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ExperimentaL Oral Medicine
Published in Samuel Dreizen, Barnet M. Levy, Handbook of Experimental Stomatology, 2020
Samuel Dreizen, Barnet M. Levy
In bone, osteocytes adjoining the necrotic area became pyknotic while those two or more lacunar spaces away were usually normal appearing. Marrow spaces adjoining the necrotic area became filled with chronic inflammatory cells. Osteoclastic activity was prominent at the periphery of the lesion. Vascular changes were found mainly in the mandible where arterioles and, occasionally, medium- and large-sized arteries were involved. The intima and media were thickened by cell proliferation producing slight to complete occlusion. Bone destruction in the alveolar part of the mandible stimulated a periosteal reaction along the inferior border that resulted in new trabeculae being laid down on the cortical plates. The amount of new bone was proportional to the amount destroyed. Osteoradionecrosis resulted primarily from radiation damage to the osteocytes and was aggravated and prolonged by blood vessel changes.
The Head and Neck
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
The incidence of some of the postoperative complications increase if the patient has had preoperative irradiation or recurrent tumor. Postoperative hematomas can be avoided to some extent by correcting coagulopathies, meticulous intra-operative hemostasis, and effective close suction away from major vessels. If a hematoma develops in the immediate postoperative period, the patient must be returned to the operative room, the wound opened, and the hematoma evacuated and all tiny bleeders coagulated. Hematomas can lead to infection, which leads to flap necrosis and carotid exposure and rupture. One third of the infections are due to Staphylococcus aureus, one third is due to anaerobic infection, and one third is due to Gram-negative organisms, mainly Bacteroides fragilis. Seromas and chylous accumulations are managed by repeated aspirations or continuous drainage. While acute small orocutantous fistulae can close spontaneously, large fistulae should be allowed to mature then be revised with closure of the intraoral part if no recurrence is noted. The overall flap complications are about 25%, with 10% considered as major complications. Long and/or kinked flaps that have not been previously delayed increase the incidence of sloughing. In addition, diabetics and atherosclerotics are candidates for sloughed flaps. Delaying some types of skin flaps can avoid to a certain extent some of these complications. Carotid rupture is managed by ligation which carries 25% mortality. Osteoradionecrosis is usually managed conservatively; however, if it progresses, the exposed bone is resected and fresh coverage is used under heavy systemic antibiotics. Uncontrolled studies indicate that hyperbaric chambers may play a role in helping such bones to granulate with spontaneous healing.
Ear Trauma
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Skull trauma from blows to the temporal, parietal or occipital region (with or without fracture of the temporal bone) is the main cause; other modes of injury are rare.102 About 60% occur without a concomitant temporal bone fracture.101 Hearing loss occurs in about 22.5% of temporal bone fractures.103 Around 16–30% of these have a conductive component, of which some will be due to transient causes such as a haemotympanum.103,104 Direct penetrating trauma is less common105,106 and may be iatrogenic as a result of intratympanic injections, particularly if there has been previous middle ear surgery or stapedectomy.107 Other causes include middle ear barotrauma, surgical trauma and lightening strike.108 Several large studies identify similar aetiologies. Drill-induced trauma to the incus during tympanomastoid surgery usually causes incudostapedial joint dislocation and a corresponding conductive hearing loss. Permanent sensorineural hearing loss is also highly likely in this situation but prophylactic disarticulation of the incus does not protect against it in a standardized guinea pig model.109 Simple manipulation of the ossicles during surgery should, however, not result in a sensorineural deficit.110 Digital pressure applied to the external auditary meatus may result in a sudden pressure change resulting in an isolated malleus fracture.96 A comprehensive forensic post-mortem study looking at head injury victims using multislice CT methods suggests that the type of energy imparted is more important than simply the amount.111 Damage to the ossicular chain may also occur secondary to osteoradionecrosis.112 Congenital incus dislocation has also been described.113
Long-term outcomes following stereotactic body radiotherapy boost for oropharyngeal squamous cell carcinoma
Published in Acta Oncologica, 2019
Sarah Baker, Gerda M. Verduijn, Steven Petit, Aniel Sewnaik, Hetty Mast, Senada Koljenović, Joost J. Nuyttens, Wilma D. Heemsbergen
Among the 182 patients available for late toxicity assessment, 47 experienced grade ≥3 late toxicity with an estimated cumulative incidence of 28% (4% 1SE) at 5 years (Figure 2). Median time to onset of grade ≥3 late toxicity was 10.0 months (3.0–77.6) after RT. The 5-year cumulative incidence of grade ≥3 mucosal ulcers or soft tissue necrosis was 18% (3% 1SE) (Figure 3). This included one patient with grade 4 toxicity (carotid blow-out which was treated successfully with surgical ligation) and one grade 5 toxicity in a patient who died from tracheal necrosis/bleeding. Among the total 30 patients who experienced grade ≥3 mucosal ulcers or soft tissue necrosis, the time from occurrence until healing was <6 months in 14 patients (47%), 6–12 months in 9 patients (30%), and > 12 months in 6 patients (20%), with one patient (3%) lost to follow-up. The 5-year cumulative incidence of grade ≥3 osteoradionecrosis (ORN) was 9% (3% 1SE) (Figure 3). Among the total 11 cases of ORN, 5 experienced fracture and/or required surgery (grade 4), and an additional one died from surgical complications (grade 5). The 5-year cumulative incidence of grade ≥3 dysphagia or weight loss was 12% (3% 1SE) (Figure 3). For comparison with the literature, crude rates of grade ≥3 dysphagia (tube feeding dependence) at 1 and 2 years were 2% (n = 4) and 2% (n = 3), respectively. Additional grade ≥3 toxicities are provided in Table 2.
Outcome of nasopharyngeal carcinoma in Finland: A nationwide study
Published in Acta Oncologica, 2018
Miia Ruuskanen, Reidar Grenman, Ilmo Leivo, Tero Vahlberg, Antti Mäkitie, Kauko Saarilahti, Tuija Wigren, Merja Korpela, Leena Voutilainen, Petri Koivunen, Heikki Irjala, Heikki Minn
Unfortunately, in one-third of the cases detailed information about late toxicity was not available, and thus, data regarding toxicity have to be considered as incomplete. The severe adverse effects reported included osteoradionecrosis in four cases, peripheral neuropathy in three cases and both abducens nerve and recurrent laryngeal nerve palsies in one patient. Ear problems were reported in 33 cases (17%), and three patients needed a mastoidectomy to treat chronic mastoiditis. Mild dysphagia was common but severe swallowing complications also occurred. One patient remained permanently dependent on percutaneous endoscopic gastrostomy and three patients required repeated dilatations for esophageal strictures. Two patients had late onset laryngeal edema, which necessitated a tracheostomy. Twenty patients (20%) developed a second primary cancer of which only two were detected within the irradiated volume: one in the soft palate 15 years later and another in the nasopharynx 17 years later.
Irradiation affects the structural, cellular and molecular components of jawbones
Published in International Journal of Radiation Biology, 2022
Sridhar Reddy Padala, Bina Kashyap, Hannah Dekker, Jopi J. W. Mikkonen, Anni Palander, Nathalie Bravenboer, Arja M. Kullaa
In this review, the effects of radiation on the structure, cells, and biomolecules of bone are discussed with an emphasis on the jawbone. Most of the studies on radiation damage to the bone have been performed in animal models and only a few studies have examined human jawbone tissues. A single fractionated dose of 2 Gy seems to be a critical threshold; above that, the effects of radiation are more detrimental. A high dose of radiation causes a rapid bone loss due to the increased osteoclastic activity and decreased bone formation whereas a low and fractionated dose of radiation has caused a downregulation of osteoclast function and a stimulation of osteoblasts. Radiation exposure will lead to a drastic decrease in bone marrow cells which are needed to prevent the destruction of the bone’s architectural integrity. Inflammation and oxidative stress occur in the response to radiation that stimulates many molecular mechanisms such as triggering an early activation of osteoclast-mediated bone loss. Radiation also affects the surrounding soft tissues causing vascular damage and fibrotic changes which may further contribute to bone alterations or disturbances in bone healing processes. Hence, the complex interaction of altered cellular, vascular, and metabolic components of bone and in the adjacent tissues following radiotherapy, promotes structural changes in the bone. As a deleterious consequence of radiation, most jaw osteoradionecrosis occurs within months or even years after the treatment. The intensity of the reaction is often variable and may depend on various parameters related to the form of radiation delivery. Therefore if we are to devise effective countermeasures to radiation-induced bone loss, it is mandatory that we clarify the precise molecular and cellular drivers behind this phenomenon. We propose further research directions should utilize human jaw tissues in order to understand the early and late dose-dependent changes evoked by radiation as ways to enhance bone health after radiotherapy.