Articular cartilage transplantation. Current and future limitations and solutions.

The ultimate goal of replacing cartilage with a bioengineered graft, autologous graft, or allograft is to replace the damaged articulating surface with tissue containing the anatomical, biomechanical, and functional properties of native articular cartilage, which will have resultant satisfactory clinical outcome. For transplanted articular cartilage to obtain the original histologic arrangement of hyaline cartilage with secure incorporation into host tissue, progressive integrated multidisciplinary research must continue. Although autologous chondrocyte transplantation of the talus is not yet FDA approved, this technique may provide the surgeons with a cutting-edge method to treat patients with nondegenerative osteochondral lesions of the talus and possibly other articulating joints of the foot.

Full-thickness burn of the foot: successful treatment with Apligraf. A case report.

Burn wounds, although uncommon in the foot, present a uniquely challenging opportunity to physicians. The keys to successful management include a proper and specific initial evaluation of the burning agent, the location, the TBSA affected, and the depth. Ultimately, proper recognition and meticulous wound care with skin grafting, when necessary, bring about the desired results. A case report of a patient with a third-degree burn over the dorsum of the left foot is presented. This case is unique in that Apligraf, a human skin equivalent, was used to gain coverage and eventual resolution of the wound. It is the authors' opinion that the use of Apligraf in this application is a viable alternative to traditional methods of skin harvesting and grafting. To the authors' knowledge, there have been no other cases reported of Apligraf use in burn wound coverage of the foot.

Articular cartilage. Anatomy, injury, and repair.

Articular cartilage plays a vital role in joint morphology. An understanding of articular cartilage anatomy and physiology will enable the physician to more fully appreciate its function and necessity. Articular cartilage is made up of four basic biological layers or zones. Each zone possesses attributes necessary to make articular cartilage as a whole strong, durable, and more able to withstand shear and axial forces through a joint. Cartilage metabolism is relatively slow in comparison with other tissues; hence, it is much more difficult for defects in cartilage to heal spontaneously. There are many ways in which articular cartilage can incur damage. Mechanical injury, be it acute or insidious, causes cartilage to fissure and fracture. This results in painful and inflamed joints along with disruption of the cartilage. Metabolic diseases also can produce joint destruction, inflammation, and pain. The resultant defects fail to heal spontaneously because of slow metabolism of cartilage. These chondral defects eventually may penetrate subchondral bone. Disruption of the layers of cartilage eventually will cause collapse and loss of integrity of the entire joint apparatus as a whole. More than 250 years ago, Hunter stated, "Ulcerated cartilage is a troublesome thing--once [it is] destroyed it is not repaired." Articular cartilage defects are very difficult to repair effectively. Cartilage defects can heal spontaneously, if the defect extends to subchondral bone. The reparative substance, fibrocartilage, is less durable and much less smooth. There are many techniques and procedures in which chondral or osteochondral defects can be filled. Promoting subchondral bleeding is the method most commonly used clinically. This allows pleuripotent cells to fill the defect with eventual fibrocartilage. Implants are gaining favor as a method of inducing a more pure, hyaline-like cartilage into cartilage defects. Gene therapy and tissue engineering are at the forefront of cartilage research today. Cartilage injury and repair remains today a very difficult topic of study. Understanding the anatomy of articular cartilage, the pathomechanics of injury, and methods available for cartilage repair, will help the physician more adequately approach treatment options.

Pentoxifylline. Adjunctive therapy in the treatment of pedal frostbite.

Frostbite injury to the extremities has the potential for disastrous effects. Prompt recognition and treatment are paramount. The use of Pentoxifylline to minimize tissue damage in the treatment of frostbite is a viable addition to the traditional therapy of rewarming soaks, pain management, and vesicle débridement. The most well known action of Pentoxifylline is its ability to increase RBC flexibility, allowing easier vascularization. This explains its indication for PVD, arterial disease, and intermittent claudication. As is explained previously, however, Pentoxifylline has multiple actions that will enhance tissue survival. The dosage of Pentoxifylline in controlled release tablet form is one 400 mg tablet three times a day with meals. The duration of treatment should be from two to six weeks. As this drug has many actions and therefore possibilities, more research is warranted with regards to its use not only with frostbite, but with other pathological processes.

Tendon pathology in the foot. The use of corticosteroid injection therapy.

Corticosteroids have been used extensively in the practice of orthopedics and podiatry. It is the authors' opinion that the issue of corticosteroids and their effect on the healing of tendon pathology has not been addressed sufficiently or answered adequately. Few studies have used a well-controlled injury model. Steroid dosage and steroid selection also appear to be random. Clinical experience in conjunction with a complete review of the literature, however, leads the authors to believe that the use of local corticosteroid injection is a valid treatment option. Local injection for painful tendon pathology is a relatively simple, safe, and effective form of treatment. The patient may experience rapid relief of pain and swelling and, on occasion, may be able to return to normal activities after one injection. With the exception of the Achilles' tendon, it is the authors' opinion that the use of local corticosteroid injection for the treatment of tendonopathy is not only an option, but an effective means of therapy. Armed with a good understanding of tendon anatomy, proper injection technique, and differing types of corticosteroids, effective results are well within reach for the patient and physician. Unlike nonsteroidal anti-inflammatory drugs (NSAIDs) or oral corticosteroids, injectable corticosteroids deal with the problem at the site, delivering needed relief while eliminating adverse systemic effects. This therapy is cost effective and has fewer potential complications than operative intervention.

Preliminary report on a method of human papillomavirus DNA extraction from verruca plantaris for polymerase chain reaction studies.

This preliminary report on the Chelex-based extraction method of HPV DNA from verruca plantaris is the first step in a series of studies on verruca plantaris undertaken, jointly, by the Departments of Podiatric Medicine and Microbiology at Des Moines University-Osteopathic Medical Center, Des Moines, Iowa. Current projects include the development of new primers for PCR studies of HPV, exploration of different viral DNA extraction methods, and surveys concerning treatment, success of therapies, and the epidemiology of verruca plantaris.

Malignant melanoma of the foot and ankle.

Malignant melanoma is a serious and devastating skin disease that podiatrists may be called upon to treat. It is pertinent that delays in diagnosis and treatment of malignant melanoma be avoided. Some of the topics discussed in this article are causes, clinical features, classification, and treatment of malignant melanoma, focusing on the foot and ankle.

Nerve injury associated with plantarflexion-inversion ankle sprains.

This article presents some of the less frequently described nerve pathologies associated with severe plantarflexion-inversion ankle sprains. It outlines the likely mechanisms of nerve injury, the typical presentations, and treatment possibilities. An anatomic review of the lower extremity, with emphasis on the neurologic structures, is also included to assist in understanding the mechanism and location of the nerve injury.

Vancomycin-resistant Enterococci infected puncture wound to the foot. A case report.

Vancomycin is often administered empirically to patients with osteomyelitis, septic arthritis, septic throbophlebitis, infected burns, and cellulitis of the lower extremities when methicillin-resistant staphylococci are suspected, or when a staphylococcus organism is suspected in a penicillin-allergic patient. Physicians must be aware of the guidelines established regarding the use of Vancomycin to avoid bacterial resistance. Physicians also must be aware of the procedures that have been developed to help contain nasocomial outbreaks of Vancomycin-resistant Enterococci.

Technetium-99, iodine-129 and tritium in the waters of the Savannah River Site.

Surface water samples were collected from streams on and around the Savannah River Site (SRS) to assess current 3H, 99Tc, and 129I concentrations in the water. The SRS is a nuclear facility operated by Westinghouse Savannah River Company for the US Department of Energy. Water quality parameters were measured at the time of collection using field portable instrumentation. The tritium activity was determined by liquid scintillation spectrometry. The isotopes, 99Tc and 129I, were determined by isotope dilution/inductively coupled plasma-mass spectrometry (D.M. Beals, Determination of technetium-99 in aqueous samples by isotope dilution inductively coupled plasma-mass spectrometry. Presented at the 3rd International Conference on Nuclear and Radiochemistry, Vienna, September 1992, unpublished data; D.M. Beals, P. Chastagner and P.K. Turner, Analysis of iodine-129 in aqueous samples by inductively coupled plasma-mass spectrometry. Presented at the 38th Annual Conference on Bioassay, Analytical and Environmental Radiochemistry, Santa Fe, NM, November 1992). Elevated activities of 3H, 99Tc, and 129I were found in some surface streams of the SRS, principally due to migration of ground water from beneath old seepage basins, however the levels in the waters leaving the SRS are well below any regulatory guidelines.

Environmental monitoring and dose assessment following the December 1991 K-reactor aqueous tritium release.

Between 22 December and 25 December 1991, approximately 570 L of tritiated water was released from the K Reactor at the Savannah River Site. Analyses of river flow rates and measured tritium concentrations showed that approximately 210 TBq of tritium had been released from the reactor and was being transported down the Savannah River. Elevated tritium concentrations in the Savannah River were first detected on 26 December 1991. The maximum measured tritium concentration at Highway 301 (a major sampling point 37 km downstream of the Savannah River Site) was 2.5 Bq mL-1. A hypothetical maximum individual located at Highway 301 would have received a drinking water dose of approximately 0.35 microSv, less than 1% of the Environmental Protection Agency's 40 microSv y-1 drinking water standard. Concentrations at the intake canals to two water treatment facilities, approximately 160 km downstream, began to rise above normal on 28 December. The population dose to users of the downstream domestic water supplies and consumers of Savannah River biota was estimated to be 4.7 x 10(-3) person-Sv.

Nifedipine potentiates cardiopulmonary baroreflex control of sympathetic nerve activity in healthy humans. Direct evidence from microneurographic studies.

Nifedipine augments baroreflex mechanisms in in vivo animal models. Previous studies in our laboratory demonstrate that nifedipine potentiates baroreflex control of heart rate and vascular resistance in normal human subjects. To further define the neuroeffector mechanism of the autonomic effects of nifedipine, we directly measured postganglionic sympathetic nerve activity to muscle (MSNA, microneurography), before and after drug administration, during selective unloading of cardiopulmonary baroreceptors with lower body negative pressure (-10 mm Hg, LBNP-10), and during the cold pressor test. Twenty-three normal subjects (age, 23 +/- 1 years; mean +/- SEM) were studied in the control state and 20 minutes after administration of either nifedipine (10 mg s.l., 10 subjects), during nitroprusside infusion (0.37 +/- 0.03 microgram/kg/min i.v., eight subjects), or 20 minutes after sublingual administration of placebo (five subjects). We measured systemic arterial pressure, central venous pressure, heart rate, and MSNA. Nifedipine and nitroprusside produced similar increases in resting heart rate and MSNA and similar decreases in central venous pressure, whereas placebo had no effect on resting hemodynamics. During LBNP-10, hemodynamic changes were not significantly different among the three treatment groups. However, the percentage increase in MSNA during LBNP-10 was significantly augmented from a 24 +/- 9% increase before nifedipine to a 56 +/- 7% increase after nifedipine (p less than 0.05). Decreases in central venous pressure with LBNP-10 were nearly identical before compared with after nifedipine. Thus, nifedipine increased the cardiopulmonary baroreflex sympathetic sensitivity (change in total MSNA per mm Hg decrease in central venous pressure during LBNP-10) from 26.5 +/- 10.7 units/mm Hg to 74.9 +/- 19.0 units/mm Hg (p less than 0.01). In contrast, administration of hemodynamically similar doses of nitroprusside resulted in an attenuation of MSNA responses to LBNP-10. During LBNP-10, MSNA increased 57 +/- 12% before nitroprusside but only 14 +/- 4% during nitroprusside (p less than 0.01). The cardiopulmonary baroreflex sympathetic sensitivity was not significantly altered by nitroprusside (45.1 +/- 12.4 units/mm Hg before compared with 33.1 +/- 20.8 units/mm Hg during nitroprusside, p = NS). Placebo had no effect on the responses to LBNP-10. Nifedipine did not augment MSNA responses to the cold pressor test. To evaluate the linearity of sympathetic responses to cardiopulmonary baroreceptor unloading, graded LBNP (0, -5, -10, and -15 mm Hg) was applied in three additional subjects before and after nifedipine (10 mg s.l.).(ABSTRACT TRUNCATED AT 400 WORDS)