Osteoarthritis (OA) is a chronic, progressive, multifactorial disease resulting in a progressive loss of articular cartilage structure and function that is most common in middle-aged and older patients. OA is involved in the loss of extracellular matrix and cartilage as well as cell number decreases within the matrix, especially in the further stages of the disease. The immune system plays a pivotal role in the pathomechanism of this condition. Both humoral and cellular mediators contribute to cartilage destruction, abnormal bone remodeling, synovitis, and joint effusion. The increasing prevalence of this disease has led to a growing interest in using animal models as the primary way to broaden the knowledge of the pathogenesis of OA and possible therapies at each stage of disease development. This review aims to describe the signs, pathogenesis, and classification of OA as well as discuss the advantages and disadvantages of some animal models. The currently used treatment methods include mesenchymal stem cells, exosomes, gene therapies, and blood-derived products. In addition, exogenous growth factors, platelet-rich plasma (PRP), platelet lysate, and autologous conditioned serum (ACS) are discussed with the application of tissue engineering techniques and biomaterials.

Osteomyelitis, a severe bone infection, poses a significant therapeutic challenge in both human and veterinary medicine, especially due to the increasing prevalence of antibiotic-resistant pathogens like methicillin-resistant Staphylococcus aureus (MRSA). Conventional treatments, including surgical debridement and systemic antibiotics, often prove inadequate due to the ability of bacteria to form biofilms and evade host immune responses. Antimicrobial peptides (AMPs), such as LL-37 and β-defensins, have emerged as a promising alternative therapeutic strategy. AMPs exhibit broad-spectrum antimicrobial activity, including efficacy against resistant strains, and possess immunomodulatory properties that can promote bone regeneration. This article comprehensively reviews AMP applications in treating osteomyelitis across both human and veterinary medicine. We discuss diverse therapeutic approaches, including free AMPs, their conjugation with biomaterials such as collagen and chitosan to enhance delivery and stability, and the development of AMP-based nanoparticles. Furthermore, we analyze preclinical and clinical findings, highlighting the efficacy and safety of AMPs in combating osteomyelitis in both human and animal patients. Finally, we explore future perspectives and challenges, such as optimizing delivery, stability, and efficacy, while minimizing cytotoxicity, and in translating AMP-based therapies into clinical practice to effectively manage this debilitating disease.

Introduction: Macrophages are crucial immune cells that play a role in tissue repair and can exhibit pro- or anti-inflammatory behaviour based on environmental stimulation. Their functional phenotype can be affected by platelet-derived products as determined by those products’ composition. When the inflammatory response caused by implantation is excessive, it can lead to rejection of the implant. Therefore, a thorough evaluation of implant haemocompatibility is necessary to minimise undesirable consequences. Material and Methods: In an in vitro study, monocyte-derived macrophages (MDMs) were obtained from the whole blood of sheep after a silicon-doped diamond-like carbon–coated implant insertion. These MDMs were then exposed to autologous platelet-derived products for functional marker analysis. Results: Platelet-poor plasma (PPP) and pure platelet-rich plasma (P-PRP) stimulation increased arginase-1 activity, while leukocyte-rich PRP stimulation produced a mixed response involving higher O₂ ⁻ (6.49 ± 2.43 nM vs non-stimulated 3.51 ± 1.23 nM, P-value < 0.05) and NO (3.28 ± 1.38 μM vs non-stimulated 2.55 ± 0.32μM, P-value < 0.05) generation. Conclusion: Using PPP and P-PRP stimulation in post-implantation procedures may contribute to the polarisation of macrophages towards the M2-like pro-resolving phenotype, thereby accelerating wound healing. This would also prevent implant degradation due to an excessive inflammatory process.

Implant insertion can evoke excessive inflammation which disrupts the healing process and potentially leads to complications such as implant rejection. Neutrophils and macrophages play a vital role in the early inflammatory phase of tissue repair, necessitating the study of cellular responses in host–implant interactions. In order to deepen the knowledge about these interactions, the response of neutrophils and macrophages to contact with selected biomaterials was examined in vitro on the basis of secretory response as well as reactive oxygen species/reactive nitrogen species (ROS/RNS) generation. Porcine neutrophils exposed to hydroxyapatite (HA) released more enzymes and generated higher levels of ROS/RNS compared to the control group. The addition of AMPNE diminished these responses. Although the results from porcine cells can provide valuable preliminary data, further validation using human cells or clinical studies would be necessary to fully extrapolate the findings to human medicine. Our study revealed that human neutrophils after contact of with HA increased the production of nitric oxide (NO) (10.00 ± 0.08 vs. control group 3.0 ± 0.11 µM, p < 0.05), while HAP or FAP did not elicit a significant response. Human macrophages cultured with HA produced more superoxide and NO, while HAP or FAP had a minimal effect, and curdlan reduced ROS/RNS generation. The addition of AMPNE to cultures with all biomaterials, except curdlan, reduced neutrophil activity, regardless of the peptides’ origin. These results highlight the potential of antimicrobial peptides in modulating excessive biomaterial/host cell reactions involving neutrophils and macrophages, enhancing our understanding of immune reactions, and suggesting that AMPNE could regulate leukocyte response during implantation.

Ozone (O₃) is a reactive oxidant increasingly applied in biomedical settings, yet its dose-dependent effects on innate immune cells, particularly those from non-human species, remain insufficiently defined. Within a One Health framework, this study examined how two clinically relevant O₃ exposure regimens (30 µg/mL and 90 µg/mL) affect porcine neutrophils and monocytes isolated from peripheral blood. Cell viability, reactive oxygen and nitrogen species (RONS) production, and the activity of key enzymes (myeloperoxidase, elastase, alkaline phosphatase, arginase) were assessed at 1 h and 24 h post-exposure. The lower dose induced mild functional activation without compromising viability, whereas the higher dose triggered pronounced oxidative stress, enhanced degranulation, and reduced neutrophil viability by more than 60%. Neutrophils exhibited a stronger and more dynamic response than monocytes, which retained viability and differentiation capacity at 30 µg/mL but showed impaired function at 90 µg/mL. These findings highlight the dual nature of O₃, where controlled exposure may support immunomodulation, while excessive dosing disrupts cell function. Defining safe and effective therapeutic windows remains critical for future applications.