Patients suffering from autoimmune diseases like rheumatoid arthritis often exhibit delayed or unsuccessful fracture healing. The fracture healing process comprises overlapping stages. The most fundamental steps are inflammation, repair, and remodeling. The inflammatory phase starts with the formation of the fracture hematoma under bioenergetically restricted conditions and is of great importance for the clinical outcome. From an immunological point of view, the fracture hematoma represents the starting point of inflammatory processes, thus initiating the healing cascade. The early inflammatory phase is disturbed in patients with autoimmune disorders and may contribute to delayed-healing or non-unions. The fracture hematoma possesses abilities such as induction of angiogenesis or periosteal cell proliferation and subsequently initiation of intramembranous bone formation underlining the fact, that in a mature fracture hematoma the initial steps of fracture healing have already taken place. The early human fracture hematoma is characterized by maturation of granulocytes and immigration of monocytes/macrophages and hematopoietic stem cells. Both T helper cells and cytotoxic T cells proliferate within the fracture hematoma and/or migrate to the fracture site. High concentration of pro-inflammatory cytokines such as IL-6, IL-8, IFNγ and TNFα are found. Immunologically restricted patients exhibit a pronounced initial inflammation. This specific microenvironment is among the crucial factors that determine fracture healing. In patients with autoimmune diseases the medicinal manipulation of the initial inflammatory milieu could be of therapeutic interest to improve the clinical outcome of fracture healing.
Disclosure of Interest None declared