Nanomedicine, Volume IIA: Biocompatibility

© 2003 Robert A. Freitas Jr. All Rights Reserved.

Robert A. Freitas Jr., Nanomedicine, Volume IIA: Biocompatibility, Landes Bioscience, Georgetown, TX, 2003 Mechanical Damage to Extracellular Matrix Proteins

Uncorrected ECM damage caused by medical nanorobots might resemble any of several human disease conditions that are associated with disruptions in the ECM. For example, muscular dystrophy may be caused by disorganization of links between the intracellular cytoskeleton and the ECM through the plasmalemmal interface [4002, 4003]. However, R. Smigrodzki notes that dystrophy usually involves very widespread damage (some of it actually killing the cells), so for this kind of damage to occur, “you would probably need a very high, prolonged level of nanorobot activity.” Nanorobot-induced ECM damage might symptomatically resemble cystic fibrosis (which also involves ECM degradation [4004]), though CF is a genetic disorder associated with defective chloride ion channel protein, not mechanical damage per se. Alternatively, nanorobots could disrupt cell-cell connections, causing symptoms analogous to certain desmosomal genetic disorders [4005] or to tumor cell disruptions of normal tissue architecture [4006]. A wide range of connective tissue disorders and mechanical tissue abnormalities are known [4007, 4008], including spontaneous arterial dissections [4009], perforating disorders of skin [4010], and genetic disorders of the ECM [4011] (though these genetic coding errors are not due to mechanical damage by an external agency). Hair follicle growth may be compromised following the disruption of epithelial-mesenchymal interactions [4012]. Even a weakened ECM in atherosclerotic plaques can cause fibrous cap rupture in the high stress (>105 N/m2) vascular shoulder regions [4013]. All of these forms of mechanical damage to ECM should be avoidable by good design – specific force and duration thresholds for ECM damage should be investigated experimentally.

Fibrosis as a consequence of injury is characterized by accumulation of excess collagen and other extracellular matrix components, resulting in the disruption of normal tissue architecture and function [4608]. Without careful design, the emplacement of artificial fiber materials in the extracellular spaces by motile fiber-laying nanorobots could induce analogous destruction of normal tissue architecture.


Last updated on 30 April 2004