The healing of tibial fracture and response of the local lymphatic system.
Szczesny G, Olszewski WL, Gewartowska M, Zaleska M, Górecki A.
Department of Surgical Research and Transplantology, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland. firstname.lastname@example.org
BACKGROUND: Damage of tissues by mechanical injury and inflammation is followed by reaction of the regional lymphoid tissue, lymphatics, and lymph nodes. In our previous lymphoscintigraphic studies, we showed that closed fractures of a lower limb cause reaction of the local lymphoid tissue. There was dilation of lymphatics draining the site of the fracture and enlargement of inguinal lymph nodes. These changes persisted even after clinical healing of the fracture. In the long-lasting nonhealing fractures, the lymphoscintigraphic pictures were different. The draining lymphatics became obliterated, and the lymph nodes disappeared.
METHODS: In this study, we tried to correlate the lymphoscintigraphic images, reflecting the immune events at the fracture site, with the immunohistochemical observations of the biopsy specimens obtained during corrective operations from the healing and nonhealing fracture gaps. Thirty-eight patients with closed fracture of the tibia without traumatic skin changes were studied.
RESULTS: We confirmed that closed tibial fracture evokes response of the regional lymphatic system. Normal fracture healing with immune cell infiltrates and foci of ossification was accompanied by dilated lymphatics and enlarged lymph nodes. Prolonged nonhealing fracture with lack of cellular reaction in the gap proceeded with decreased mass of lymph nodes.
CONCLUSION: This study provides evidence for existence of a functional axis between wound of bone and surrounding soft tissue and the local lymphatic (immune) system. We hypothesize that the fast healing is regulated by influx into the wound of lymph node regulatory cells, whereas prolonged healing causes gradual exhaustion of the regional lymph node functional elements, and reciprocally impairment in sending regulatory cells to the fracture gap.
PMID: 18090016 [PubMed - in process]