These implants must be designed and installed with care. Stress shielding occurs when plates or screws carry too large of a portion of the bones load, causing atrophy. This problem is reduced, but not eliminated, by the use of low-modulus materials, including titanium and its alloys. The heat generated by the friction of installing hardware can accumulate easily and damage bone tissue, reducing the strength of the connections. If dissimilar metals are installed in contact with one another (i.e., a titanium plate with cobalt-chromium alloy or stainless steel screws), galvanic corrosion will result. The metal ions produced can damage the bone locally and may cause systemic effects as well. Other
A Cochrane review of low-intensity pulsed ultrasound to speed healing in newly broken bones found insufficient evidence to justify routine use. Other reviews have found tentative evidence of benefit. It may be an alternative to surgery for established nonunions. Children
In children, whose bones are still developing, there are risks of either a growth plate injury or a greenstick fracture. A greenstick fracture occurs due to mechanical failure on the tension side. That is since the bone is not so brittle as it would be in an adult, it does not completely fracture, but rather exhibits bowing without complete disruption of the bones cortex in the surface opposite the applied force. Growth plate injuries, as in Salter-Harris fractures, require careful treatment and accurate reduction to make sure that the bone continues to grow normally.
These smears typically show plasmablasts and, in some cases, other malignant cells that have the morphology of anaplastic cells (i.e., large pleomorphic cells) or the Reed-Sternberg cells associated with Hodgkin disease. As detected by immunostaining methods, the malignant cells typically express molecular marker proteins such as CD45 (which is not expressed on mature plasma cells) as well as activation and plasma cell marker proteins such as CD30, MUC1, CD38, syndecan 1, and IRF4/MUM1; they do not express B-cell molecular marker proteins such as PAX5, CD19, CD29, or CD79a. The cells may also express many of the structural and non-structural gene abnormalities cited in the Pathophysiology section. By definition, individuals with PEL are infected by Kaposis sarcoma-associated herpesvirus (HHV-8 or KSHV/HHV8) and therefore evidence malignant cells that express products of this virus such as LANA1. In most cases, these individuals are also infected with EBV and therefore evidence malignant cells that express products of this virus such as EBER1/2 nuclear RNAs. Cases associated with HIV/AIDS test positive for antibodies directed against this virus. (PEL occurs in the absence of HHV-8 and HIV, although this is rare.) Individuals with PEL that is associated with cirrosis due to hepatitis evidence positive serum tests for the hepatitis virus B antigen (HBsAg) or one of the various tests for hepatitis C antigen. Extracavitary PEL is diagnosed based on findings that their mass lesions contain the same or very similar types of malignant cells and the same set of blood and serum findings as those that are found in cavitary PEL.