A mixed methods exploration of physiotherapist's approaches to analgesic use among patients with hip osteoarthritis.

OBJECTIVE: To explore how physiotherapists currently address analgesic use among patients with hip osteoarthritis, and their beliefs about the acceptability of prescribing for these patients. METHODS: A cross-sectional questionnaire was mailed to 3126 UK-based physiotherapists. Approaches to analgesic use among patients with hip osteoarthritis were explored using a case vignette. Semi-structured telephone interviews were undertaken with 21 questionnaire responders and analysed thematically. SETTING: UK. PARTICIPANTS: Physiotherapists who had treated a patient with hip osteoarthritis in the previous 6 months. RESULTS: Questionnaire response: 53% (n=1646). One thousand one hundred forty eight physiotherapists reported treating a patient with hip osteoarthritis in the last 6 months (applicable responses), of whom nine (1%) were non-medical prescribers. Nearly all physiotherapists (98%) reported that they would address analgesic use for the patient with hip osteoarthritis, most commonly by signposting them to their GP (83%). Fifty six percent would discuss optimal use of current medication, and 33%, would discuss use of over-the-counter medications. Interviews revealed that variations in physiotherapists' approaches to analgesic use were influenced by personal confidence, patient safety concerns, and their perceived professional remit. Whilst many recognised the benefits of analgesia prescribing for both patients and GP workload, additional responsibility for patient safety was a perceived barrier. CONCLUSIONS: How physiotherapists currently address analgesic use with patients with hip osteoarthritis is variable. Although the potential benefits of independent prescribing were recognised, not all physiotherapist want the additional responsibility. Further guidance supporting optimisation of analgesic use among patients with hip OA may help better align care with best practice guidelines and reduce GP referrals.

Regulation of RAW264.7 macrophage polarization on smooth and rough surface topographies by galectin-3.

Recognition of topographical features induces phenotypic changes in macrophages although the receptors and signaling pathways are not completely characterized. As integrin molecules in focal adhesions/podosomes are in intimate contact with topography and topography modulates the NFkB pathway through cholesterol enriched raft-associated adhesive signaling structures we hypothesized that a cell-surface signaling complex comprised of galectin-3 together with its ligand CD98 and integrinß1 is important for topography-directed lineage determination. This study used polished, sand blasted and acid etched (SLA) surfaces and two novel grooved topographies (G1 and G2) produced by anisotropic etching of Si <1 1 0> to evaluate the role of galectin-3 in macrophage polarization in RAW 264.7 macrophages, as determined by gene expression and morphology. In the presence of the galectin-3 inhibitor, lactose, the M2 marker (mannose receptor) was down-regulated while the M1 marker (iNOS) was up-regulated on smooth and rough surfaces. This skewing of phenotype suggests a role for galectin-3 in macrophage polarization towards the M2 phenotype. Additionally, we evaluated the role of PI3K on polarization using PI3K inhibitor LY294002. We found that the M2 marker was down-regulated on both PO (surface polished) and G1 surfaces implicating PI3K in lineage determination. We also found that surface topography altered cell morphology; macrophages had a larger area on G2 surfaces. Lactose treatment significantly reduced the cell area on all topographies suggesting that the galectin-3 is also involved in signaling complexes triggering the rearrangement of the actin cytoskeleton. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2499-2509, 2017.

Perineal resuturing versus expectant management following vaginal delivery complicated by a dehisced wound (PREVIEW): a nested qualitative study.

OBJECTIVE: To explore women's lived experiences of a dehisced perineal wound following childbirth and how they felt participating in a pilot and feasibility randomised controlled trial (RCT). DESIGN: A nested qualitative study using semistructured interviews, underpinned by descriptive phenomenology. PARTICIPANTS AND SETTING: A purposive sample of six women at 6-9 months postnatal who participated in the RCT were interviewed in their own homes. RESULTS: Following Giorgi's analytical framework the verbatim transcripts were analysed for key themes. Women's lived experiences revealed 4 emerging themes: (1) Physical impact, with sub-themes focusing upon avoiding infection, perineal pain and the impact of the wound dehiscence upon daily activities; (2) Psychosocial impact, with sub-themes of denial, sense of failure or self-blame, fear, isolation and altered body image; (3) Sexual impact; and (4) Satisfaction with wound healing. A fifth theme 'participating in the RCT' was 'a priori' with sub-themes centred upon understanding the randomisation process, completing the trial questionnaires, attending for hospital appointments and acceptability of the treatment options. CONCLUSIONS: To the best of our knowledge, this is the first qualitative study to grant women the opportunity to voice their personal experiences of a dehisced perineal wound and their views on the management offered. The powerful testimonies presented disclose the extent of morbidity experienced while also revealing a strong preference for a treatment option. TRIAL REGISTRATION NUMBER: ISRCTN05754020; results.

Novel grooved substrata stimulate macrophage fusion, CCL2 and MMP-9 secretion.

Rough surface topographies on implants attract macrophages but the influence of topography on macrophage fusion to produce multinucleated giant cells (MGC) and foreign body giant cells (FBGC) is unclear. Two rough novel grooved substrata, G1 and G2, fabricated by anisotropic etching of Silicon <110> crystals without the use of photolithographic patterning, and a control smooth surface (Pol) were produced and replicated in epoxy. The surfaces were compared for their effects on RAW264.7 macrophage morphology, gene expression, cyto/chemokine secretion, and fusion for one and five days. Macrophages on grooved surfaces exhibited an elongated morphology similar to M2 macrophages and increased cell alignment with surface directionality, roughness and cell culture time. Up-regulated expression of macrophage chemoattractants at gene and protein level was observed on both grooved surfaces relative to Pol. Grooved surfaces showed time-dependent increase in soluble mediators involved in cell fusion, CCL2 and MMP-9, and an increased proportion of multinucleated cells at Day 5. Collectively, this study demonstrated that a rough surface with surface directionality produced changes in macrophage shape and macrophage attractant chemokines and soluble mediators involved in cell fusion. These in vitro results suggest a possible explanation for the observed accumulation of macrophages and MGCs on rough surfaced implants in vivo. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 2243-2254, 2016.

The effect of surface topography on cell shape and early ERK1/2 signaling in macrophages; linkage with FAK and Src.

Implant surface topography can modulate macrophage behavior during wound healing by the production of proinflammatory cytokines. This study investigated the activation of FAK, Src, and ERK1/2 signaling intermediates of the proinflammatory ERK1/2 pathway in RAW 264.7 macrophages in response to polished (P), coarse-grit-blasted (B), acid etched (E), and grit-blasted and etched (SLA) surface topographies. In addition, the effects of these topographies on cell spreading, vinculin organization, and viability were determined. Macrophages on the SLA surface changed from predominantly well-spread cells to ones with a more spherical morphology over time. In contrast, macrophages on the P surface changed from being predominantly spherical cells to well spread. The morphological changes were associated with changes in the distribution of vinculin. The overall patterns of the pFAK, pSrc, pERK1/2 levels as well as pERK1/2 nuclear translocation associated with cell shape with greater activation being seen with a more spread morphology. These results suggest that surface topography differentially activates signaling pathways that affect cell function and raise the possibility that topographies can be designed to optimize desired cell responses.

The effect of surface roughness on RAW 264.7 macrophage phenotype.

Monocyte-derived cells, including macrophages and foreign body giant cells, can determine the performance of implanted devices. Upon contact with biomaterials, macrophages can be activated into a classic inflammatory (M1) or wound-healing (M2) phenotype. Previously, we showed that high macrophage density on rough SLA implants was associated with early bone formation. This study examined a possible mechanism, namely, surface roughness activation of macrophages to the M2 phenotype to enhance bone formation on the SLA surface. RAW 264.7 macrophages were seeded on SLA or smooth (Po) epoxy substrates and the expression of the M1 and M2 specific markers, NOS2 and Arg-1 measured by qPCR on days 1, 3, and 5. Additionally, secretion of inflammation-associated cytokines and chemokines was studied by antibody arrays and ELISAs. Controls included RAW 264.7 macrophages primed into the M1 or M2 phenotypes by LPS/IFN-γ and IL-4, respectively. Rough SLA surfaces did not activate Arg-1 and NOS2 expression, but relative to Po surfaces MCP-1 and MIP-1α were upregulated after 5 days, whereas the secretion of the M1-associated chemokine IP-10 was lowered. RAW 264.7 macrophages on the SLA surface thus adopted elements of an M2-like phenotype, suggesting that when implanted the SLA surfaces may enhance wound repair.

Infection control in digital intraoral radiography: evaluation of microbiological contamination of photostimulable phosphor plates in barrier envelopes.

BACKGROUND AND OBJECTIVE: The detectors (both solid-state sensors and photostimulable phosphor [PSP] plates) used for digital intraoral radiography cannot be autoclaved, and barriers are typically used to prevent the spread of infection. The aim of this study was to determine the effectiveness of a barrier envelope system for PSP plates. METHODS: Disinfected PSP plates were aseptically inserted into barrier envelopes and placed in a periapical location. One PSP plate was placed in each of 28 patients, and 12 plates in each of 2 volunteers (D.S.M., J.D.W.). After retrieval, each PSP plate was removed from its barrier envelope, immersed in trypticase soy broth and aliquots were plated on trypticase soy agar. Bacterial colonies were counted 2 days later. RESULTS: Fifty-two PSP plates in barrier envelopes were evaluated for contamination. Quality assurance of the PSP plates before clinical placement revealed defects in the integrity of 4 barrier envelopes, caused by forceps-related damage or failure to achieve a uniform seal. These defects allowed substantial contamination. Contamination also occurred as a result of failure to extract the PSP plate from the barrier envelope cleanly. Of the 44 barriers with no obvious defects that were placed by either final-year dental students or a radiologist, only 3 allowed bacterial contamination of the PSP plate. CONCLUSION: Detectors contained in barrier envelopes remain a potential source of contamination. PSP plates must be disinfected between removal from a contaminated barrier envelope and placement in a new barrier envelope. In addition, placement into the barrier envelope should ideally be carried out under aseptic conditions. Finally, the integrity of each sealed barrier envelope must be verified visually before release to the clinic.

The effect of surface topography on early NFκB signaling in macrophages.

Surface topography modulates macrophage expression of pro-inflammatory cytokines through triggering of a number of different signaling pathways. In this article, we investigated the early activation of the NFκB pathway in RAW 264.7 macrophages in response to four surface topographies: mechanically polished (PO), coarse sand blasted (CB), acid etched (AE), and sandblasted and acid etched (SLA). We found that activation of the NFκB pathway was topography dependent. The PO and CB surfaces showed the highest level of activation, followed by the AE, then the SLA. Addition of suboptimal stimulatory concentrations of lipopolysaccharide (LPS) enhanced the response. Second, we determined that topography dependent cell signaling occurred in the absence of fetal bovine sera in the media. Third, we demonstrated that disruption of the lipid rafts by removal of cholesterol from cells in suspension using methyl ß cyclodextrin (MßCD) affected signaling through the NFκB pathway and transcription of the pro-inflammatory cytokine IL-1 ß, but did not affect cell adhesion, spreading or morphology. The number of macrophages adhered to the surfaces after 30 min followed the order PO, CB, AE, and SLA. In conclusion, our study suggests that one mechanism by which surface topography modulates activation of the NFκB pathway is through cholesterol-enriched raft-associated adhesive/signaling structures.

The CCL3 family of chemokines and innate immunity cooperate in vivo in the eradication of an established lymphoma xenograft by rituximab.

The therapeutic mAb rituximab induced the expression of the CCL3 and CCL4 chemokines in the human lymphoma line BJAB following binding to the CD20 Ag. Induction of CCL3/4 in vitro was specific, was observed in several cell lines and freshly isolated lymphoma samples and also took place at the protein level in vitro and in vivo. To investigate the role of these beta-chemokines in the mechanism of action of rituximab, we synthesized a N-terminally truncated CCL3 molecule CCL3(11-70), which had antagonist activity on chemotaxis mediated by either CCL3 or BJAB supernatant. We also set up an established s.c. BJAB tumor model in athymic mice. Rituximab, given weekly after tumors had reached 250 mm2, led to complete disappearance of the lymphoma within 2-3 wk. Treatment of mice with cobra venom factor showed that complement was required for rituximab therapeutic activity. Treatment of BJAB tumor bearing mice every 2 days with the CCL3(11-70) antagonist, starting 1 wk before rituximab treatment, had no effect on tumor growth by itself, but completely inhibited the therapeutic activity of the Ab. To determine whether CCL3 acts through recruitment/activation of immune cells, we specifically depleted NK cells, polymorphonuclear cells, and macrophages using mAbs, clodronate treatment, or Rag2-/-cgamma-/- mice. The data demonstrated that these different cell populations are involved in BJAB tumor eradication. We propose that rituximab rapidly activates complement and induces beta-chemokines in vivo, which in turn activate the innate immunity network required for efficient eradication of the bulky BJAB tumor.

Effect of titanium surface topography on macrophage activation and secretion of proinflammatory cytokines and chemokines.

The macrophage has a major role in normal wound healing and the reparative process around implants. Murine macrophage-like cells RAW 264.7 were used to investigate the effect of titanium surfaces on macrophage activation and secretion of proinflammatory cytokines [interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha] and chemokines (monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha). Four topographies were used: those produced by mechanically polishing, coarse sand blasting, acid etching, and sandblasting and acid etching (SLA). Macrophages were plated on the four titanium surfaces at a population density of 5 x 10(5) cells/mL/well. Tissue culture plastic and tissue culture plastic plus lipopolysaccharide (LPS) served as negative and positive control, respectively. In addition, all surfaces were tested for their effects on macrophages in the presence of LPS. Supernatants were collected for assays after 6, 24, and 48 h and the numbers of macrophages attached to the surfaces were quantified using the DAPI (4,6-di-amidino-2-phenylindole) assay. Cytokine and chemokine levels were measured with sandwich enzyme-linked immunosorbent assays. Statistical comparison between the surfaces and the controls was determined by using the two-way analysis of variance including interaction effect (two tailed and p < or = 0.05). Unstimulated macrophages increased their secretion of the proinflammatory cytokine (TNF-alpha) when attached to rough surfaces (acid etching and SLA, p < or = 0.05). In macrophages stimulated with LPS, the roughest surface SLA produced higher levels of IL-1 beta, IL-6, and TNF-alpha at 24 and 48 h than all other surfaces (p < or = 0.05). Surface topography also modulated the secretion of the chemokines monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha by macrophages. Unstimulated macrophages attached to the SLA surface down-regulated their production of chemokines (p < or = 0.05) whereas LPS-stimulated macrophages attached to the SLA surface up-regulated their production (p < or = 0.05). Moreover, the SLA surface was found to act synergistically with LPS as well as the combination of blasting and etching features of the SLA surface resulted in significant release of proinflammatory cytokines and chemokines by stimulated macrophages at 24 and 48 h (p < or = 0.05). This in vitro study has demonstrated that surface topography, in particular the SLA surface, modulated expression of proinflammatory cytokines and chemokines by macrophages in a time-dependent manner.

Proinflammatory cytokine profiles in pulp fibroblasts stimulated with lipopolysaccharide and methyl mercaptan.

Pulpal disease is intimately associated with the immune system's response to bacteria products. Clinical pathology is mediated in part by the production of pyrogenic cytokines, especially interleukin (IL)-1, tumor necrosis factor (TNF)-alpha, and IL-6. Methyl mercaptan (CH3SH), a volatile sulfur compound produced by anaerobic Gram-negative bacteria, has been shown to contribute to the production of IL-1 by human mononuclear cells. In this report, we investigated the production of IL-1, TNF-alpha, and IL-6 by human pulp fibroblasts when stimulated for various periods of time with lipopolysaccharide (LPS) with or without the presence of CH3SH. We found that LPS and CH3SH had no effect on the production of IL-1 or TNF-alpha. However, LPS stimulated IL-6 production, and this production was augmented when CH3SH was present. We conclude that the volatile sulfur compound CH3SH plays a role in activation and modulation of the immune response through its role in production of IL-6.

Post-onset inhibition of murine arthritis using combined chemokine antagonist therapy.

OBJECTIVE: To investigate the effect of targeting the chemotaxis of monocytes and polymorphonuclear monocytes (PMNs) in situ in MRL-Faslpr arthritis. METHODS: MRL-Faslpr mice were injected intradermally with complete Freund's adjuvant and cellular infiltration into the joint was monitored. Once clinical disease developed, the animals received one of three treatments: MCP-1(9-76); MCP-1(9-76) plus Gro-alpha(8-73); or control peptide, MCP-1 Ala. The bimalleolar ankle width was measured for 11 days and histological examination of the joints was then assessed. RESULTS: Cellular infiltration started after the onset of ankle swelling, and increased progressively. The incidence of swelling and the histopathology was reduced after day 6 of treatment in the MCP-1(9-76)-treated mice. Mice treated with the two antagonists MCP-1(9-76) and Gro-alpha(8-73) displayed a further significant reduction in disease parameters. CONCLUSION: Treatment after disease onset with chemotactic antagonists for monocytes and PMNs significantly alleviated both the swelling and the histopathology seen in arthritis, suggesting that chemokine antagonists are an effective anti-inflammatory therapy.

The effect of lactation in the post-partum arthritis of MRL-lpr/fasmice.

OBJECTIVE: To investigate the effects of lactation on the post-partum arthritic flare in MRL-lpr/fas mice. METHODS: Three groups of mice were investigated. Group 1: females whose litters were weaned at termination of the experiment; group 2: females whose litters were weaned at parturition; group 3: females who were not bred. Clinical evaluation was carried out at 5-day intervals following parturition. Blood samples were also collected during the course of the experiment and assayed for corticosterone and prolactin. Histological evaluation of the joints was assessed at day 30. RESULTS: The incidence of swelling and erythema, the bimalleolar ankle width and the histopathology were significantly reduced by removal of the litters at parturition. This correlated well with a decrease seen in prolactin levels in these females. Corticosterone, an immunomodulatory glucocorticoid, did not play a significant role in the arthritic flare. CONCLUSION: Our findings suggest that prolactin levels contribute to the inflammation seen in MRL-lpr/fas mice following parturition.

Photodynamic therapy in immune (non-oncological) disorders: focus on benzoporphyrin derivatives.

This review examines the efficacy of photodynamic therapy in the treatment of immunological disorders. Photodynamic therapy (PDT) is a 2-step procedure. Firstly, a photosensitiser is introduced into the body, where it accumulates selectively in cells with elevated metabolism, such as cancer cells or activated cells of the immune system. Second, light is applied at a wavelength that excites the photosensitiser, producing a variety of short-lived oxygen-derived species. The effect is dependent on the doses of both photosensitiser and activating light. The mechanisms of action of PDT are multifactorial. Induction of high levels of oxidative stress results in necrotic cell death, while lower intensity oxidative stress initiates apoptosis. Sublethal doses may result in the modification of cell surface receptor expression levels and cytokine release and consequently influence cell behaviour. Immunomodulatory PDT (IPDT) utilises mainly apoptotic and sublethal doses. The studies reported here utilise verteporfin, a benzoporphyrin-derived chlorin-like photosensitiser. Veteporfin is a second generation photosensitiser, displaying rapid clearance and consequently a reduced period of skin photosensitivity compared with the first generation photosensitiser, porfimer sodium. In vivo studies showed that IPDT was effective in alleviating immunopathology in murine models of arthritis, contact hypersensitivity, experimental allergic encephalomyelitis and retention of allogeneic skin grafts. Based on these findings, early stage clinical trials with IPDT were initiated recently for the treatment of psoriasis, psoriatic arthritis and rheumatoid arthritis. While verteporfin has been the photosensitiser which pioneered IPDT, a new benzoporphyrin derivative photosensitiser, QLT0074, is under development. This has demonstrated an enhanced avidity for target cells as well as improved clearance characteristics.

The peripheral benzodiazepine receptor ligand PK 11195 inhibits arthritis in the MRL-lpr mouse model.

OBJECTIVE: Mice of the MRL-lpr strain develop a severe autoimmune arthritic condition when primed with complete Freund's adjuvant. The pathology is similar to that seen in human rheumatoid arthritis. We investigated whether PK 11195, a powerful ligand for peripheral benzodiazepine receptors, would have preventative or therapeutic effects in this model. METHODS: MRL-lpr mice were primed with complete Freund's adjuvant at 13-14 weeks of age. Daily PK 11195 injections were started on the same day as priming to test for preventative effects. Daily PK 11195 injections were started 10 days after priming to test therapeutic effects. RESULTS: PK 11195 showed both preventative and therapeutic effects. At 1 mg/kg/day, it inhibited disease onset. At 3 mg/kg/day, it inhibited established disease progression. CONCLUSION: The evidence suggests that PK 11195 may be the prototype of a new class of anti-inflammatory agents.

Uptake of verteporfin by articular tissues following systemic and intra-articular administration.

Photodynamic therapy (PDT) using the photosensitizer BPD-Verteporfin (liposomal benzoporphyrin derivative-monoacid ring A) has been shown in previous studies to be effective in the amelioration of inflammatory arthritis in both the MRL-lpr mouse and the New Zealand White (NZW) rabbit models, and could potentially offer alleviation of certain inflammation-related symptoms of rheumatoid arthritis. Time and dose dependency of BPD-MA tissue uptake was carried out in the inflamed synovium and other articular and peri-articular tissues following intravenous and intra-articular administration in the NZW rabbit model. As some articular and peri-articular tissues are difficult to extract, this study uses a rapid fluorimetric sampling of tissues following dissolution in Soluene 350. Our results showed that i.v. injected BPD-MA preferentially distributed in the inflamed synovium, and in tissues with a high degree of vascularization. Little or no association was found with avascular tissues such as cartilage and tendons. Clearance from the synovium was rapid, supporting earlier rather than late light treatment. Much higher association of BPD-MA with the synovium was achieved using intra-articular injection, and BPD-MA concentrations were maintained at relatively steady levels for several hours. These observations support the possibility that PDT could offer a safe, highly versatile clinical option for the management of inflamed joints in autoimmune disorders.

Amelioration of antigen-induced arthritis in rabbits by induction of apoptosis of inflammatory cells with local application of transdermal photodynamic therapy.

OBJECTIVE: To study the efficacy and mechanism of local transdermal photodynamic therapy (tPDT) in rabbits with antigen-induced arthritis (AIA). METHODS: AIA in rabbits on day 14 postinduction was treated with an intravenous injection of benzoporphyrin-derivative monoacid ring A (BPD; Verteporfin) and subsequent transdermal exposure of the knee joint to light. BPD uptake and PDT-induced apoptosis of the synovium was studied applying fluorescence confocal microscopy and immunohistochemistry. The (histo)pathology of the joints was assessed at day 28. RESULTS: Treatment with tPDT resulted in significant amelioration of synovial inflammation and an almost complete prevention of pannus formation and bone and cartilage destruction. BPD uptake was detectable in activated T cells and macrophages, and there was significant PDT-induced increase in the number of apoptotic cells in the synovium. CONCLUSION: Because photodynamic therapy is both specific and noninvasive, our findings suggest that it could be used for treating arthritic joints in humans.

An antagonist of monocyte chemoattractant protein 1 (MCP-1) inhibits arthritis in the MRL-lpr mouse model.

An antagonist of human monocyte chemoattractant protein (MCP)-1, which consists of MCP-1(9-76), had previously been characterized and shown to inhibit MCP-1 activity in vitro. To test the hypothesis that, by inhibiting endogenous MCP-1, the antagonist has antiinflammatory activity in vivo, we examined its effect in the MRL-lpr mouse model of arthritis. This strain spontaneously develops a chronic inflammatory arthritis that is similar to human rheumatoid arthritis. Daily injection of the antagonist, MCP-1(9-76), prevented the onset of arthritis as monitored by measuring joint swelling and by histopathological evaluation of the joints. In contrast, controls treated with native MCP-1 had enhanced arthritis symptoms, indicating that the inhibitory effect is specific to the antagonist. In experiments where the antagonist was given only after the disease had already developed, there was a marked reduction in symptoms and histopathology, although individuals varied in the magnitude of the response. The mechanism of inhibition of disease is not known, although the results suggest that it could be more complex than the competitive inhibition of ligand binding that is observed in vitro. The demonstration of the beneficial effects of an MCP-1 antagonist in arthritis suggests that chemokine receptor antagonists could have therapeutic application in inflammatory diseases.

An investigation into the relation between step height and ground reaction forces in step exercise: a pilot study.

The aim of this study was to investigate the effect that changing step height had on ground reaction force. Using a randomised crossover design, 12 volunteers with no previous experience of step aerobics were recruited to perform at three different step heights: 6, 8 and 10 inches. Subjects performed a basic step at a cadence of 120 beats/min and performed three one minute trials during which ground reaction force was measured. Measurement of peak impact force, time to achieve peak impact, and total time of foot contact was made, and impulse of the force was calculated. Statistically significant differences were found to exist for peak impact force between the 6 and 8 inch and 6 and 10 inch, but not between the 8 and 10 inch conditions. No significant differences were found in any other parameters. The study supports the present advice that participants should use low step heights, and possible mechanisms of injury are discussed.