Multimodular Assessment of a Traumatic Bone Cyst Overlapped with Apical Periodontitis

Table 1

Etiopathogenetic theories of the TBC.

°	Theory	Statement
1	Traumatic-hemorrhagic	A trauma can lead to intramedullary hemorrhage. Compromised vascular supply, edema, and aseptic bone necrosis caused by the trauma lead the blood clot to liquefy. In the area, lytic enzymes are released, and osteoclastic bone resorption is activated. The expansion of the cavity seems to be sustained by the edema and blood extravasation.
2	Infective	A small, low-grade, chronic infection of bone marrow is involved in the pathogenesis
3	Lesion degeneration	A developing tumor or lesion (i.e., hemangioma, lymphoma, fibrous-osseous dysplasia, or central giant cell granuloma) undergoes liquid degeneration, leaving behind an empty cavity.
4	Local thrombosis	A local thrombosis can generate either a local ischemia with necrosis of bone marrow and blockage of interstitial fluid drainage leading to the formation and expansion of an intraosseous cavity.
5	Developmental	A failure of mesenchymal tissue to form bone and cartilage occurs and instead generates immature synovial cavities, which coalesce to form a larger connective tissue-lined defect.
6	Systemic disease	An imbalance between osteoclastic and osteoblastic activity, parathyroid disease, or a peculiarity in vessel walls or blood coagulation can predispose to the development of a TBC.