Nonosseous accumulation of bone-seeking radiopharmaceuticals.

Wegener’s Granulomatosis: Extraosseous Uptake in HDP Bone Scintigraphy- A Case Report

“…In this case, diffuse hepatic uptake of MDP was probably due to hepatic hypoxic necrosis resulted from respiratory failure caused by granulomatosis inflammation and necrotizing vasculitis. There are several reports where diffuse hepatic uptake occured due to respiratory failure (7,8).The possible pathophysiology of increased liver uptake of Tc-99m MDP may be due to the presence of necrotic or degenerative tissue that sets free intracellular calcium and phosphorus complexes in liver (8).…”

Extraosseous uptake of technetium-99m methylene diphosphonate by an acute territorial cerebral infarct in a classical biodistribution pattern

“…Enhanced regional vascularity and permeability, extracellular fluid expansion, elevated tissue calcium concentration, presence of tracer avid other metallic ions, adsorption onto immature collagen and binding to denatured proteins are some of the mechanisms, which lead to extraosseous uptake. [23] Such extraosseous uptake in the brain is rare, occurring in less than 0.2% of patients undergoing bone scintigraphy. [4] Acute infarcts of the brain show increased tracer uptake because of the following pathophysiology: (i) the ischemic damage to cellular membranes result in rapid intracellular influx of calcium leading to calcium precipitation within the mitochondria and (ii) denatured proteins also act as substrates for calcium deposition.…”

“…[4] Acute infarcts of the brain show increased tracer uptake because of the following pathophysiology: (i) the ischemic damage to cellular membranes result in rapid intracellular influx of calcium leading to calcium precipitation within the mitochondria and (ii) denatured proteins also act as substrates for calcium deposition. [3] Established territorial infarcts of the brain show uptake of tracer in a well-defined pattern in the skull region depending upon the blocked artery. [45] If the ischemic changes are widespread and bilateral, for example in hypoxic ischemic encephalopathy, Tc-99m MDP is seen in laminar distribution and watershed territories matching the vascular insult.…”

“…[7] Sometimes tracer is localized in extra axial locations also such as hematomas, meningiomas, metastases and dural calcifications. [38] One rare instance of primary cerebral amyloidoma having increased bone tracer accumulation has been documented in the literature. [9]…”

Non-osseous uptake on Tc99m methylene diphosphonate in multiple muscles confirmed on SPECT/computed tomography

“…[1] The pathogenesis of uptake of bone scanning agents in soft-tissue is multi-factorial; one of the primary underlying factors is excess calcium in the soft-tissue. [2] Scintigraphy with Tc-99m MDP delineates a wide spectrum of non-osseous disorders, i.e., Neoplastic, hormonal, inflammatory, ischemic, traumatic, excretory, and artifactual entities demonstrate abnormal soft-tissue uptake of Tc-99m MDP. [3] Mechanisms leading to increased extraosseous Tc-99m MDP uptake include extracellular fluid expansion, enhanced regional vascularity and permeability, and elevated tissue calcium concentration.…”