ABSTRACT
INTRODUCTION: Bacteria can enter the bloodstream through simple actions such as brushing teeth, flossing, and even chewing food, increasing the chance of hematogenous seeding of prosthetic joints. Antibiotics before dental work in patients with orthopedic hardware is a topic of debate because of concerns for antibiotic resistance. Patients with dentures theoretically avoid this risk due to the lack of teeth and their maintenance. Most periprosthetic joint infections (PJIs) that occur in the first six months after surgery are due to wound infection, whereas late PJIs are more commonly caused by hematogenous seeding. MATERIALS AND METHODS: Charts from patients who received primary total joint arthroplasty were interrogated for the condition of their teeth at the time of operation. If the patient had a PJI, the time from surgery and the organism responsible were noted. Multivariate linear regressions were performed for statistical analysis to compare rates of dental status, infection, comorbidities, and demographics. RESULTS: From the 1,500 charts reviewed, patients with teeth and edentulous had similar rates of comorbidities. PJI patients had higher rates of chronic kidney disease than patients who did not have the infection. The overall rate of infections in patients with teeth was 2.14%, close to the national average. The rate of infection in patients without teeth was 0.78%. Patients with teeth have a higher rate of infection one month or longer from surgery than edentulous patients. CONCLUSIONS: There was an increased infection rate in patients with teeth at six months and greater since the primary total joint arthroplasty. The organisms responsible for many of the PJIs are commonly found in the mouth of humans. Having teeth is a potential risk factor for late PJI.
ABSTRACT
PURPOSE OF THE REVIEW: Diabetes mellitus is a chronic metabolic disorder commonly encountered in orthopedic patients. Both type 1 and type 2 diabetes mellitus increase fracture risk and impair fracture healing. This review examines complex etiology of impaired fracture healing in diabetes. RECENT FINDINGS: Recent findings point to several mechanisms leading to orthopedic complications in diabetes. Hyperglycemia and chronic inflammation lead to increased formation of advanced glycation end products and generation of reactive oxygen species, which in turn contribute to the disruption in osteoblast and osteoclast balance leading to decreased bone formation and heightening the risk of nonunion or delayed union as well as impaired fracture healing. The mechanisms attributing to this imbalance is secondary to an increase in pro-inflammatory mediators leading to premature resorption of callus cartilage and impaired bone formation due to compromised osteoblast differentiation and their apoptosis. Other mechanisms include disruption in the bone's microenvironment supporting different stages of healing process including hematoma and callus formation, and their resolution during bone remodeling phase. Complications of diabetes including peripheral neuropathy and peripheral vascular disease also contribute to the impairment of fracture healing. Certain diabetic drugs may have adverse effects on fracture healing. The pathophysiology of impaired fracture healing in diabetic patients is complex. This review provides an update of the most recent findings on how key mediators of bone healing are affected in diabetes.