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Human allografts of iliac bone and marrow in periodontal osseous defects.

The purpose of this study was to statistically compare the bone regeneration and/or remodeling that occurred in human periodontal osseous defects treated with frozen allogenic, cancellous, iliac bone and marrow grafts, to defects treated by nongrafted flap curettage using a split-mouth protocol. Six patients were selected to participate in the study. These patients exhibited bilateral intrabony periodontal defects that had been refractory to nonsurgical periodontal therapy. Twenty-three intrabony defects were treated by osseous grafting using allogenic iliac bone and marrow and 32 intrabony defects were treated by open debridement procedures. The bony regeneration in each defect treated was evaluated by probing measurements taken from a fixed reference made at the initial surgery and at reentry 1 year after transplantation. The overall results of this study demonstrated that the percentage of osseous regeneration that occurred in intrabony defects treated by allogenic bone and marrow grafting was statistically greater than that which occurred in defects treated by nongrafted flap curettage procedures.

Adult↗

Clinical evaluation of porous and nonporous hydroxyapatite in the treatment of human periodontal bony defects.

The purpose of this study was to investigate the effectiveness of a synthetic nonporous hydroxyapatite graft material (OrthoMatrix HA-500), a porous replamineform hydroxyapatite graft material (Interpore 200), and a debrided control with respect to defect fill. Twelve adult patients having periodontitis and three similar angular osseous defects as verified by radiographic analysis and clinical probe depths greater than or equal to 5 mm were selected. Clinical parameters gathered prior to surgical intervention and at identified postoperative visits included plaque index, probing depth, and standardized radiographic examination. Customized acrylic stents were used as fixed reference guides for the insertion of endodontic silver points to the base of each defect during both initial and 6-month reentry surgeries. A total of 36 defects were randomly assigned to one of three treatment modalities such that 12 defects received OrthoMatrix HA-500, 12 received Interpore 200, and 12 served as debrided controls. Comparison of nonporous hydroxyapatite, porous replamineform hydroxyapatite, and debrided control treatment modalities revealed a statistically significant improvement (P less than 0.05) in the mean per cent of defect resolved in only those sites treated with nonporous hydroxyapatite. Similar positive trends were seen in the sites treated with nonporous hydroxyapatite for mean reentry defect depth and mean defect fill although these were not statistically significant (P greater than 0.05). No other significant differences were noted.

Adult↗

Evaluation of a bioactive glass alloplast in treating periodontal intrabony defects.

This study evaluated the use OF bioactive glass (BG) for repairing/regenerating periodontal intrabony defects. Fourteen systemically healthy patients participated. Each patient had 2 contralateral sites with > or = 6 mm clinical probing depth and radiographic evidence of an intrabony defect. One defect was treated with flap debridement plus BG (test) and the other with flap debridement alone (control). Baseline measurements included gingival index (GI), plaque index (PI), position of the free gingival margin (S/FGM), clinical attachment level (CAL), probing depth (PD), and mobility. At the time of surgery and at surgical reentry (9 to 13 months later), hard tissue measurements included: stent to defect base, bone crest to defect base, and defect width at the bone crest. One-way repeated ANOVA was used to analyze the treatment effect. Friedman's test was used to detect any significant changes of GI, PI and mobility at different time periods (baseline, 3 months, 6 months, and reentry). For multivariate analysis, the random coefficients mixed effect model was applied to adjust the intra-correlation effect. Both treatments resulted in decreased PD and gain of CAL. These changes were only significant (P < 0.05) for the BG treated sites (PD reduction = 1.24+/-0.43 mm, CAL gain = 0.87+/-0.38 mm) from baseline. Defect fill was significant for test (1.1+/-0.4 mm) and control (1.4+/-0.4 mm) alike (P < or = 0.01). Although BG treated sites had more PD reduction and CAL gain than debridement only controls, there were no statistically significant differences between groups for any parameter measured. Further studies are required to clarify the beneficial effects, if any, of BG alloplast in treating periodontal intrabony defects.

Adult↗

Hydroxyapatite cement implant for regeneration of periodontal osseous defects in humans.

A newly developed calcium phosphate cement used to promote bone regeneration in craniofacial defects was examined to determine its potential for treatment of periodontal osseous defects. Sixteen patients with moderate to severe periodontal disease and 2 bilaterally similar vertical bony defects received initial therapy including scaling and root planing followed by treatment with either calcium phosphate cement, flap curettage (F/C) or debridement plus demineralized freeze-dried bone allograft (DFDBA). Standardized radiographs were exposed at baseline and 12 months postsurgery for computer assisted densitometric image analysis (CADIA). The extent of the bony defect was determined during initial and 12 month re-entry surgery. Within 6 months of implant placement, 11 of 16 patients treated with calcium phosphate cement exfoliated all or most of the implant through the gingival sulcus. At all 16 test sites, a narrow radiolucent gap formed by 1 month postsurgery at the initially tight visual interface between the radiopaque calcium phosphate cement and the walls of the bony defect. Mean probing depth reduction and clinical attachment gain at sites treated with calcium phosphate cement were 1.6 mm and 1.3 mm, respectively at 1 year. Minimal bony defect fill was accompanied by mean crestal resorption of 1.4 mm. Alveolar crestal resorption at sites with calcium phosphate cement was statistically significant (P=0.001). These findings contrasted with the more favorable outcomes for controls treated with DFDBA or F/C. DFDBA sites exhibited probing depth reduction of 3.1 mm, clinical attachment gain of 2.9 mm, and defect fill of 2.4 mm. Respective clinical changes at F/C sites were 2.4 mm, 1.4 mm, and 1.1 mm. CADIA revealed clinically significant trends between the three treatment modalities at various areas-of-interest. Based on the findings of this study, there is no rationale available to support the use of hydroxyapatite cement implant in its current formulation for the treatment of vertical intrabony periodontal defects.

Absorptiometry, Photon↗

Treatment of intrabony defects with bovine-derived xenograft alone and in combination with platelet-rich plasma: a randomized clinical trial.

BACKGROUND: In the treatment of periodontal intrabony defects, the benefits of adding platelet-rich plasma (PRP) to a bone replacement grafting material have not been tested. The purpose of this study was to compare the clinical outcomes obtained by the combination of PRP and a bovine derived xenograft (BDX) to those obtained from the use of the bone replacement graft alone. METHODS: Thirteen patients were enrolled in a randomized, split mouth, double-masked clinical trial. Bilateral defects were matched according to their intrasurgical measurements. Qualifying defects had loss of attachment of > or = 6 mm, a radiographically detectable defect of > or = 4 mm, at least two remaining osseous walls, and not primarily related to a furcation involvement. After the hygienic phase, at the baseline examination, probing depth (PD), clinical attachment level (CAL), and recession (REC) were measured. During open flap debridement, the defects were randomly assigned to receive either BDX mixed with PRP or BDX alone. Baseline osseous intrasurgical measurements were obtained. Post-surgical follow-up and maintenance were performed and PD, CAL, and REC were remeasured at 6 months. The mean baseline and 6-month PD, CAL, and REC of the deepest buccal and lingual measurements related to the defect for each group were computed. The change from baseline to 6 months for each parameter measured was calculated. Pre- and postoperative comparisons were made between treatment groups at 6 months. RESULTS: Randomization of the defects resulted in comparable groups (P > or = 0.05). At 6 months, paired t test comparisons within groups showed statistically significant benefits with both treatment modalities (P < or = 0.05). The mean changes (delta) at 6 months for the test and the control groups at the deepest sites were: PD reduction: 3.54 and 2.53 mm; CAL gain: 3.15 and 2.31 mm; and REC: -0.38 and -0.23 mm, respectively. Paired t test comparisons yielded significant differences between treatments for PD and CAL (P < or = 0.05). CONCLUSION: In this 6-month clinical trial, the addition of a high concentration of autologous platelets to a bovine derived xenograft to treat intrabony defects significantly improved their clinical periodontal response.

Adult↗

Accuracy of cone beam computed tomography for periodontal defect measurements.

BACKGROUND: Periodontal diagnosis relies heavily on traditional two-dimensional radiographic assessment. Despite efforts in improving reliability, current methods of detecting bone level changes over time or determining three-dimensional architecture of osseous defects are inadequate. To address these issues, computed tomography (CT) has been explored because of its ability to produce accurate three-dimensional imaging, but limitations such as radiation, machine size, and cost have made this approach impractical. Recently, cone beam computed tomography (CBCT) has turned this concept into potential reality because these lower-cost small machines produce high-quality data. Yet there is little research to establish periodontal bone measurement using CBCT as a valid method. Therefore, the aim of this study was to compare CBCT measurements of periodontal defects to traditional methods. METHODS: Artificial osseous defects were created on mandibles of dry skulls. CBCT scanning, periapical radiography (PA), and direct measurements using a periodontal probe were compared to an electronic caliper that was used as a standard reference. RESULTS: Linear measurements for all defects revealed no statistical differences between bone sounding, radiography, and CBCT. There was a significant difference when comparing isolated interproximal measurements using a probe versus the caliper (P<0.001) but no significant difference for CBCT or radiography. All bony defects were identifiable and measurable directly or with CBCT. In comparison, buccal and lingual defects could not be measured with radiographs. CONCLUSIONS: Overall, all three modalities are useful for identifying interproximal periodontal defects. Compared to radiographs, the three-dimensional capability of CBCT offers a significant advantage because all defects can be detected and quantified.

Alveolar Bone Loss↗

Stability of clinical and radiographic results after guided tissue regeneration in infrabony defects.

BACKGROUND: The aim of this 5-year follow-up study was to evaluate clinically and radiographically the long-term results after guided tissue regeneration (GTR) therapy of infrabony defects using non-resorbable and bioabsorbable barriers. METHODS: Thirty-one patients with periodontitis and 50 infrabony defects that had been treated using GTR were recruited. Eleven defects were treated with non-resorbable expanded polytetrafluoroethylene membranes and 39 defects with bioabsorbable barriers. At baseline and 6 and 60 +/- 3 months after surgery, clinical parameters and standardized radiographs were obtained. During surgery and 60 +/- 3 months thereafter, the distance from the cemento-enamel junction to the base of the bony defect (vertical probing bone level [PBL-V]) was measured. Bone gain was evaluated using digital subtraction radiography. RESULTS: At 6 and 60 +/- 3 months after GTR, there was a statistically significant (P <0.001) reduction of probing depth (6 months: 4.31 +/- 1.76 mm; 60 months: 3.95 +/- 1.62 mm) and vertical clinical attachment level gains (CAL-V) (6 months: 3.34 +/- 1.66 mm; 60 months: 2.97 +/- 1.53 mm). From 6 to 60 months after GTR, three infrabony defects exhibited CAL-V loss >2 mm, and a small, statistically not significant mean CAL-V loss of 0.39 +/- 1.60 mm was observed. From baseline to 60 +/- 3 months, a significant PBL-V gain of 1.78 +/- 2.67 mm (P <0.001) and increase in bone density were observed (P = 0.003). CONCLUSION: The CAL-V gain achieved after GTR in infrabony defects using both non-resorbable and bioabsorbable barriers was stable after 5 years in 47 of 50 defects.

Absorbable Implants↗

Cell origin and differentiation in the repair of full-thickness defects of articular cartilage.

The origin and differentiation of cells in the repair of three-millimeter-diameter, cylindrical, full-thickness drilled defects of articular cartilage were studied histologically in New Zealand White rabbits. The animals were allowed to move freely after the operation. Three hundred and sixty-four individual defects from 122 animals were examined as long as forty-eight weeks postoperatively. In the first few days, fibrinous arcades were established across the defect, from surface edge to surface edge, and this served to orient mesenchymal cell ingrowth along the long axes. The first evidence of synthesis of a cartilage extracellular matrix, as defined by safranin-O staining, appeared at ten days. At two weeks, cartilage was present immediately beneath the surface of collagenous tissue that was rich in flattened fibrocartilaginous cells in virtually all specimens. At three weeks, the sites of almost all of the defects had a well demarcated layer of cartilage containing chondrocytes. An essentially complete repopulation of the defects occurred at six, eight, ten, and twelve weeks, with progressive differentiation of cells to chondroblasts, chondrocytes, and osteoblasts and synthesis of cartilage and bone matrices in their appropriate locations. At twenty-four weeks, both the tidemark and the compact lamellar subchondral bone plate had been re-established. The cancellous woven bone that had formed initially in the depths of the defect was replaced by lamellar, coarse cancellous bone. Autoradiography after labeling with 3H-thymidine and 3H-cytidine demonstrated that chondrocytes from the residual adjacent articular cartilage did not participate in the repopulation of the defect. The repair was mediated wholly by the proliferation and differentiation of mesenchymal cells of the marrow. Intra-articular injections of 3H-thymidine seven days after the operation clearly labeled this mesenchymal cell pool. The label, initially taken up by undifferentiated mesenchymal cells, progressively appeared in fibroblasts, osteoblasts, articular chondroblasts, and chondrocytes, indicating their origin from the primitive mesenchymal cells of the marrow. Early traces of degeneration of the cartilage matrix were seen in many defects at twelve to twenty weeks, with the prevalence and intensity of the degeneration increasing at twenty-four, thirty-six, and forty-eight weeks. Polarized light microscopy demonstrated failure of the newly synthesized repair matrix to become adherent to, and integrated with, the cartilage immediately adjacent to the drill-hole, even when light microscopy had shown apparent continuity of the tissue. In many instances, a clear gap was seen between repair and residual cartilage.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

The effect of recombinant human bone morphogenetic protein-2 (rhBMP-2) on the healing of full-thickness defects of articular cartilage.

Articular cartilage has a limited capacity for repair. We investigated the effect of rhBMP-2 (recombinant human bone morphogenetic protein-2) on the healing of full-thickness osteochondral defects in adult New Zealand White rabbits. A single defect, three millimeters wide by three millimeters deep, was created in the trochlear groove of the right femur in eighty-nine rabbits. The defect was either left empty, filled with a plain collagen sponge, or filled with a collagen sponge impregnated with five micrograms of rhBMP-2. The animals were killed at four, eight, or twenty-four weeks, and the repair tissue was examined histologically and evaluated with use of a grading scale. The defects also were examined immunohistochemically for the presence of type-II collagen at four and eight weeks. The rate of bone repair was evaluated with fluorescent labeling of bone at two and four weeks and with use of fluorescence microscopy at eight weeks. Treatment with rhBMP-2 greatly accelerated the formation of new subchondral bone and improved the histological appearance of the overlying articular surface. At twenty-four weeks, the thickness of the repair cartilage was 70 per cent that of the normal adjacent cartilage and a new tidemark usually had formed between the repair cartilage and the underlying subchondral bone. The average total scores on the histological grading scale were significantly better (p < 0.01) for the defects treated with rhBMP-2 than for the untreated defects (those left empty or filled with a plain collagen sponge) at all time-points. Immunostaining with an antibody against type-II collagen showed the diffuse presence of this cartilage-specific collagen throughout the repair cartilage in the treated defects. The untreated defects demonstrated minimum staining with this antibody.

Animals↗

The effect of implants loaded with autologous mesenchymal stem cells on the healing of canine segmental bone defects.

Bone marrow has been shown to contain a population of rare mesenchymal stem cells that are capable of forming bone, cartilage, and other connective tissues. We examined the effect of cultured autologous mesenchymal stem cells on the healing of critical-sized (twenty-one-millimeter-long) segmental defects in the femora of adult female dogs. Autologous mesenchymal stem cells were isolated from bone marrow, grown in culture, and loaded onto porous ceramic cylinders consisting of hydroxyapatite (65 per cent) and beta-tricalcium phosphate ceramic (35 per cent). The animals were randomly assigned to one of three groups. In Group A (six dogs), a porous ceramic cylinder that had been loaded with autologous mesenchymal stem cells was implanted in the defect. In Group B (six dogs), a ceramic cylinder that had not been loaded with cells was placed in the defect. In Group C (three dogs), the defect was left untreated (no ceramic cylinder was implanted). Radiographs were made immediately after the operation and at four-week intervals. At sixteen weeks, the animals were killed, the involved femora were removed, and undecalcified histological sections from the defects and adjacent bone were prepared. Histological and histomorphometric studies were carried out to examine the healing of the defects and the formation of bone in and around the ceramic implants. Atrophic non-union occurred in all of the femora that had untreated defects, and only a small amount of trabecular bone formed at the cut ends of the cortex of the host bone in this group. In contrast, radiographic union was established rapidly at the interface between the host bone and the implants that had been loaded with mesenchymal stem cells. Numerous fractures, which became more pronounced with time, developed in the implants that had not been loaded with cells. Histological and morphometric analyses demonstrated that both woven and lamellar bone had filled the pores of the implants that had been loaded with mesenchymal stem cells; the amount of bone was significantly greater (p < 0.05) than that found in the pores of the implants that had not been loaded with cells. In addition, a large collar of bone (mean maximum thickness, 3.14 millimeters) formed around the implants that had been loaded with cells; this collar became integrated and contiguous with callus that formed in the region of the periosteum of the host bone. The collar of bone remodeled during the sixteen-week period of study, resulting in a size and shape that were comparable with those of the segment of bone that had been resected. Callus did not develop around the cortex of the host bone or around the defect in any of the specimens in the other two groups.

Animals↗

Noninvasive imaging predicts failure load of the spine with simulated osteolytic defects.

BACKGROUND: The clinical management of lytic tumors of the spine is currently based on geometric measurements of the defect. However, the mechanical behavior of a structure depends on both its material and its geometric properties. Quantitative computed tomography and dual-energy x-ray absorptiometry were investigated as noninvasive tools for measuring the material and geometric properties of vertebrae with a simulated lytic defect. From these measures, yield loads were predicted with use of composite beam theory. METHODS: Thirty-four fresh-frozen cadaveric spines were segmented into functional spinal units of three vertebral bodies with two intervertebral discs at the thoracic and lumbar levels. Lytic defects of equal size were created in one of three locations: the anterior, lateral, or posterior region of the vertebra. Each spinal unit was scanned with use of computed tomography and dual-energy x-ray absorptiometry, and axial and bending rigidities were calculated from the image data. Each specimen was brought to failure under combined compression and forward flexion, and the axial load and bending moment at yield were recorded. RESULTS: Although the relative defect size was nearly constant, measured yield loads had a large dispersion, suggesting that defect size alone was a poor predictor of failure. However, image-derived measures of structural rigidity correlated moderately well with measured yield loads. Furthermore, with use of composite beam theory with quantitative computed tomography-derived rigidities, vertebral yield loads were predicted on a one-to-one basis (concordance, r(c) = 0.74). CONCLUSIONS: Although current clinical guidelines for predicting fracture risk are based on geometric measurements of the defect, we have shown that the relative size of the defect alone does not account for the variation in vertebral yield loads. However, composite beam theory analysis with quantitative computed tomography-derived measures of rigidity can be used to prospectively predict the yield loads of vertebrae with lytic defects. CLINICAL RELEVANCE: Image-predicted vertebral yield loads and analytical models that approximate loads applied to the spine during activities of daily living can be used to calculate a factor of fracture risk that can be employed by physicians to plan appropriate treatment or intervention.

Absorptiometry, Photon↗

Immunolocalization of matrix metalloproteinases in partial-thickness defects in pig articular cartilage. A preliminary report.

BACKGROUND: Partial-thickness defects in mature articular cartilage do not heal spontaneously. Attempts at repair often result in limited integration between the repair tissue and the surrounding cartilage, with formation of chondrocyte clusters adjacent to a zone of cartilage necrosis. In wound repair, spatially and temporally controlled expression of matrix metalloproteinases and their inhibitors have been implicated in proteolytic degradation of damaged extracellular matrix components, but the sequence of events following damage to cartilage is unknown. To determine this sequence, we studied the distribution of matrix metalloproteinases and their inhibitors during early in vivo repair of partial-thickness defects in pig articular cartilage. METHODS: With use of a model that elicits the ingrowth of mesenchymal cells into partial-thickness defects, partial-thickness defects were created in knee joint cartilage. The distributions of matrix metalloproteinase-1, 2, 3, 9, 13, and 14; tissue inhibitors of metalloproteinase-1 and 2; and the neoepitope DIPEN341 specifically generated following matrix metalloproteinase cleavage of aggrecan were determined by immunolocalization of repair tissue and surrounding cartilage excised from immature pigs during the first eight weeks of repair and from adult minipigs at eight days and three weeks. RESULTS: Synthesis of matrix metalloproteinase-13 was usually confined to hypertrophic chondrocytes in immature cartilage and to the radial zone in adult cartilage. Following injury, strong induction of matrix metalloproteinase-13 synthesis was observed in chondrocyte clusters surrounding lesions in all of the animals. The migration of macrophages into defects was prominent at two and eight days, with synthesis and deposition of matrix metalloproteinase-9 onto damaged cartilage matrix and newly synthesized matrix in the defect. The DIPEN341 neoepitope was localized to damaged cartilage matrix at eight days and six weeks, indicating partial degradation of aggrecan. Focal synthesis of matrix metalloproteinase-1, 3, and 14 and of tissue inhibitor of metalloproteinase-1 occurred at later times, suggesting continuous remodeling of the increasingly compact repair tissue. CONCLUSIONS: The expression of matrix metalloproteinase-13 by normal hypertrophic chondrocytes and the induction of synthesis in chondrocyte clusters adjacent to the zone of cartilage necrosis suggest that this enzyme participates in the pericellular proteolysis required for lacunar expansion. The localization of matrix metalloproteinase-9 to damaged cartilage matrix suggested matrix proteolysis, which was confirmed with DIPEN341 localization. Reduced matrix metachromasia persisted and was colocalized with DIPEN341 at six weeks. However, under the conditions investigated, there was only limited proteolytic degradation in the zone of cartilage necrosis. This may render the zone mechanically weakened, thereby contributing to subsequent instability of the region, and may form a barrier to integration of repair tissue with viable cartilage. CLINICAL RELEVANCE: Osteoarthritis initially involves the superficial layers of cartilage. The development of procedures to promote the healing or repair of early defects will have major advantages in terms of disease alleviation as well as economic importance. Identification of the enzymes involved in the early repair of partial-thickness defects in articular cartilage is clinically relevant because proteolysis of damaged matrix has to take place in order for repair tissue to integrate with surrounding healthy cartilage.

Aggrecans↗

Effect of bone morphogenetic protein-2-expressing muscle-derived cells on healing of critical-sized bone defects in mice.

BACKGROUND: Cells that express bone morphogenetic protein-2 (BMP-2) can now be prepared by transduction with adenovirus containing BMP-2 cDNA. Skeletal muscle tissue contains cells that differentiate into osteoblasts on stimulation with BMP-2. The objectives of this study were to prepare BMP-2-expressing muscle-derived cells by transduction of these cells with an adenovirus containing BMP-2 cDNA and to determine whether the BMP-2-expressing muscle-derived cells would elicit the healing of critical-sized bone defects in mice. METHODS: Primary cultures of muscle-derived cells from a normal male mouse were transduced with adenovirus encoding the recombinant human BMP-2 gene (adBMP-2). These cells (5 yen 10(5)) were implanted into a 5-mm-diameter critical-sized skull defect in female SCID (severe combined immunodeficiency strain) mice with use of a collagen sponge as a scaffold. Healing in the treatment and control groups was examined grossly and histologically at two and four weeks. Implanted cells were identified in vivo with use of the Y-chromosome-specific fluorescent in situ hybridization (FISH) technique, and their differentiation into osteogenic cells was demonstrated by osteocalcin immunohistochemistry. RESULTS: Skull defects treated with muscle cells that had been genetically engineered to express BMP-2 had >85% closure within two weeks and 95% to 100% closure within four weeks. Control groups in which the defect was not treated (group 1), treated with collagen only (group 2), or treated with collagen and muscle cells without adBMP-2 (group 3) showed at most 30% to 40% closure of the defect by four weeks, and the majority of the skull defects in those groups showed no healing. Analysis of injected cells in group 4, with the Y-chromosome-specific FISH technique showed that the majority of the transplanted cells were located on the surfaces of the newly formed bone, but a small fraction (approximately 5%) was identified within the osteocyte lacunae of the new bone. Implanted cells found in the new bone stained immunohistochemically for osteocalcin, indicating that they had differentiated in vivo into osteogenic cells. CONCLUSIONS: This study demonstrates that cells derived from muscle tissue that have been genetically engineered to express BMP-2 elicit the healing of critical-sized skull defects in mice. The cells derived from muscle tissue appear to enhance bone-healing by differentiating into osteoblasts in vivo. CLINICAL RELEVANCE: Ex vivo gene therapy with muscle-derived cells that have been genetically engineered to express BMP-2 may be used to treat nonhealing bone defects. In addition, muscle-derived cells appear to include stem cells, which are easily obtained with muscle biopsy and could be used in gene therapy to deliver BMP-2.

Animals↗

Healing of a critical-sized defect in the rat femur with use of a vascularized periosteal flap, a biodegradable matrix, and bone morphogenetic protein.

BACKGROUND: The purpose of this study was to evaluate the osseous healing of a critical-sized femoral defect in a rat model with use of recombinant human bone morphogenetic protein-2 (rhBMP-2), a matrix fabricated of D,D-L,L-polylactic and hyaluronan acid (OPLA-HY), and a vascularized periosteal flap. METHODS: The carrier matrix OPLA-HY with or without rhBMP-2 was implanted in a 1-cm-long femoral defect and secured with a plate and screws. In some groups, a vascularized periosteal flap was harvested from the medial surface of the tibia. In group 1, the femoral defects in the animals were filled with the OPLA-HY matrix alone; in group 2, the OPLA-HY matrix was covered by the vascularized periosteal flap; in group 3, 20 mug of rhBMP-2 was added to the OPLA-HY matrix; and in group 4, the femoral defect containing the OPLA-HY matrix and 20 mug of rhBMP-2 was wrapped circumferentially by the vascularized periosteal flap. The presence and density of new bone formation in the femoral defect were evaluated radiographically, histologically, and with histomorphometry at four and eight weeks postoperatively. RESULTS: Groups 1 and 2, which were not treated with rhBMP-2, showed no radiographic or histologic evidence of mature bone formation at four or eight weeks. Both groups 3 and 4, which were treated with rhBMP-2, demonstrated excellent bone formation. However, with the periosteal flap, group 4 demonstrated more bone formation on histomorphometric analysis at eight weeks (43.1%) than did group 3 (28.3%) (p < 0.01). Additionally, heterotopic bone formed outside the boundaries of the defect in eight of the fifteen animals in group 3, which had no periosteal flap. CONCLUSIONS: Bone-tissue engineering with use of the OPLA-HY matrix and rhBMP-2 produced good bone formation in the rat femoral defect model. However, the addition of a vascularized periosteal flap significantly increased bone formation within the boundaries of the defect and prevented heterotopic ossification.

Animals↗

Does thalidomide cause second generation birth defects?

The proposed association between thalidomide and second generation birth defects is an improbable hypotheses which lacks, so far, any credible scientific foundation. However, the media have chosen to give it extensive coverage. So much so that even the hard-headed scientist may start wondering if there is anything in it. However, there is no reason to suppose that people with birth defects caused by exposure to thalidomide during embryonic life have any greater or lesser chance of producing children with birth defects. This appears to be the case in practice. The question could be reworded to, 'Can thalidomide be responsible for identical, or similar, birth defects in 2 generations of the same family?' For such a phenomenon to be possible, a mechanism must be proposed and there appear to be only 2 possible candidates. The first is that the defects in the parent, originating during embryonic life, have somehow been transmitted to the next generation. The second is that thalidomide is a mutagen as well as a teratogen. The first mechanism can be excluded, since Lamarckism has long since been abandoned by scientists. The hypothesis that thalidomide is a mutagen and might be responsible for birth defects in the children of thalidomide-damaged people is without any scientific foundation. Birth defects appear to be no more common amongst the children of thalidomide-affected parents than in the general population. It is important that thalidomide-affected adults are firmly reassured on this point. Most of them have now completed their own families, but they may still worry about their grandchildren. Therefore, unless and until further supportive evidence is reported by a separate and independent source, the answer to the question, 'Can thalidomide cause second generation defects?' is a very definite 'No.'

Abnormalities, Drug-Induced↗

Effect of hyperbaric oxygen treatment on incorporation of an autogenous cancellous bone graft in a nonunion diaphyseal ulnar defect in cats.

OBJECTIVE: To determine whether hyperbaric oxygen treatment (HBOT) would affect incorporation of an autogenous cancellous bone graft in diaphyseal ulnar defects in cats. ANIMALS: 12 mature cats. PROCEDURE: Bilateral nonunion diaphyseal ulnar defects were created in each cat. An autogenous cancellous bone graft was implanted in 1 ulnar defect in each cat, with the contralateral ulnar defect serving as a nongrafted specimen. Six cats were treated by use of hyperbaric oxygen at 2 atmospheres absolute for 90 minutes once daily for 14 days, and 6 cats were not treated (control group). Bone labeling was performed, using fluorochrome markers. Cats were euthanatized 5 weeks after implanting, and barium sulfate was infused to evaluate vascularization of grafts. Ulnas were evaluated by use of radiography, microangiography, histologic examination, and histomorphometric examination. RESULTS: Radiographic scores did not differ between treatment groups. Microangiographic appearance of grafted defects was similar between groups, with all having adequate vascularization. Differences were not observed between treated and nontreated groups in the overall histologic appearance of decalcified samples of tissue in grafted defects. Mean distance between fluorescent labels was significantly greater in cats given HBOT than in nontreated cats. Median percentage of bone formation in grafted defects was significantly greater in cats given HBOT. CONCLUSIONS: Hyperbaric oxygen treatment increased the distance between fluorescent labels and percentage of bone formation when incorporating autogenous cancellous bone grafts in induced nonunion diaphyseal ulnar defects in cats, but HBOT did not affect revascularization, radiographic appearance, or qualitative histologic appearance of the grafts.

Animals↗

Pathogenesis of corneal epithelial defects: role of plasminogen activator.

Previous studies have suggested that the plasminogen activator (PA)/plasmin system has important roles in the pathogenesis of epithelial defects and stromal ulceration. The current studies were performed to localize PA species and identify them as tissue-type PA (tPA) or urokinase-like PA (uPA) as the two have distinct regulatory properties potentially related to the mechanisms of defect formation and ulceration. To determine the locations and types of PA species, antibodies to tPA or to uPA or the drug amiloride (a drug that inhibits uPA but not tPA) were incorporated into fibrin/fibronectin (Fn) clots overlying frozen sections to block regional fibrinolysis. Normal rabbit eyes showed tPA activity in association with corneal epithelium, corneal endothelium, and ciliary body/iris. After epithelial scrape or alkali burn, corneal tPA activity was detected initially in the defect zone colinear with fibrin/Fn and was symmetrical to resurfacing epithelium. The observation that initial fibrinolysis occurs in the defect zone, known to contain fibrin/Fn, suggests that tPA from blood (limbal vascular endothelium) and/or from corneal epithelium has become bound to (and activated on) the fibrin/Fn. PA activity was also associated with the leading edges of migrating epithelium post-scrape and post-burn and was not inhibited by antibodies to either tPA or uPA but was inhibited by amiloride. After complete closure of the primary defect post-scrape, only tPA appeared to be associated with the epithelium in that all PA activity was inhibited by antibodies to tPA. The observation that leading edge activity post-burn, in correlation with the formation of secondary defects, continues to be inhibitable by amiloride but not by antibodies to tPA suggests that uPA remains abnormally on the leading edge, and that sustained uPA activity in that location results in inappropriate degradation of subepithelial fibrin/Fn to result in a defect. Successful regulation of uPA activity at the leading edge of corneal epithelium post-burn would be expected to be useful therapeutically in the healing of epithelial defects and the prevention of stromal ulceration.

Animals↗

Free fat transplant prevents osseous reunion of skull defects. A new approach in the treatment of craniosynostosis.

Free fat tissue transplant to correct premature epiphyseal fusion of long bones has been successfully used to prevent re-ossification after bone bridge resection. In the present study we have applied this principle in the prevention of osseous reunion of the bone defect in the calvaria of the rabbit. In two-week-old animals standard bone defects were made on both sides of the sagittal suture to the temporal bone. The dura was left intact. On the right side a free autogenous fat transplant was placed to fill the bone defect. On the left side the control defect was left without fat interposition. The skull defects were examined postoperatively at three weeks, three months, and eight months. The control defects reossified within three weeks. The bone defects with fat tissue transplant were found to be open and of original size at eight months postoperatively. On the transplanted side histological examination revealed living fat cells filling the gap. Osteogenesis was inhibited and reunion of the bone edges was prevented. All the control bone defects were filled by lamellar bone. The use of free fat tissue transplant can be a useful alternative, serving as a biological interposition material in the surgical treatment of craniosynostosis.

Adipose Tissue↗