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Biomedical subjects

J J Jacobs

Publications and source records attributed to J J Jacobs.

At least 19 recordsLinked to original sources

Differential lymphocyte reactivity to serum-derived metal-protein complexes produced from cobalt-based and titanium-based implant alloy degradation.

The lymphocyte response to serum protein complexed with metal from implant alloy degradation was investigated in this in vitro study using primary human lymphocytes from healthy volunteers (n = 10). Cobalt chromium molybdenum alloy (Co-Cr-Mo, ASTM F-75) and titanium alloy (Ti-6Al-4V, ASTM F-136) beads (70 microm) were incubated in agitated human serum at 37 degrees C to simulate naturally occurring metal implant alloy degradation processes. Particulate free serum samples that had been incubated with metal were then separated into molecular weight based fractions. The amounts of soluble Cr and Ti within each serum fraction were measured and correlated with lymphocyte proliferation response to the individual serum fractions. Lymphocytes from each subject were cultured with 11 autologous molecular weight based serum fractions either with or without added metal. Two molecular weight ranges of human serum proteins were associated with the binding of Cr and Ti from Co-Cr-Mo and Ti implant alloy degradation (at <30 and 180-250 kDa). High molecular weight serum proteins ( approximately 180 kDa) demonstrated greater lymphocyte reactivity when complexed with Cr alloy and Ti alloy than low (5-30 kDa) and midrange (30-77 kDa) serum proteins. When the amount of lymphocyte stimulation was normalized to both the moles of metal and the moles of protein within each fraction (metal-protein complex reactivity index), Cr from Co-Cr-Mo alloy degradation demonstrated approximately 10-fold greater reactivity than Ti in the higher molecular weight serum proteins ( approximately 180 kDa). This in vitro study demonstrated a lymphocyte proliferative response to both Co-Cr-Mo and Ti alloy metalloprotein degradation products. This response was greatest when the metals were complexed with high molecular weight proteins, and with metal-protein complexes formed from Co-Cr-Mo alloy degradation.

Absorbable Implants↗

An automated method for the quantification of immunostained human Langerhans cells.

Allergic contact dermatitis is a frequent and increasing health problem. For ethical reasons, the current animal tests used to screen for contact sensitizers should be replaced by in vitro alternatives. Contact sensitizers have been shown to accelerate Langerhans cell (LC) migration from human organotypic skin explant cultures (hOSECs) more rapidly than non-sensitizers and it has been proposed that the hOSEC model could be used to screen for sensitizers. However, chemically induced decreases in epidermal LC numbers need to be accurately quantified if the alterations in epidermal LC numbers are to form the basis of an alternative system for screening contact sensitizers in vitro. As manual counting of LCs is labour intensive and subject to intra- and inter-personal variation we developed an image analysis routine, using the Leica QWin image analysis software, to quantify LCs in situ using immunohistochemically stained skin sections. LCs can be identified using antibodies against the membrane molecule CD1a or the Lag antibody, which recognises cytoplasmic Birbeck granules. Quantification of epidermal LC number using the image analysis software had a much lower inter-person variation than when the same specimens were counted manually, using both the anti-Lag and CD1a antibodies. The software-aided quantification of epidermal LCs provides an accurate method for measuring chemically-induced changes in LC numbers.

Antigens, CD1↗

The potential role of the osteoblast in the development of periprosthetic osteolysis: review of in vitro osteoblast responses to wear debris, corrosion products, and cytokines and growth factors.

Limited information is available on the responses of osteoblasts to wear debris, corrosion products, and cytokines and on the roles of altered osteoblast functions in the development of periprosthetic bone loss. Wear debris-challenged osteoblasts exhibit altered functions resulting in the loss of their capacity to produce bone matrix and to replace the resorbed bone. Also, osteoblasts may secrete cytokines, which act in a paracrine fashion to recruit inflammatory cells into the periprosthetic space and to stimulate osteoclastic bone resorption. These effects may be mediated in part by ionic metal dissolution products. We review the mechanisms by which altered osteoblast functions, in response to particulate wear debris, corrosion products, and cytokines and growth factors, may contribute to the development and the progression of periprosthetic osteolysis.

Corrosion↗

Evaluation of metallic and polymeric biomaterial surface energy and surface roughness characteristics for directed cell adhesion.

Directed cell adhesion remains an important goal of implant and tissue engineering technology. In this study, surface energy and surface roughness were investigated to ascertain which of these properties show more overall influence on biomaterial-cell adhesion and colonization. Jet impingement was used to quantify cellular adhesion strength. Cellular proliferation and extracellular matrix secretion were used to characterize colonization of 3T3MC fibroblasts on: HS25 (a cobalt based implant alloy, ASTM F75), 316L stainless steel, Ti-6Al4V (a titanium implant alloy), commercially pure tantalum (Ta), polytetrafluoroethylene (PTFE), silicone rubber (SR), and high-density polyethylene (HDPE). The metals exhibited a nearly five-fold greater adhesion strength than the polymeric materials tested. Generally, surface energy was proportional to cellular adhesion strength. Only polymeric materials demonstrated significant increased adhesion strength associated with increased surface roughness. Cellular adhesion on metals demonstrated a linear correlation with surface energy. Less than half as much cellular proliferation was detected on polymeric materials compared to the metals. However the polymers tested demonstrated greater than twice the amount of secreted extracellular matrix (ECM) proteins on a per cell basis than the metallic materials. Thus, surface energy may be a more important determinant of cell adhesion and proliferation, and may be more useful than surface roughness for directing cell adhesion and cell colonization onto engineered tissue scaffoldings.

3T3 Cells↗

Long-term followup of the Miller-Galante total knee replacement.

One hundred seventy-two consecutive cemented Miller-Galante-I total knee arthroplasties in 155 patients were compared with 109 consecutive cemented Miller-Galante-II total knee arthroplasties in 92 patients. The average followup was 11 years (range, 8-15 years) and 9 years (range, 8-10 years), respectively. Of the 172 Miller-Galante-I arthroplasties, there have been 21 revisions; 15 patellar revisions; two included femoral revisions attributable to abrasion. Six additional well-fixed femoral and tibial components were revised: two for early instability, one for pain, one for periprosthetic fracture, and two for infection. No component had aseptic loosening or osteolysis. Using revision or loosening of any components as the end point, the Kaplan-Meier 10-year survivorship was 84.1% +/- 4.1%. Of the 109 Miller-Galante-II arthroplasties, there have been no component revisions, no aseptic loosening, and no osteolysis. Using revision or loosening of any components as the end point, the Kaplan-Meier 10-year survivorship was 100%. The Miller-Galante knee systems showed excellent fixation with no loosening and no osteolysis at as many as 15 years. Additionally, there have been no component revisions for late instability at as many as 15 years. Finally, the high prevalence of patellofemoral complications with the Miller-Galante-I design has been obviated with the Miller-Galante-II design.

Adult↗

Problems with cementless total knee arthroplasty at 11 years followup.

One hundred two patients with 131 consecutive cementless total knee arthroplasties that retained the posterior cruciate ligament were followed up prospectively. The average age of the patients was 58 years (range, 32-75 years). The mean followup on the surviving knee arthroplasties was 11 years (range, 7-16 years). The patellar component was metal-backed in the first 112 (85%) knees, cementless all-polyethylene in the last 17 (13%) knees, and two knees had a prior patellectomy. Forty-four metal-backed patellar components (48%) were revised; nine were loose, and 35 had polyethylene wear through. Thirteen femoral components (12%) were revised because of femoral abrasion from a failed metal-backed patellar component. No other femoral component was revised, loose, or had osteolysis develop. Nine (8%) tibial components had failure of ingrowth; eight have been revised. Partial radiolucencies occurred in 53% of the tibias. Thirteen (12%) small osteolytic lesions developed, all around screws or screw holes in the tibial components. At an average of 11 years followup, cementless fixation yielded mixed results: cementless femoral fixation was excellent and metal-backed patellar components had a 48% patellar revision rate. Cementless tibial components had an 8% aseptic loosening rate and a 12% incidence of small osteolytic lesions. Based on these results, the authors have abandoned cementless fixation in total knee arthroplasty.

Adult↗

Gout-induced arthropathy after total knee arthroplasty: a report of two cases.

Gout, although relatively rare in joint replacements, can present as an acute or chronic painful knee or hip arthroplasty. Gout and acute infection of a joint replacement can be difficult to differentiate, with the physical examination and laboratory study results frequently being similar. Both conditions can present with a rapid onset of joint pain, swelling, erythema, and constitutional symptoms, including fevers and malaise. Laboratory findings in both conditions often include an elevated leukocyte count, erythrocyte sedimentation rate, and C-reactive protein level. Negatively birefringent, needle-shaped crystals in the synovial fluid confirm the diagnosis of gout. The mistaken diagnosis of septic arthritis in a joint replacement with crystal-induced synovitis can lead to inappropriate open debridement or component removal. The current study includes a review of the literature and presents two cases of gout after total knee arthroplasty. These cases suggest that in situations of suspected sepsis without synovial fluid crystals, operative intervention is indicated with a presumed diagnosis of septic arthritis. The identification of chalky white or yellow deposits in the synovium or bone is highly suggestive of gout. The definitive diagnosis is made by polarized light histologic evaluation of these tissues. If these deposits are present in the absence of a positive preoperative culture, positive Gram stain for bacteria, or component loosening, component retention is indicated.

Aged↗

Osteolysis: basic science.

Since the recognition of aseptic loosening by Charnley in the early 1960s, much information has been gained on the basic science of periprosthetic bone loss. Initially termed cement disease, it now generally is accepted that, in most instances, osteolysis is a manifestation of an adverse cellular response to phagocytosable particulate wear and corrosion debris, possibly facilitated by local hydrodynamic effects. Tissue explant, animal, and cell culture studies have allowed us to compile an appreciation of the complexity of cellular interactions and chemical mediators involved in osteolysis. Cellular participants have been shown to include the macrophage, osteoblast, fibroblast, and osteoclast. The plethora of chemical mediators that are responsible for the cellular responses and effects on bone include prostaglandin E2, tumor necrosis factor-alpha, interleukin-1, and interleukin 6. However, an increasing number of other proinflammatory and antiinflammatory cytokines, prostenoids, and enzymes have been shown to play important roles in this process. The ultimate goal of basic research is to develop novel strategies for evaluation and treatment of patients with osteolysis. Although initial animal studies are promising for possible pharmacologic treatment and prevention of osteolysis, well-controlled human trials are required before agents such as bisphosphonates can be recommended for general clinical use.

Animals↗

Ruptured intracranial mycotic aneurysm: an unusual infectious complication following craniofacial surgery.

The case of a child with Apert syndrome is presented in which the development and rupture of an intracranial mycotic aneurysm occurred secondary to multiple infectious complications following craniofacial surgery. An endovascular procedure was utilized in an attempt to embolize the aneurysm and parent vessel. The patient recovered from her infections, but retained a residual right hemiparesis and left cranial nerve III palsy at the time of discharge. To our knowledge, this is the first report of a mycotic aneurysm developing after a craniofacial procedure. Risk factors leading to aneurysm formation in this case are presented, as well as a literature review of neurological complications following craniofacial surgery.

Acrocephalosyndactylia↗

Primary repair of intraoperative disruption of the medical collateral ligament during total knee arthroplasty.

BACKGROUND: Intraoperative disruption of the medial collateral ligament during total knee arthroplasty is an uncommon complication that is frequently treated by implanting a prosthesis with varus-valgus constraint. To our knowledge, no data have been published on primary repair or reattachment of the medial collateral ligament and implantation of a minimally constrained posterior-stabilized or cruciate-retaining prosthesis. This retrospective study evaluates the hypothesis that satisfactory clinical results, at a minimum of two years, can be achieved with immediate repair or reattachment of the medial collateral ligament and without a constrained total knee prosthesis. METHODS: Of 600 knees treated with primary total knee arthroplasty, sixteen (in fourteen patients) sustained either a midsubstance disruption of the medial collateral ligament or an avulsion of the ligament from bone during the procedure. Preoperatively, all patients had either neutral or varus alignment and an intact medial collateral ligament. Midsubstance tears were treated with direct primary repair, and avulsions of the ligament off the tibia or femur were treated with suture-anchor reattachment to bone. All patients wore a hinged knee brace, with no limit to the range of motion, for six weeks postoperatively. Clinical and radiographic data were gathered prospectively as part of a database that was ongoing throughout the period of study; the cohort of patients was assembled retrospectively by searching that database. RESULTS: No patients were lost to follow-up. The mean duration of follow-up was forty-five months (range, twenty-four to ninety-five months). The Hospital for Special Surgery knee scores increased from a mean of 47 points (poor) preoperatively to a mean of 93 points (excellent) at the time of final follow-up. On physical examination, no patient had a Hospital for Special Surgery score in the fair or poor range and all patients had regained normal stability in the coronal plane both at full extension and at 30 degrees of flexion. No patient required knee-bracing beyond the initial six-week postoperative period. The range of motion at the time of final follow-up averaged 108 degrees (range, 85 degrees to 125 degrees ), although one knee required manipulation under anesthesia to obtain a satisfactory range of motion. No arthroplasties required revision. Radiographic examination demonstrated appropriate limb alignment in all patients at the time of final follow-up. CONCLUSIONS: Intraoperative disruption of the medial collateral ligament can be treated with primary repair or reattachment of the ligament to bone and postoperative bracing with good results; this avoids the potential disadvantages associated with the use of varus-valgus constrained implants.

Aged↗

The effects of particulate wear debris, cytokines, and growth factors on the functions of MG-63 osteoblasts.

BACKGROUND: Particle-challenged cells release cytokines, chemokines, and eicosanoids, which contribute to periprosthetic osteolysis. The particle-induced activation of macrophages and monocytes has been extensively studied, but only limited information is available on the response of osteoblasts to particulate wear debris. This study examines the effects of particulate wear debris, proinflammatory cytokines, and growth factors on osteoblast functions. METHODS: MG-63 osteoblasts were treated with metal particles (titanium, titanium alloy, and chromium orthophosphate) or polymeric particles (polyethylene and polystyrene) of phagocytosable sizes or were treated with exogenous cytokines and growth factors. The kinetics of particle phagocytosis and the number of engulfed particles were assessed with use of fluoresceinated particles. Cell proliferation was determined according to [3H]-thymidine incorporation, and cell viability was determined by either fluorescein diacetate uptake or trypan blue exclusion. Expressions of osteoblast-specific genes were quantified with Northern blot hybridization, and the secretions of osteoblast-specific proteins and cytokines were analyzed by enzyme-linked immunosorbent assays. RESULTS: MG-63 osteoblasts phagocytosed particles and became saturated after twenty-four hours. A maximum of forty to sixty particles per cell were phagocytosed. Each type of particle significantly suppressed procollagen alpha1[I] gene expression (p<0.05), whereas other osteoblast-specific genes (osteonectin, osteocalcin, and alkaline phosphatase) did not show significant changes. Particle-stimulated osteoblasts released interleukin-6 (p<0.05) and a smaller amount of transforming growth factor-beta1. Particles reduced cell proliferation in a dose-dependent manner without affecting cell viability (p<0.05). Exogenous tumor necrosis factor-alpha also enhanced the release of interleukin-6 (p<0.01) and transforming growth factor-beta1 (p<0.05), whereas the secretion of transforming growth factor-beta1 was increased by insulin-like growth factor-I and prostaglandin E2 as well. Insulin-like growth factor-I and transforming growth factor-beta1 significantly increased procollagen alpha1[I] gene expression in osteoblasts (p<0.05), while tumor necrosis factor-alpha and prostaglandin E2 significantly suppressed procollagen alpha1[I] gene expression (p<0.01). In contrast, neither exogenous nor endogenous interleukin-6 had any effect on other cytokine secretion, on proliferation, or on procollagen alpha1[I] gene expression. The transcription inhibitor actinomycin D reduced both procollagen alpha1[I] transcription and interleukin-6 production. Inhibitors of protein synthesis (cyclohexamide) and intracellular protein transport (brefeldin A and monensin) blocked the release of interleukin-6, but none of these compounds influenced the suppressive effect of titanium on procollagen alpha1[I] gene expression. CONCLUSIONS: MG-63 osteoblasts phagocytose particulate wear debris, and this process induces interleukin-6 production and suppresses type-I collagen synthesis. Osteoblast-derived interleukin-6 may induce osteoclast differentiation and/or activation, but the resorbed bone cannot be replaced by new bone because of diminished osteoblast function (reduced type-I collagen synthesis). Exogenous cytokines (tumor necrosis factor-alpha and interleukin-1beta), growth factors (insulin-like growth factor-I and transforming growth factor-beta1), and prostaglandin E2 can modify particulate-induced alterations of osteoblast functions.

Biocompatible Materials↗

Metal sensitivity in patients with orthopaedic implants.

All metals in contact with biological systems undergo corrosion. This electrochemical process leads to the formation of metal ions, which may activate the immune system by forming complexes with endogenous proteins. Implant degradation products have been shown to be associated with dermatitis, urticaria, and vasculitis. If cutaneous signs of an allergic response appear after implantation of a metal device, metal sensitivity should be considered. Currently, there is no generally accepted test for the clinical determination of metal hypersensitivity to implanted devices. The prevalence of dermal sensitivity in patients with a joint replacement device, particularly those with a failed implant, is substantially higher than that in the general population. Until the roles of delayed hypersensitivity and humoral immune responses to metallic orthopaedic implants are more clearly defined, the risk to patients may be considered minimal. It is currently unclear whether metal sensitivity is a contributing factor to implant failure.

Antibody Formation↗

Focal osteolysis at the junctions of a modular stainless-steel femoral intramedullary nail.

BACKGROUND: During routine follow-up of patients treated with a three-piece stainless-steel modular femoral nail, osteolysis and periosteal reaction around the modular junctions of some of the nails were noted on radiographs. The purpose of this study was to evaluate the prevalence, etiology, and clinical relevance of these radiographic findings. METHODS: Forty-four femoral fractures or nonunions in forty-two patients were treated with a modular stainless-steel femoral intramedullary nail. Seventeen nails were excluded, leaving twenty-seven intramedullary nails in twenty-seven patients for this study. All patients had had a femoral diaphyseal fracture; nineteen had had an acute fracture and eight, a nonunion. These twenty-seven patients returned for radiographs, a physical examination, assessment of functional outcomes, assessment of thigh pain with a visual analog scale, determination of serum chromium levels, and nail removal if desired. A control group of sixteen patients treated with a one-piece stainless-steel femoral intramedullary nail was evaluated with use of the same outcome measures and was compared with the group treated with the modular femoral nail with regard to prevalence of thigh pain and serum chromium levels. Twelve modular femoral nails were removed according to the study protocol. The modular nail junctions were analyzed for corrosion products, and histopathologic analysis of tissue specimens from the femoral canal was performed. RESULTS: The twenty-seven patients were seen at a mean of twenty-one months after fracture fixation; twenty-six of the twenty-seven fractures healed. Twenty-three femora had at least one of three types of abnormalities-osteolysis, periosteal reaction, or cortical thickening--localized to one or both modular junctions. Eighteen patients had severe reactions, defined as osteolysis of > or =2 mm, cortical thickening of > or =5 mm, and/or a periosteal reaction (group 1). Nine patients had mild or no reactions (group 2). Serum chromium levels in group 1 (mean, 1.27 ng/ mL; range, 0.34 to 3.12 ng/mL) were twice as high as those in group 2 (mean, 0.53 ng/mL; range, 0.12 to 1.26 ng/mL). However, this difference did not reach significance with the numbers available. The differences in serum chromium levels between group 1 and the control group with a one-piece nail (mean, 0.26 ng/mL; range, 0.015 to 1.25 ng/mL) (p<0.01) and a control group without an implant (mean, 0.05 ng/mL; range, 0.015 to 0.25 ng/ mL) (p<0.01) were significant. The level of thigh pain recorded on the visual analog scale was also significantly different between group 1 and the control group with a one-piece implant (p = 0.03). Retrieved modular nails had signs of fretting corrosion as well as stainless-steel corrosion products adherent to the junction where the osteolysis occurred. Histologic and spectrographic analysis revealed two types of corrosion products that were consistent with stainless-steel within the peri-implant tissue and were associated with a foreign-body granulomatous response. CONCLUSIONS: The presence of corrosion products at the taper junctions suggests that particulate debris was a major factor in the etiology of the radiographic findings of osteolysis, periosteal reaction, and cortical thickening. Serum chromium levels were substantially elevated in the patients with a modular femoral nail, and such levels may serve as a marker of fretting corrosion of these devices.

Adult↗

Cementless acetabular reconstruction after acetabular fracture.

BACKGROUND: Total hip arthroplasty in patients with posttraumatic arthritis has produced results inferior to those in patients with nontraumatic arthritis. The use of cementless acetabular reconstruction, however, has not been extensively studied in this clinical context. Our purpose was to compare the intermediate-term results of total hip arthroplasty with a cementless acetabular component in patients with posttraumatic arthritis with those of the same procedure in patients with nontraumatic arthritis. We also compared the results of arthroplasty in patients who had had prior operative treatment of their acetabular fracture with those in patients who had had prior closed treatment of their acetabular fracture. METHODS: Thirty total hip arthroplasties were performed with use of a cementless hemispheric, fiber-metal-mesh-coated acetabular component for the treatment of posttraumatic osteoarthritis after acetabular fracture. The median interval between the fracture and the arthroplasty was thirty-seven months (range, eight to 444 months). The average age at the time of the arthroplasty was fifty-one years (range, twenty-six to eighty-six years), and the average duration of follow-up was sixty-three months (range, twenty-four to 140 months). Fifteen patients had had prior open reduction and internal fixation of their acetabular fracture (open-reduction group), and fifteen patients had had closed treatment of the acetabular fracture (closed-treatment group). The results of these thirty hip reconstructions were compared with the intermediate-term results of 204 consecutive primary total hip arthroplasties with cementless acetabular reconstruction in patients with nontraumatic arthritis. RESULTS: Operative time (p < 0.001), blood loss (p < 0.001), and perioperative transfusion requirements (p < 0.001) were greater in the patients with posttraumatic arthritis than they were in the patients with nontraumatic arthritis. Of the patients with posttraumatic arthritis, those who had had open reduction and internal fixation of their acetabular fracture had a significantly longer index procedure (p = 0.01), greater blood loss (p = 0.008), and a higher transfusion requirement (p = 0.049) than those in whom the fracture had been treated by closed methods. Eight of the fifteen patients with a previous open reduction and internal fixation required an elevated acetabular liner compared with one of the fifteen patients who had been treated by closed means (p = 0.005). Two of the fifteen patients with a previous open reduction and internal fixation required bone-grafting of acetabular defects compared with seven of the fifteen patients treated by closed means (p = 0.04). The thirty patients treated for posttraumatic arthritis had an average preoperative Harris hip score of 41 points, which increased to 88 points at the time of follow-up; there was no significant difference between the open-reduction and closed-treatment groups (p = 0.39). Twenty-seven patients (90%) had a good or excellent result. There were no dislocations or deep infections. The Kaplan-Meier ten-year survival rate, with revision or radiographic loosening as the end point, was 97%. These results were similar to those of the patients who underwent primary total hip arthroplasty for nontraumatic arthritis. CONCLUSIONS: The intermediate-term clinical results of total hip arthroplasty with cementless acetabular reconstruction for posttraumatic osteoarthritis after acetabular fracture were similar to those after the same procedure for nontraumatic arthritis, regardless of whether the acetabular fracture had been internally fixed initially. However, total hip arthroplasty after acetabular fracture was a longer procedure with greater blood loss, especially in patients with previous open reduction and internal fixation. Previous open reduction and internal fixation predisposed the hip to more intraoperative instability but less bone deficiency.

Acetabulum↗

Posterior cruciate ligament-retaining total knee arthroplasty in patients with rheumatoid arthritis.

BACKGROUND: Although initial reports on posterior cruciate ligament-retaining total knee arthroplasty in patients with rheumatoid arthritis have been encouraging, a high rate of late instability necessitating revision has been reported recently. The purpose of the present prospective study was to analyze the results of posterior cruciate ligament-retaining total knee arthroplasty in patients with rheumatoid arthritis. METHODS: Seventy-two posterior cruciate ligament-retaining total knee arthroplasties in fifty-one patients with rheumatoid arthritis were studied prospectively. All procedures were performed with the Miller-Galante I prosthesis. Eighteen patients (twenty-four knees) died before the eight-year follow-up and one patient (two knees) was lost to follow-up, leaving forty-six knees (thirty-two patients) for review. These forty-six knees were evaluated clinically (with particular attention to posterior instability) and radiographically at annual intervals for a mean of 10.5 years (range, eight to fourteen years). RESULTS: Forty-four (95%) of forty-six knees had a good or excellent result at a mean of 10.5 years. However, nine (13%) of the original seventy-two knees had revision of the implant, with six of the revisions performed because of failure of a metal-backed patellar component. The rate of survival at ten years was 93% 4% with femoral or tibial revision for any reason as the end point and 81% 5% with any reoperation as the end point. There was no aseptic loosening in any knee. Posterior instability was identified clinically and/or radiographically in two (2.8%) of the original seventy-two knees; both unstable knees were in the same patient. CONCLUSION: Posterior cruciate ligament-retaining total knee arthroplasty yielded satisfactory clinical and radiographic results in patients with rheumatoid arthritis at intermediate-term follow-up (mean, 10.5 years). Therefore, we believe that it remains an excellent treatment option for these patients.

Adult↗

Second-generation cementless total hip arthroplasty. Eight to eleven-year results.

BACKGROUND: Second-generation cementless femoral components were designed to provide more reliable ingrowth and to limit distal osteolysis by incorporating circumferential proximal ingrowth surfaces. We examined the eight to eleven-year results of total hip arthroplasty with a cementless, anatomically designed femoral component and a cementless hemispheric acetabular component. METHODS: Ninety-two consecutive primary total hip arthroplasties with implantation of a femoral component with a circumferential proximal porous coating (Anatomic Hip) and a cementless hemispheric porous-coated acetabular component (Harris-Galante II) were performed in eighty-five patients. These patients were prospectively followed clinically and radiographically. Six patients (seven hips) died and five patients (seven hips) were lost to follow-up, leaving seventy-four patients (seventy-eight hips) who had been followed for a mean of ten years (range, eight to eleven years). The mean age at the time of the arthroplasty was fifty-two years. RESULTS: The mean preoperative Harris hip score of 51 points improved to 94 points at the time of final follow-up; 86% of the hips had a good or excellent result. Thigh pain was reported as mild to severe after seven hip arthroplasties. No femoral component was revised for any reason, and none were loose radiographically at the time of the last follow-up. Two hips underwent acetabular revision (one because of dislocation and one because of loosening). Kaplan-Meier survivorship analysis was performed with revision or loosening of any component as the end point. The ten-year survival rate was 96.4% +/- 2.1% for the total hip prosthesis, 100% for the femoral component, and 96.4% +/- 2.1% for the acetabular component. Radiolucencies adjacent to the nonporous portion of the femoral component were seen in sixty-eight (93%) of the -seventy-three hips with complete radiographic follow-up. Femoral osteolysis proximal to the lesser trochanter was noted in four hips (5%). No osteolysis was identified distal to the lesser trochanter. Periacetabular osteolysis was identified in twelve hips (16%). Five patients underwent exchange of the acetabular liner because of polyethylene wear. CONCLUSIONS: This second-generation cementless, anatomically designed femoral component provided excellent clinical and radiographic results with a 100% survival rate at ten years. The circumferential porous coating of this implant improved ingrowth and prevented distal osteolysis at a mean of ten years after the arthroplasty.

Acetabulum↗

The basic science of periprosthetic osteolysis.

Despite improvements in the techniques, materials, and fixation of total joint replacements, wear and its sequelae continue to be the main factors limiting the longevity and clinical success of arthroplasty. Since Charnley first recognized aseptic loosening in the early 1960s, a tremendous amount of information has been gained on the basic science of osteolysis. Tissue explant, animal, and cell culture studies have allowed development of an appreciation of the complexity of cellular interactions and chemical mediators involved in these processes. Cellular participants have been shown to include the macrophage, osteoblast, fibroblast, and osteoclast. The plethora of chemical mediators that are responsible for the cellular interactions and effects on bone primarily include PGE2, TNF-alpha, IL-1, and IL-6. Recent and ongoing work in the field of signaling pathways will continue to advance our understanding of the mechanisms of periprosthetic bone loss. Although initial animal studies are promising for the development of possible pharmacologic agents for the treatment and prevention of osteolysis, well controlled human trials are required.

Adult↗

Orthopaedic implant related metal toxicity in terms of human lymphocyte reactivity to metal-protein complexes produced from cobalt-base and titanium-base implant alloy degradation.

Metal toxicity from sources such as orthopaedic implants was investigated in terms of immune system hyper-reactivity to metal implant alloy degradation products. Lymphocyte response to serum protein complexed with metal from implant alloy degradation was investigated in this in vitro study using primary human lymphocytes from healthy volunteers (n = 10). Cobalt chromium molybdenum alloy (Co-Cr-Mo, ASTM F-75) and titanium alloy (Ti-6Al-4V, ASTM F-136) beads (70 microm) were incubated in agitated human serum at 37 degrees Celsius to simulate naturally occurring metal implant alloy degradation processes. Particulate free serum samples, which were incubated with metal, were then separated into molecular weight based fractions. The amounts of soluble Cr and Ti within each serum fraction were measured and correlated with lymphocyte proliferation response to the individual serum fractions. Lymphocytes from each subject were cultured with 11 autologous molecular weight based serum fractions either with or without added metal. Two molecular weight ranges of human serum proteins were associated with the binding of Cr and Ti from Co-Cr-Mo and Ti implant alloy degradation (at < 30 and 180-330 kDa). High molecular weight serum proteins (approximately 180 kDa) demonstrated greater lymphocyte reactivity when complexed with metal released from Co-Cr-Mo alloy and Ti alloy than with low (5-30 kDa) and midrange (30-77 kDa) serum proteins. When the amount of lymphocyte stimulation was normalized to both the moles of metal and the moles of protein within each fraction (Metal-Protein Complex Reactivity Index, MPCRI), Cr from Co-Cr-Mo alloy degradation demonstrated approximately 10 fold greater reactivity than Ti in the higher molecular weight serum proteins (approximately 180-250 kDa). This in vitro study demonstrated a lymphocyte proliferative response to both Co-Cr-Mo and Ti alloy metalloprotein degradation products. This response was greatest when the metals were complexed with high molecular weight proteins, and with metal-protein complexes formed from Co-Cr-Mo alloy degradation.

Adult↗