The biological interface between an orthopedic implant and the surrounding host tissue may have a dramatic effect upon clinical outcome. Desired effects include bony ingrowth (osseointegration), stimulation of osteogenesis (osteoinduction), increased vascularization, and improved mechanical stability. Implant loosening, fibrous encapsulation, corrosion, infection, and inflammation, as well as physical mismatch may have deleterious clinical effects. This is particularly true of implants used in the reconstruction of load-bearing synovial joints such as the knee, hip, and the shoulder. The surfaces of orthopedic implants have evolved from solid-smooth to roughened-coarse and most recently, to porous in an effort to create a three-dimensional architecture for bone apposition and osseointegration. Total joint surgeries are increasingly performed in younger individuals with a longer life expectancy, and therefore, the postimplantation lifespan of devices must increase commensurately. This review discusses advancements in biomaterials science and cell-based therapies that may further improve orthopedic success rates. We focus on material and biological properties of orthopedic implants fabricated from porous metal and highlight some relevant developments in stem-cell research. We posit that the ideal primary and revision orthopedic load-bearing metal implants are highly porous and may be chemically modified to induce stem cell growth and osteogenic differentiation, while minimizing inflammation and infection. We conclude that integration of new biological, chemical, and mechanical methods is likely to yield more effective strategies to control and modify the implant-bone interface and thereby improve long-term clinical outcomes.

Like any foreign object, orthopaedic implants are susceptible to infection when introduced into the human body. Without additional preventative measures, the absolute number of annual prosthetic joint infections will continue to rise, and may exceed the capacity of health care systems in the near future. Bacteria are difficult to eradicate from synovial joints due to their exceptionally diverse taxonomy, complex mechanistic attachment capabilities, and tendency to evolve antibiotic resistance. When a primary orthopaedic implant fails from prosthetic joint infection, surgeons are generally challenged by limited options for intervention. In this review, we highlight the etiology and taxonomic groupings of bacteria known to cause prosthetic joint infections, and examine their key mechanisms of attachment. We propose that antimicrobial strategies should focus on the most harmful bacteria taxa within the context of occurrence, taxonomic diversity, adhesion mechanisms, and implant design. Patient-specific identification of organisms that cause prosthetic joint infections will permit assessment of their biological vulnerabilities. The latter can be targeted using a range of antimicrobial techniques that exploit different colonization mechanisms including implant surface attachment, biofilm formation, and/or hematogenous recruitment. We anticipate that customized strategies for each patient, joint, and prosthetic component will be most effective at reducing prosthetic joint infections, including those caused by antibiotic-resistant and polymicrobial bacteria.

Many species have been heavily exploited by man leading to local extirpations, yet few studies have attempted to unravel subsequent recolonization histories. This has led to a significant gap in our knowledge of the long-term effects of exploitation on the amount and structure of contemporary genetic variation, with important implications for conservation. The Antarctic fur seal provides an interesting case in point, having been virtually exterminated in the nineteenth century but subsequently staged a dramatic recovery to recolonize much of its original range. Consequently, we evaluated the hypothesis that South Georgia (SG), where a few million seals currently breed, was the main source of immigrants to other locations including Livingston Island (LI), by genotyping 366 individuals from these two populations at 17 microsatellite loci and sequencing a 263 bp fragment of the mitochondrial hypervariable region 1. Contrary to expectations, we found highly significant genetic differences at both types of marker, with 51% of LI individuals carrying haplotypes that were not observed in 246 animals from SG. Moreover, the youngest of three sequentially founded colonies at LI showed greater similarity to SG at mitochondrial DNA than microsatellites, implying temporal and sex-specific variation in recolonization. Our findings emphasize the importance of relict populations and provide insights into the mechanisms by which severely depleted populations can recover while maintaining surprisingly high levels of genetic diversity.

Antarctic fur seals (AFS) are an ecologically important predator and a focal indicator species for ecosystem-based Antarctic fisheries management. This species suffered intensive anthropogenic exploitation until the early 1900s, but recolonized most of its former distribution, including the southern-most colony at Cape Shirreff, South Shetland Islands (SSI). The IUCN describes a single, global AFS population of least concern; however, extensive genetic analyses clearly identify four distinct breeding stocks, including one in the SSI. To update the population status of SSI AFS, we analyzed 20 years of field-based data including population counts, body size and condition, natality, recruitment, foraging behaviors, return rates, and pup mortality at the largest SSI colony. Our findings show a precipitous decline in AFS abundance (86% decrease since 2007), likely driven by leopard seal predation (increasing since 2001, p << 0.001) and potentially worsening summer foraging conditions. We estimated that leopard seals consumed an average of 69.3% (range: 50.3–80.9%) of all AFS pups born each year since 2010. AFS foraging-trip durations, an index of their foraging habitat quality, were consistent with decreasing krill and fish availability. Significant improvement in the age-specific over-winter body condition of AFS indicates that observed population declines are driven by processes local to the northern Antarctic Peninsula. The loss of SSI AFS would substantially reduce the genetic diversity of the species, and decrease its resilience to climate change. There is an urgent need to reevaluate the conservation status of Antarctic fur seals, particularly for the rapidly declining SSI population.