0.99 to 0.39. A genome wide scan identified suggestive QTL (LOD>2.2) for femoral shaft width on chromosome 14q (LOD=2.69 at position 99 cM), calcar femorale at chromosome 2p (LOD=3.97 at position 194 cM) and at the X chromosome (LOD=3.01 at position 77 cM), femoral neck width on chromosome 5p (LOD=2.28 at position 0 cM), femoral head width on chromosome 11q (LOD=2.30 at position 131 cM) and 15q (LOD=3.11 at position 90 cM), and pelvic axis length on chromosome 4q (LOD=4.16 at position 99 cM) and 17q (LOD=2.80 at position 112 cM). Comparison with published data in 437 pairs of premenopausal sisters from the same geographical region suggested that 3 of the 7 autosomal QTL were male-specific. This study demonstrates that bone structure at the proximal femur in healthy men is highly heritable. The occurrence of sex-specific genes in humans for bone structure has important implications for the pathogenesis and treatment of osteoporosis.     

Aneuploidy and Skeletal Health

The normal human chromosome complement consists of 46 chromosomes comprising 22 morphologically different pairs of autosomes and one pair of sex chromosomes. Variations in either chromosome number and/or structure frequently result in significant mental impairment and/or a variety of other clinical problems, among them, altered bone mass and strength. Chromosomal syndromes associated with specific chromosomal abnormalities are classified as either numerical or structural and may involve more than one chromosome. Aneuploidy refers to the presence of an extra copy of a specific chromosome, or trisomy, as seen in Down’s syndrome (trisomy 21), or the absence of a single chromosome, or monosomy, as seen in Turner syndrome (a single X chromosome in females: 45, X). Aneuploidies have diverse phenotypic consequences, ranging from severe mental retardation and developmental abnormalities to increased susceptibility to various neoplasms and premature death. In fact, trisomy 21 is the prototypical aneuploidy in humans, is the most common genetic abnormality associated with longevity, and is one of the most widespread genetic causes of intellectual disability. In this review, the impact of trisomy 21 on the bone mass, architecture, skeletal health, and quality of life of people with Down syndrome will be discussed.     

椎体松质骨的三维构筑学成像研究

目的研究骨量和松质骨显微结构的变化,及其与骨质疏松症骨折发生之间的关系。方法研究采用相对较为成熟的螺旋CT扫描三维重建,并借助工程学上的Euler定律,以活体无创三维成像方法,对小梁骨的结构和连接性进行观察和分析。结果随着年龄的增长,横向排列的骨小梁逐渐消失,纵向骨小梁变细,与周围的小梁逐步失去其连接性;二维横断面图像在小梁连接性描述上有一定的局限性,原因是小梁骨在垂直方向的走向并非规律有序。由于松质骨的显微结构具有不同的类型,它们之间不能等同比较。结论三维结构连接性和连接密度的结果显示板状型的小梁具有较高的连接密度和较小的连接性;而杆状型的小梁则连接密度较低和连接性较好。     

Ulnar avascular necrosis? You be the judge

Posttraumatic diaphyseal malunions of paediatric forearm fractures are associated with a considerable decrease in functional capacity. Corrective osteotomy and plating may be indicated to retrieve normal function and decrease the pain of the forearm. We present a case of a patient with malunited forearm to be treated with a corrective osteotomy. Intraoperatively, however, we visualized a grossly osteonecrotic ulna. After we removed the tourniquet and drilled 3 holes into the bone and still appreciated no active bleeding, we decided to abort the ulna osteotomy. Subsequent bone biopsy and bone scan results returned at the one and a half year follow-up clinical visit revealed that the visual appearance of the bone was misleading; however we are unaware of this finding in the literature. It is our intention that this case report draws attention to this possible outcome secondary to paediatric both bone forearm fractures and provide information about a presumably rare case in hopes of quantifying this complication and determining the true incidence of an abnormal ulna appearance.     

髂骨皮瓣修复手掌部毁损伤

目的 探讨应用吻合旋髂深动脉的髂骨皮瓣一期修复手掌部毁损伤所致多根掌骨复合组织缺损的疗效.方法 1996年以来,对8例手掌部毁损伤所致多根掌骨复合组织缺损,采用吻合旋髂深动脉的髂骨皮瓣重建手掌,并一期修复肌腱、神经.其中2根掌骨缺损3例,3根3例,4根2例.6例肌腱、神经缺损在2～3cm以内,通过短缩植骨,获得肌腱、神经的直接缝合;1例2～5掌骨缺损通过一期"y"形截骨,增加骨承载面,减小了骨瓣切取宽度;1例通过传统骨移植单独重建第一掌骨.获得了拇指单独活动功能;2例合并掌骨头缺损者一期行掌指关节成形术.结果 8例骨皮瓣全部存活.7例伤口 I期愈合,1例因术后皮瓣肿胀,拆除部分缝线,获得Ⅱ期愈合.术后随访1～3年.临床骨愈合时间为3～5周,全部获得骨性愈合.供区无明显并发症.术后手功能评定:优1例,良5例,可1例,差1例;优良率为75%.结论 应用吻合旋髂深动脉的髂骨皮瓣移植重建手掌,并一期修复肌腱和神经,可以较好地恢复手的外形和功能,是手掌毁损伤修复重建的一种有效治疗方法.     

The use of artificial dermis for reconstruction of full thickness scalp burn involving the calvaria

The incidence of extensive full thickness scalp burn involving the calvaria is rare and can be very difficult to reconstruct, as the application of local or free tissue transfer is limited. Although wound closure can be achieved with bone debridement and immediate or delayed split-thickness autografting, the result may be problematic due to unstable skin graft surface. The use of artificial dermis that may provide stable thick coverage in the treatment scalp and skull burn has rarely been reported in literature. We encountered two patients who suffered from severe head burns involving the calvarium. Following debridement including the necrotic bone, the artificial dermis (Integra) was used for immediate wound coverage which was 15 cmx10 cm in one case and 5 cmx6 cm in another. Three weeks later, ultra-thin skin grafting was placed on the neodermis. Compared to split-thickness skin graft, this technique provides a thicker coverage for wound closure. Neither skin breakdown nor ulceration was noted in the 1-year follow-up. This paper reports the successful use of artificial dermis for reconstruction of severe scalp burn with calvarial bone involvement.     

A rare karyotype of nonmosaic isodicentric (Y) (p11.31) with azoospermia and short stature

Chromosome aberration is one of the common causes of male infertility. Isodicentric chromosome is a chromosomal aberration in which two arms of a chromosome are identical in morphology and genetics and connected by two centromeres. We firstly reported a case of infertile male with nonmosaic 46, X, idic (Y) (qter-p11.31::p11.31-qter) but with the sex-determining region Y (SRY). The broken site is the chromosome Y (p11.31). The patients' clinical phenotype was azoospermia and short stature. Fluorescence in situ hybridisation (FISH), chromosomal microarray comparative genomic hybridisation (array CGH) and related molecular analysis were performed. Azoospermia of this case may be caused by the abnormal chromosome structure, which leads to abnormal chromosome synapsis in spermatogenesis. Loss of genes in PAR1 and gain of genes copies in azoospermia factor (AZF) region on the Y chromosome may also contribute to the pathogenesis of azoospermia.     

Post-traumatic forearm nonunion in healthy skeletally immature children: A report on 15 cases

BackgroundNonunion is a rare but severe complication following forearm fracture in skeletally immature patients. The purpose of this study is to describe a case series of pediatric forearm nonunions treated at our Institute.Materials and methodWe retrospectively reviewed medical charts and radiographs of healthy children affected by post-traumatic nonunion of the forearm, from April 1992 to July 2015. An overall series of 15 cases was included in the study. Nonunion developed at ulna in 5 cases and at radius in 10 cases, at a mean time of 9 months (range 6–12) from fracture. Surgical treatment was performed in 14 cases out of 15. Stabilization of the nonunion was achieved with Kirschner wires (5 cases), plates (4 cases), rush rods (2 cases) and unilateral external fixator (3 cases). Iliac crest bone autograft was used in 11 cases, strut cortical bone allograft was used in 2 cases while in one case no bone graft was applied. In 2 cases an additional shortening osteotomy of the ulnar shaft was necessary to obtain adequate compression of the bone fragments. Cast immobilization was maintained for 6 to 8 weeks after surgery, then a brace was applied for further 8 to 12 weeks.ResultsThe average follow-up was 54 months (range 12–129); nonunion healed in 14 cases (93%) at an average time of 4 months (range 2–8). One case of nonunion did not heal 12 months after surgery; other complications included: radio-ulnar fusion and radial nerve palsy (1 case), myositis ossificans at the ulna (1 case), olecranon bursitis with residual elbow stiffness (1 case). One case was treated conservatively and healed after 18 months with residual malalignment.ConclusionsThe present study describes the largest series of pediatric forearm nonunions in the current literature. Whether the surgical management of pediatric forearm nonunion provides satisfactory results in terms of bone healing, it may be accompanied by several complications, permanent sequelae and residual functional impairment. Any effort must be undertaken to avoid this serious complication.     

The clinical use of autologous marrow to improve osteogenic potential of bone grafts in pediatric orthopedics

The high osteogenic potential of living autologous marrow cells can be combined with foreign bone to enhance new bone formation. Xenogeneic bone was combined with autologous red marrow and used in 23 patients aged 5-17 years. Kiel bone was impregnated with marrow aspirated from the iliac crest and, apart from one case of lesion recurrence, gave excellent results in all patients under conditions covering a wide range of indications for bone grafting. Unlimited supplies of xenograft bone and other bone substitutes can be rendered osteogenic by a simple procedure. Combining fresh autologous red marrow with other types of bank bone allograft or xenograft, or even with biological or synthetic biocompatible material that favors the induction of new bone, may provide even better results.     

The restoration of resected mandibles in children without the use of bone grafts

Following resection of the mandible for various types of neoplastic disease, six patients between the ages of 5 and 14 were followed for a period of 8 to 12 years after osseous surgical reconstructive surgery. It was found in children of this age group that a surgical technique may be employed which will effect complete bone regeneration without the use of bone graft materials. All six of the patients spontaneously regenerated large segments of the mandible from full-body ostectomy to hemimandibulectomy defects. The surgical procedure involves the use of a titanium mesh implant between the ostectomized bone fragments to maintain the surrounding soft tissues in a distracted position. It is found that if the soft tissues of the growing child are surgically prepared using the described technique, a new periosteum and bone will be formed along the titanium mesh implant. The titanium mesh may be removed at a later date or, depending on its method of placement, may be allowed to remain as the child grows, regenerating additional bone structure. It was found that in only one case was additional grafting necessary to obtain osseous union between the spontaneously regenerated mandibular bone and the host-bone ostectomized fragments. The technique is advocated for bone restoration in cases of large osseous discontinuity defects of the mandible in children.