The influence of directional preference on lateral patellar dislocation: a case report.

BACKGROUND: There is little consensus on the conservative management of lateral patellar dislocations (LPD). Mechanical diagnosis and therapy (MDT) is an established classification system in the spinal and extremity population. This case report describes the use of MDT in the management and classification of a patient with LPD. CASE DESCRIPTION: The patient was a 20-year-old female with a 3-month history of left knee pain precipitated by a lateral patellar dislocation. The patient described pain and a feeling of instability with standing and walking and limitations in work and recreational activities which involve lifting, squatting, and running. Based on the patient's response to repeated end range knee movements, the patient was found to have a directional preference (DP) for knee extension and instruction in performance of knee extension DP exercises was provided. OUTCOMES: The patient's knee examination and subsequent intervention included her responses to repeated end range knee movements. Her knee pain was abolished, and strength, function, and motion were fully restored in five visits. A minimal clinically important difference (MCID) was achieved on the Lower Extremity Functional Scale (LEFS). At discharge, the patient was able to independently manage symptoms and perform all work and recreational activities at a pre-injury level and these improvements were maintained at a 9-month follow-up. DISCUSSION: There are various management strategies for lateral patellar dislocation. This case demonstrated the use of classifying, subgrouping, and treating a patient with lateral patellar dislocation using the principle of DP. CONCLUSION: The patient's outcomes suggest that MDT may be used in the nonoperative management of people with LPD who present with a DP.

Cartilage ultrastructure after high pressure freezing, freeze substitution, and low temperature embedding. II. Intercellular matrix ultrastructure - preservation of proteoglycans in their native state.

The extracellular matrix of epiphyseal cartilage tissue was preserved in a state believed to resemble closely that of native tissue following processing by high pressure freezing, freeze substitution, and low temperature embedding (HPF/FS). Proteoglycans (PG) were preserved in an extended state and were apparent as a reticulum of fine filamentous threads throughout the matrix. Within this network, two morphologically discrete components were discernible and identified with the carbohydrate and protein components of PG molecules. Numerous points of contact were clearly visible between components of the PG network and cross-sectioned collagen fibrils and also between PG components and chondrocytic plasmalemmata. These observations provide direct morphological indication that such relationships may exist in native epiphyseal cartilage tissue.

Cartilage resorption in the tibial epiphyseal plate of growing rats.

An electron microscopic study of the tibial epiphyseal plates of growing rats reveals that the resorption of unmineralized and mineralized cartilage occurs by two different mechanisms. During resorption the unmineralized transverse cartilaginous walls between chondrocytes are invaded by capillary sprouts. At the resorption zone, numerous cytoplasmic processes derived primarily from the perivascular cells and, to a lesser extent, from the endothelial cells of the sprouts penetrate and appear to lyse the unmineralized transverse cartilaginous walls. Hydrolases released from the degenerating chondrocytes and/or capillary sprouts may also participate in this process. The second resorption mechanism involves the mineralized longitudinal cartilaginous septa. Resorption of these septa is mediated by chondroclasts whose fine structure is identical with that of osteoclasts. The active surface of the chondroclasts has a ruffled border. The surface membrane of the chondroclasts is relatively smooth on either side of the ruffled border and lies in direct apposition with the underlying mineralized cartilage. This observation suggests that the microenvironment in the zone of resorption may be maintained by the neighboring unruffled surfaces of the chondroclasts, which thus seal off and segregate the active portions of these cells.

Cartilage ultrastructure after high pressure freezing, freeze substitution, and low temperature embedding. I. Chondrocyte ultrastructure--implications for the theories of mineralization and vascular invasion.

Electron microscopic examination of epiphyseal cartilage tissue processed by high pressure freezing, freeze substitution, and low temperature embedding revealed a substantial improvement in the preservation quality of intracellular organelles by comparison with the results obtained under conventional chemical fixation conditions. Furthermore, all cells throughout the epiphyseal plate, including the terminal chondrocyte adjacent to the region of vascular invasion, were found to be structurally integral. A zone of degenerating cells consistently observed in cartilage tissue processed under conventional chemical fixation conditions was not apparent. Hence, it would appear that cell destruction in this region occurs during chemical processing and is not a feature of cartilage tissue in the native state. Since these cells are situated in a region where tissue calcification is taking place, the implication is that the onset and progression of cartilage calcification are, at least partially, controlled by the chondrocytes themselves. The observation that the terminal cell adjacent to the zone of vascular invasion is viable has important implications in relation to the theory of vascular invasion. This may now require reconceptualization to accommodate the possibility that active cell destruction may be a precondition for vascular invasion.

Synthesis of cartilage matrix by mammalian chondrocytes in vitro. I. Isolation, culture characteristics, and morphology.

We describe the isolation and the ultrastructural characteristics of adult bovine articular chondrocytes in vitro. Slices of bovine articular cartilage undergo sequential digestions with pronase and collagenase in order to release cells. Chondrocytes are plated at high density (1 x 10(5) cells/cm2) in culture dishes or roller bottles with Ham's F-12 medium, supplemented with 10% fetal bovine serum. Before culture, chondrocytes are freed of surrounding territorial matrix. Within the first few days of culture they re-establish a territorial matrix. As time progresses, chondrocytes synthesize both territorial and extraterritorial matrices. The matrices are rich in collagen fibrils and ruthenium red-positive proteoglycans. These features are most apparent in mass roller cultures in which aggregates of cells and matrix appear as long streaks and nodules. This morphology reveals an organization of chondrocytes and their matrices that is similar to that of the parent articular cartilage in vivo.

Connective tissue growth factor does not affect transforming growth factor-beta 1-induced Smad3 phosphorylation and T lymphocyte proliferation inhibition.

Transforming growth factor-beta 1 (TGF-beta(1)) is a key regulator of immune tolerance. TGF-beta(1) controls T lymphocyte activation and is involved in the immunosuppressive function and generation of regulatory T lymphocytes. Connective tissue growth factor (CTGF) has an essential role in the formation of connective tissue and blood vessels. CTGF expression is induced by TGF-beta(1) in several cell types and CTGF mediates several of the downstream actions of TGF-beta(1). Since little is known about the potential synergy between CTGF and TGF-beta(1) in T lymphocyte biology, the purpose of the present study was to determine whether CTGF can modulate TGF-beta(1)-mediated effects on human CD4+ T lymphocytes. Human recombinant CTGF was expressed in HEK293 cells. rCTGF was biologically active demonstrated by induction of proliferation in the endothelial cell line EA hy 926. rCTGF alone did not potentiate or diminish anti-CD3-induced CD4+ T lymphocyte proliferation and did not activate the Smad signaling pathway in CD4+ T lymphocytes. Furthermore, rCTGF did not attenuate TGF-beta(1)-mediated inhibition of CD4+ T lymphocyte proliferation and TGF-beta(1)-induced Smad signaling in CD4+ T lymphocytes. These results indicate that rCTGF had no detectable effects of its own on human CD4+ T lymphocytes and did not potentiate the effects of low amounts of TGF-beta(1) on human CD4+ T lymphocytes. Overall, these data support the hypothesis that CTGF does not act on CD4+ T lymphocytes.

Isolation and study of an acquired inhibitor of human coagulation factor V.

A coagulation Factor V inhibitor developed in a man 75 yr of age in association with an anaplastic malignancy and drug treatment (including the aminoglycoside antibiotic, gentamicin). The patient did not bleed abnormally, despite both surgical challenge and plasma Factor V activity of less than 1%. The inhibited plasma had grossly prolonged prothrombin and activated partial thromboplastin times, but a normal thrombin time. Mixing studies indicated progressive coagulation inhibition with normal plasma, but not with Factor V-deficient plasma, and reversal of coagulation inhibition by the addition of bovine Factor V to the patient's plasma. 1 ml of patient plasma inhibited the Factor V activity of 90 ml of normal human plasma. The inhibitor was isolated by sequential affinity chromatography on protein A-Sepharose and Factor V-Sepharose. The IgG isolate markedly inhibits the activity of prothrombinase assembled from purified Factors Xa and Va, calcium ion, and phospholipid vesicles, and partially inhibits prothrombinase assembled from purified Factor Xa, calcium ion, and normal platelets. The Factor V of platelets, however, appears relatively inaccessible to the antibody, inasmuch as platelets isolated from whole blood supplemented for 8 h with the antibody functioned normally with respect to platelet Factor V-mediated prothrombinase function. The absence of obvious hemorrhagic difficulties in the patient, the total inhibition of plasma Factor V by the inhibitor, and the apparent inaccessibility of platelet Factor V to the inhibitor specifically implicate platelet Factor V in the maintenance of hemostasis.

Peri-implant inflammation defined by the implant-abutment interface.

An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 +/- 691 vs. 2398 +/- 1077 neutrophils/mm(2)). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.

A procedure to define natural groundwater conditions of groundwater bodies in Germany.

Commissioned by Germany's Working Group of the Federal States on Water Problems (LAWA) the authors developed a procedure to define natural groundwater conditions from groundwater monitoring data. The distribution pattern of a specific groundwater parameter observed by a number of groundwater monitoring stations within a petrographically comparable groundwater typology is reproduced by two statistical distribution functions, representing the "natural" and "influenced" components. The range of natural groundwater concentrations is characterized by confidence intervals of the distribution function of the natural component. The applicability of the approach was established for four hydrochemically different groundwater typologies occurring throughout Germany. Based on groundwater monitoring data from 7920 groundwater monitoring stations, 15 different hydrochemical parameters were evaluated for each groundwater typology. For all investigated parameters the range of natural groundwater concentrations has been identified. According to the requirements of the EC Water Framework Directive (article 17) (WFD) this study is a basis for the German position to propose criteria for assessing a reference state for a "good groundwater chemical status".

BM 21.0955, a potent new bisphosphonate to inhibit bone resorption.

A total of 300 new bisphosphonates were screened for their effect on bone resorption in the rat. Among these, 1-hydroxy-3-(methylpentylamino)propylidenebisphosphonate (BM 21.0955) was selected for detailed investigation. It inhibited arotinoid-stimulated bone resorption as assessed by calcemia in thyroparathyroidectomized rats at a SC dose as low as 0.001 mg P (0.016 mumol) per kg body weight per day. The compound was thus about 2, 10, 50, and 500 times more potent than risedronate, alendronate, pamidronate, and clodronate, respectively. Intravenous administration was as effective as subcutaneous, and oral administration was 100 times less effective. The effect after one administration decreased with time but was still measurable after 2 weeks. Nonstimulated bone resorption assayed by the urinary excretion of radiolabeled tetracycline from lifelong prelabeled animals was also inhibited. This effect started 3 days after a single dose and was still maximal after 7 days. Histomorphometric analysis of the tibial metaphysis in growing intact rats also showed an inhibition of bone resorption along with an increase in bone mass. The number of osteoclasts increased in animals treated with 0.01 and 0.1 mg P per kg (0.16 and 1.6 mumol/kg) body weight SC but decreased in animals given 1 mg P per kg (16.1 mumol/kg), showing that the inhibition of bone resorption was not due to an inhibition of osteoclast recruitment. No inhibition of mineralization occurred. This new bisphosphonate appears to have great potential for use in human bone disease.

Establishment and characterization of two immortalized cell lines of the osteoblastic lineage.

Osteoblastic cells were cloned by culturing rat calvariae cells in agarose in the presence of TGF-beta and EGF. Two bone cell lines were established by immortalizing such an osteoblastic clonal cell population by the introduction of the avian v-mycOK10 gene in the form of a mouse ecotropic retrovirus. Although originating from the same clonal cell population, the two lines exhibited somewhat differing properties. IRC10/30-myc1 expressed alkaline phosphatase (AP), showed PTH- and PGE2-induced cAMP production, synthesized mainly collagen type I and a minor fraction of type III, and produced mRNA for the bone-specific protein osteocalcin. IRC10/30-myc3 did not express AP, showed no PTH responsiveness, and synthesized only about one-third as much collagen as IRC10/30-myc1 (4 versus 12% of total protein synthesis). However, the cell line IRC10/30-myc3 was induced to synthesize cAMP by PGE2 and produced osteocalcin mRNA. When cultured in vivo in diffusion chambers, both lines proved to be osteogenic. Besides bone, both lines also formed cartilage and fibrous tissue. Thus, by immortalizing a clonal cell population of the osteoblastic phenotype, cell lines expressing varying properties can emerge. Furthermore, the expression of alkaline phosphatase and PTH-inducible adenylate cyclase are not prerequisites for a cell to form bone in vivo. Finally, cells expressing the phenotype of differentiated osteoblasts, including osteocalcin synthesis, still have a multipotential differentiation capacity and form bone and cartilage in vivo.

Ruthenium hexammine trichloride (RHT)-mediated interaction between plasmalemmal components and pericellular matrix proteoglycans is responsible for the preservation of chondrocytic plasma membranes in situ during cartilage fixation.

Treatment of cartilage tissue with the cationic dye ruthenium hexammine trichloride (RHT) prior to fixation has been shown to prevent the detachment of chondrocytic plasmalemmata from the pericellular matrix and the aqueous extraction of proteoglycans during the subsequent fixation procedures. However, plasmalemmal rupture is prevented only by the simultaneous addition of RHT and the dialdehydic fixative glutaraldehyde. It is proposed that RHT forms an electrostatic cross-linkage between anionic components within the chondrocytic plasmalemma and proteoglycans of the pericellular matrix; experimental support for this hypothesis is presented. The precise nature of the plasmalemmal components with which RHT interacts is unknown. However, since their anionic properties are apparently lost following treatment with chondroitinase ABC, it seems likely that they represent chondroitin sulfate groups of membrane intercalated proteoglycans.

Is longitudinal bone growth influenced by diurnal variation in the mitotic activity of chondrocytes of the growth plate?

The diurnal variations in the mitotic index, height, and rate of linear bone growth were determined and correlations between these parameters examined. Young, unweaned, female Wistar rats were housed under standardized conditions, labeled with a fluorochrome 60 h before sacrifice, and killed at intervals throughout a 24-h period, specifically 0600, 1200, 1800, and 2400. The proximal tibial epiphyseal growth plates were collected and processed, and the mitotic index, growth plate height, and the rate of linear bone growth were measured. The mitotic index measured at 0600 was significantly higher than that measured at 1800 and 2400. Growth plates of rats sacrificed at 1200 were taller than those of rats sacrificed at 1800, but there was no difference between heights of growth plates from rats sacrificed at other times. Daily growth rate for all rats averaged 283.9 microns/day and there were no statistically significant differences between daily growth rates measured at any time period. Our findings imply that in comparative, quantitative structural studies of animal groups, sacrifice should be carried out at identical times of the day, since, given a constant speed of vascular ingrowth and diurnal variation in width, relative diurnal accumulation and depletions of cells may take place. We also suggest that the daily growth rate and mitotic index be measured directly and not be considered a function of the height of the growth plate.

Enhanced bone apposition to a chemically modified SLA titanium surface.

Increased surface roughness of dental implants has demonstrated greater bone apposition; however, the effect of modifying surface chemistry remains unknown. In the present study, we evaluated bone apposition to a modified sandblasted/acid-etched (modSLA) titanium surface, as compared with a standard SLA surface, during early stages of bone regeneration. Experimental implants were placed in miniature pigs, creating 2 circular bone defects. Test and control implants had the same topography, but differed in surface chemistry. We created the test surface by submerging the implant in an isotonic NaCl solution following acid-etching to avoid contamination with molecules from the atmosphere. Test implants demonstrated a significantly greater mean percentage of bone-implant contact as compared with controls at 2 (49.30 vs. 29.42%; p = 0.017) and 4 wks (81.91 vs. 66.57%; p = 0.011) of healing. At 8 wks, similar results were observed. It is concluded that the modSLA surface promoted enhanced bone apposition during early stages of bone regeneration.

Persistent acute inflammation at the implant-abutment interface.

The inflammatory response adjacent to implants has not been well-investigated and may influence peri-implant tissue levels. The purpose of this study was to assess, histomorphometrically, (1) the timing of abutment connection and (2) the influence of a microgap. Three implant designs were placed in the mandibles of dogs. Two-piece implants were placed at the alveolar crest and abutments connected either at initial surgery (non-submerged) or three months later (submerged). The third implant was one-piece. Adjacent interstitial tissues were analyzed. Both two-piece implants resulted in a peak of inflammatory cells approximately 0.50 mm coronal to the microgap and consisted primarily of neutrophilic polymorphonuclear leukocytes. For one-piece implants, no such peak was observed. Also, significantly greater bone loss was observed for both two-piece implants compared with one-piece implants. In summary, the absence of an implant-abutment interface (microgap) at the bone crest was associated with reduced peri-implant inflammatory cell accumulation and minimal bone loss.

Quantitation of chondrocyte performance in growth-plate cartilage during longitudinal bone growth.

The longitudinal growth of bone depends on the activities of individual chondrocytes of the growth plate. Each chondrocyte remains in a fixed location throughout its life, and there accomplishes all of its functions. Although a cell may perform several or all of its activities simultaneously, one of these will usually predominate during a particular phase of its life. The two most prominent stages are those of cellular proliferation and hypertrophy (including the mineralization of matrix) before the resorption of tissue during vascular invasion. By applying recently developed stereological procedures and improved methods for the fixation of cartilage, we compared cellular shape modulation, various ultrastructural parameters (surface areas or volumes of endoplasmic reticulum, Golgi membranes, and mitochondria), the production of matrix, and cellular turnover for proliferating and hypertrophic chondrocytes within the proximal tibial growth plate of the rat. By the late hypertrophic stage, fourfold and tenfold increases in the mean cellular height and volume, respectively, and a threefold increase in the mean volume of the matrix per cell were achieved. The high metabolic activity of hypertrophic cells was reflected by a twofold to fivefold increase in the mean cellular surface area of rough endoplasmic reticulum, the Golgi membranes, and the mean cellular mitochondrial volume. Rates of longitudinal growth were determined by fluorochrome labeling and incident-light fluorescence microscopy. Using these values and the stereological estimators describing cellular height, the rates of cellular turnover were calculated. The rapid progression of the vascular invasion front was found to eliminate, for each column of cells, one chondrocyte every three hours; that is, eight cells a day. The maintenance of a steady-state structure for growth-plate cartilage in rats in a steady state of growth thus necessitates efficient compensation for these losses, which is achieved by a high rate of cellular proliferation and rapid hypertrophy.

Crestal bone changes around titanium implants. A histometric evaluation of unloaded non-submerged and submerged implants in the canine mandible.

BACKGROUND: Today, implants are placed using both non-submerged and submerged approaches, and in 1- and 2-piece configurations. Previous work has demonstrated that peri-implant crestal bone reactions differ radiographically under such conditions and are dependent on a rough/smooth implant border in 1-piece implants and on the location of the interface (microgap) between the implant and abutment/restoration in 2-piece configurations. The purpose of this investigation was to examine histometrically crestal bone changes around unloaded non-submerged and submerged 1- and 2-piece titanium implants in a side-by-side comparison. METHODS: A total of 59 titanium implants were randomly placed in edentulous mandibular areas of 5 foxhounds, forming 6 different implant subgroups (types A-F). In general, all implants had a relatively smooth, machined coronal portion as well as a rough, sandblasted and acid-etched (SLA) apical portion. Implant types A-C were placed in a non-submerged approach, while types D-F were inserted in a submerged fashion. Type A and B implants were 1-piece implants with the rough/smooth border (r/s) at the alveolar crest (type A) or 1.0 mm below (type B). Type C implants had an abutment placed at the time of surgery with the interface located at the bone crest level. In the submerged group, types D-F, the interface was located either at the bone crest level (type D), 1 mm above (type E), or 1 mm below (type F). Three months after implant placement, abutment connection was performed in the submerged implant groups. At 6 months, all animals were sacrificed. Non-decalcified histology was analyzed by evaluating peri-implant crestal bone levels. RESULTS: For types A and B, mean crestal bone levels were located adjacent (within 0.20 mm) to the rough/smooth border (r/s). For type C implants, the mean distance (+/- standard deviation) between the interface and the crestal bone level was 1.68 mm (+/- 0.19 mm) with an r/s border to first bone-to-implant contact (fBIC) of 0.39 mm (+/- 0.23 mm); for type D, 1.57 mm (+/- 0.22 mm) with an r/s border to fBIC of 0.28 mm (+/- 0.21 mm); for type E, 2.64 mm (+/- 0.24 mm) with an r/s border to fBIC of 0.06 mm (+/- 0.27 mm); and for type F, 1.25 mm (+/- 0.40 mm) with an r/s border to fBIC of 0.89 mm (+/- 0.41 mm). CONCLUSIONS: The location of a rough/smooth border on the surface of non-submerged 1-piece implants placed at the bone crest level or 1 mm below, respectively, determines the level of the fBIC. In all 2-piece implants, however, the location of the interface (microgap), when located at or below the alveolar crest, determines the amount of crestal bone resorption. If the same interface is located 1 mm coronal to the alveolar crest, the fBIC is located at the r/s border. These findings, as evaluated by non-decalcified histology under unloaded conditions, demonstrate that crestal bone changes occur during the early phase of healing after implant placement. Furthermore, these changes are dependent on the surface characteristics of the implant and the presence/absence as well as the location of an interface (microgap). Crestal bone changes were not dependent on the surgical technique (submerged or non-submerged).

Influence of the size of the microgap on crestal bone changes around titanium implants. A histometric evaluation of unloaded non-submerged implants in the canine mandible.

BACKGROUND: Endosseous implants can be placed according to a non-submerged or submerged approach and in 1- or 2-piece configurations. Recently, it was shown that peri-implant crestal bone changes differ significantly under such conditions and are dependent on a rough/smooth implant border in 1-piece implants and on the location of an interface (microgap) between the implant and abutment/restoration in 2-piece configurations. Several factors may influence the resultant level of the crestal bone under these conditions, including movements between implant components and the size of the microgap (interface) between the implant and abutment. However, no data are available on the impact of possible movements between these components or the impact of the size of the microgap (interface). The purpose of this study was to histometrically evaluate crestal bone changes around unloaded, 2-piece non-submerged titanium implants with 3 different microgap (interface) dimensions and between implants with components welded together or held together by a transocclusal screw. METHODS: A total of 60 titanium implants were randomly placed in edentulous mandibular areas of 5 hounds forming 6 different implant subgroups (A through F). In general, all implants had a relatively smooth, machined suprabony portion 1 mm long, as well as a rough, sandblasted, and acid-etched (SLA) endosseous portion, all placed with their interface (microgap) 1 mm above the bone crest level and having abutments connected at the time of first-stage surgery. Implant types A, B, and C had a microgap of < 10 microns, approximately 50 microns, or approximately 100 microns between implant components as did types D, E, and F, respectively. As a major difference, however, abutments and implants of types A, B, and C were laser-welded together, not allowing for any movements between components, as opposed to types D, E, and F, where abutments and implants were held together by abutment screws. Three months after implant placement, all animals were sacrificed. Non-decalcified histology was analyzed histometrically by evaluating peri-implant crestal bone changes. RESULTS: For implants in the laser-welded group (A, B, and C), mean crestal bone levels were located at a distance from the interface (IF; microgap) to the first bone-to-implant contact (fBIC) of 1.06 +/- 0.46 mm (standard deviation) for type A, 1.28 +/- 0.47 mm for type B, and 1.17 +/- 0.51 mm for type C. All implants of the non-welded group (D, E, and F) had significantly increased amounts of crestal bone loss, with 1.72 +/- 0.49 mm for type D (P < 0.01 compared to type A), 1.71 +/- 0.43 mm for type E (P < 0.02 compared to type B), and 1.65 +/- 0.37 mm for type F (P < 0.01 compared to type C). CONCLUSIONS: These findings demonstrate, as evaluated by non-decalcified histology under unloaded conditions in the canine mandible, that crestal bone changes around 2-piece, non-submerged titanium implants are significantly influenced by possible movements between implants and abutments, but not by the size of the microgap (interface). Thus, significant crestal bone loss occurs in 2-piece implant configurations even with the smallest-sized microgaps (< 10 microns) in combination with possible movements between implant components.

Recombinant human bone morphogenetic protein-2 stimulation of bone formation around endosseous dental implants.

BACKGROUND: Successful endosseous implant placement requires that the implant be stable in alveolar bone. In certain cases, the implant can be stabilized in native bone but some part of the implant is not covered by bone tissue. This often occurs during placement of implants into extraction sites or in areas where bone resorption has occurred and the ridge width is not sufficient to completely surround the implant. In those cases, the clinician usually employs a procedure to encourage bone formation. These procedures typically include a bone graft and/or membrane therapy. Recent advances have led to the isolation, cloning, and production of recombinant human proteins that stimulate bone formation. One of these bone morphogenetic proteins (rhBMP-2) has been extensively studied in animal models and is currently being tested in human clinical trials. METHODS: In this study, rhBMP-2 was tested using a collagen sponge carrier to stimulate bone formation in defects in the canine mandible around endosseous dental implants. Six animals had a total of 48 implants placed. rhBMP-2 with the collagen carrier was implanted around 24 of these, the remainder having only the collagen carrier placed. Half the sites were covered with a nonresorbable expanded polytetrafluoroethylene membrane. Histologic analysis was performed after 4 and 12 weeks. The area of new bone formed, percentage of bone-to-implant contact in the defect area, and percentage fill of the defect was calculated. RESULTS: The addition of rhBMP-2 resulted in significantly greater amounts of new bone area and percentage of bone-to-implant contact and with more percentage fill after 4 and 12 weeks of healing. The area of new bone formed was reduced after 4 weeks when a membrane was present but after 12 weeks, there was no significant difference between membrane and non-membrane treated sites. In some specimens, new bone was found coronal to the membranes, with rhBMP-2-treated sites having greater amounts than non-rhBMP-2-treated sites. CONCLUSIONS: These data demonstrate that a bone differentiation factor significantly stimulates bone formation in peri-implant bone defects in the canine mandible. In addition, bone-to-implant contact was significantly enhanced along the rough implant surface. Membrane-treated sites had less new bone formation after 4 weeks of healing but were similar to non-membrane sites after 12 weeks. These results demonstrate that rhBMP-2 can be used to stimulate bone growth both around and onto the surface of endosseous dental implants placed in sites with extended peri-implant osseous defects.

Biologic width around titanium implants. A histometric analysis of the implanto-gingival junction around unloaded and loaded nonsubmerged implants in the canine mandible.

The use of endosseous dental implants as transmucosal devices necessitates the successful integration of three different tissues: bone, connective tissue, and epithelium. So far, studies have predominantly focused on hard tissue integration. Much less is known about soft tissues. This study examined the dimensions of the implantogingival junction in relation to clinically healthy unloaded and loaded nonsubmerged implants. In total, 69 titanium plasma-sprayed (TPS) and sandblasted acid-etched (SLA) implants were placed in an alternating fashion in six foxhounds and allowed to heal for 3 months. Two dogs were sacrificed after the initial healing period. The remaining four dogs had crowns fabricated that were allowed to function for up to 12 months. These animals were sacrificed after 3 and 12 months of loading. Histometric analysis of undecalcified histologic sections included the evaluation of the sulcus depth (SD), the dimensions of the junctional epithelium (JE), and the connective tissue contact (CTC). Mean values in the 3 month unloaded group were 0.49 mm for SD, 1.16 mm for JE, and 1.36 mm for CTC. These dimensions were 0.50 mm for SD, 1.44 mm for JE, and 1.01 mm for CTC for the 3 month loaded group. After 12 months of loading, these values were 0.16 mm for SD, 1.88 mm for JE, and 1.05 mm for CTC. The sum of these measurements was similar for the different time points and similar to the same dimensions around teeth. TPS and SLA surfaces had no influence on the evaluated parameters (P > 0.05). The data suggest that a biologic width exists around unloaded and loaded nonsubmerged one-part titanium implants and that this is a physiologically formed and stable dimension as is found around teeth.