Incidence and pathophysiology

The reported incidence is variable. Comparison is difficult because of differences between studied population (radiotherapy alone, technique of radiation, brachytherapy, surgery more radiotherapy, policy of dental management...). Overall the incidence has considerably decreased for the last twenty years and in recent series the incidence is inferior to 5 %5,9-12.

Early the role of vascular damage in the pathophysiology of osteoradionecrosis has been advocated13,14. Its pathogenesis has been studied in a animal model in which high dose, fractionated megavoltage (equivalent to 70 Gy in 35 fractions of Cobalt 60) was administered to the mandible of rhesus monkeys15. Blood vessels in the periodontum, periosteum, haversian bone and marrow were reduced in number and calibre (by obliterative endarteritis, fibrosis, periarteritis).

Similar histologic changes have been observed in human specimens, with fibrosis of the marrow spaces7'16'17. The vascularisation of the mandible is precarious. All areas of the craniofacial skeleton other than the mandibular body are supplied by periosteal and muscular perforators that are very redundant. The entire posterior segment of the mandible receives most of its blood supply from the surrounding musculature18. In contrast, the inferior alveolar artery has been shown to be primary nutrient source of the mandibular body18,19. Additionally, the atherosclerotic changes in the inferior alveolar artery precede those in the others vessels of the head and neck20.

Initially sepsis was considered as an very important factor of the pathogenesis of osteoradionecrosis. Meyer21 defined the classic triad as radiation, trauma and infection. Osteoradionecrosis and osteomyelitis were synonym. Introduction of sepsis by a trauma in avascular bone produced osteomyelitis. Irradiated bone was thought to be susceptible to infection because of its inability to defend against bacteria due to decreased vascularity13-15,22-26. The presence of bone sepsis hasn't been clearly demonstrated in early studies. Epstein5 cultured the necrotic sites of 26 cases of osteoradionecrosis with aerobic techniques, however no pathogens has were identified. Happonen27 used immunocytochemics methods to detect microorganisms in osteoradionecrosis : Actinomyces sp. was found in all five cases, whereas its presence has been detected with conventional method (microbiologic culture) in only one case. In all patients mixed infection was found in microbiologic cultures (Streptococcus viridans was the most common). Others publications report cases of Actinomycosis in osteoradionecrosis28,29. Nevertheless the presence of microorganisms in necrotic bone does not prejudge their role in pathogenes is. Marx7 studied the necrotic bone: no organisms (aerobic, anaerobic or fungal) could be cultured or observed in the deep bone, although many different organisms were identified in all cases of osteomyelitis and infected bone grafts, both superficial and deep. In osteoradionecrosis the organisms were limited to the surface of bone exposed to the oral environment. He concluded by replacing the classic sequence of radiation-trauma-infection with a sequence of radiation, hypoxic-hypovascular-hypocellular, tissue breakdown induced or not by trauma (collagen lysis and cellular death exceeding synthesis and cellular replication), chronic non-healing wounds. The same author, recording TcPO2 of central radiation port, has shown there was no evidence of spontaneous microvascular revascularization with time17. It was recently suggested that osteoradionecrosis may be induced by a predominantly fibro-atrophic mechanism30.

0 0

Post a comment