The ischemic osteonecrosis Maxillofacial beginning to study in 1915 by Black (4), calling it “chronic osteitis ”.
This author demonstrated the occurrence of bone death “cell to cell” with the creation of “pockets” alveolar intramedullary up to 5 cm. in diameter with the ability to produce extensive bone destruction without pus. Other authors also studied this process, but it was in the 70s and 80s
When he began to investigate the association between pain and neurogenic maxillofacial osteonecrosis, proposing the termneuralgia-inducing cavitional osteonecrosis (NICO), translated al castilian as osteopathy cavitary alveolar.
NICO of the jaws was defined as a chronic neurogenic pain syndrome caused by alveolar bone necrosis and intraosseous cavity formation of significant size.
At first, the formation of these cavities intraosseous was associated with persistence after extractions of chronic infectious processes in the alveolar bone of the jaws.
ETIOPATHOGENESIS AND HISTOPATHOLOGY
The pathogenic mechanism originally proposed supposed alveolar bone infection that occurred in turn one osteomyelitis localized neuropathic effects on the trigeminal nerve.
The formation and location of bone cavities in the jaw bones attributed to dental or surgical treatments that regenerate well and which persisted or establishing a bacterial infection.
The pathology described in 1976 in patients considered pathognomonic orofacial pain, including intraosseous stared cavities and some fibrous tissue necrotic bone spicule mixed with vascular. Microorganisms were detected in all the samples studied finding numerous bacterial agents involved
In 1992, Bouquot y Cols. (7) reported the possible pathogenic mechanism for the development of alveolar osteopathy cavity. The initiating factor would be to conduct an extraction which, together with a trigger, would produce the NICO. As the authors reported triggers five. In the first of these patients may have a local or systemic immunodeficiency, thus preventing bacterial destruction. Another process would especially pathogenic bacteria present in the bone tissue and fibrosis induce lack of vascularization. The third mechanism involved would refer to decreased blood flow to the jaws, which produce hypoxia or myocardial core and lower resistance to the development of oral infections.
The fourth theory would etiopatogéncia neutrófilios relative lack and / or macrophages, which produce a decrease in chemotaxis, phagocytosis and proteolytic enzymes, thereby increasing the infection The latter process is the absence or decrease of growth factors required intraosseous for new bone formation as well as an alteration in the pH in the bone tissue, causing a decrease in the potential osteoinductivo.
This paper also described the histopathology of these lesions which predominated marrow fibrosis, bone necrosis with medullary necrosis and inflammatory infiltrate. Normal marrow was detected in 33% of samples and new bone reagent formed in 20.5% of cases.
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