Page 136 - Effects of radiotherapy and hyperbaric oxygen therapy on oral microcirculation Renee Helmers

Chapter 7
HBOT and wound healing
In an experimental model it was demonstrated for the first time that continuous microcirculation measurements using SDF imaging enabled evaluating wound status by quantifying the vascular regeneration during the healing process over time. The results in Chapter 3 suggested that HBOT positively influenced vascular regeneration as indicated by the elevated FCD in surgically raised oral mucosal flaps in comparison to healing under normal conditions. The findings of this study support the available evidence that HBOT has a beneficial effect on vascularization and wound blood perfusion.7,11,12,14,16
Onset of late IR injury in oral mucosa and bone
LRTI develops in months to years after RT and the progression to tissue necrosis becomes clinically apparent when tissue breakdown occurs. Elucidating the onset of late microvascular IR injury might aid the early detection of tissue deterioration and thereby could promote early diagnosis and the effectuation of timely (preventive) therapies. In Chapter 4 a translational model was introduced that aimed to capture early microvascular alterations associated with the onset of late IR injury. Noninvasive and prospective (11 weeks after RT) measurements of the IR oral mucosal microcirculation with the use of the SDF-device did not show lasting microvascular density changes compared to baseline. However, when angiomorphology was considered, telangiectasias were clearly observed after a single dose of 30 Gy corresponding with post-IR microcirculatory effects as described in other scientific reports.2,9,10,15 Gradually with cumulative doses of 22.4 Gy, 26 Gy, 30 Gy and 32 Gy, histological changes developed that presented in the form of decreased vascularity, fibrosis of soft tissue and bone. Moreover, a single dose of 30 Gy histologically provoked necrosis of teeth and bone tissue and a lack of osteoblast lining (periosteum) was observed. These histological findings are in line with previous reports in the literature associated with ORN in human mandibles.4
The discrepancy between observations in oral mucosal microcirculation and the histological alterations in the underlying bone suggests that soft tissue microcirculation remains unhindered until LRTI progresses in the underlying bone. It might implicate a process where soft tissue secondarily succumbs to underlying bone necrosis. The histologically observed absence of periosteum might be a precursor to soft tissue ulceration. However, the model presented
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