There are many programmed cell death pathways, but some cells show a greater preference for some over the other. I'm wondering as to why if necrosis is an inflammatory response that causes damage to neighboring cells, why some cells would prefer this as opposed to a more controlled mechanism such as apoptosis or even autophagy.
There is actually no preference for apoptosis or necrosis in cells of the human body - both types can occur in all cells and they have different triggers. The main differences can be seen in this figure (from here):
Apoptosis (also called programmed cell death) has three different triggers (intrinsic, extrinsic and Perforin/Granzyme pathways), see the image below for details (from reference 1):
All three activate different components and caspases in the beginning but finally all activate Caspase 3, which finally activates endonucleases (which degrade the chromosomal DNA), Proteases (which degrade the proteins in the nucleus and the cytoskeleton) which leads to the degradation of the cell. In the end apoptotic bodies are formed from the cell. Additionally the mitochondria break down and release cytochrome c and ATP. Their release from the cell attracts macrophages which take up and eliminate the apoptotic bodies and in turn release cytokines which suppress an inflammatory response.
Apoptosis goes on in a ordered way and does not trigger any further reactions in neighbouring cells (except these receive the same signal). See also reference 1 and 2 for more details.
Necrosis is triggered by external stimuli of the cell as injury of tissues or toxins from infections. Necrotic cells swell, while there internal structures are in a state of unregulated degradation. Finally the membrane will burst and set free cytochrome c and phosphatidylserines from the membranes which cause inflammation in the affected tissue. The necrotic cells are not removed by macrophages which allows the released interior of the cell to spread further and cause problems. See reference 2 and 3 for more details.
Necrosis is usually not as a beneficial process, but there are also publications which see the process as a specific form of cell death (see reference 4).
The answer given above by Chris is correct, but does leave out one relatively recently discovered method of cell death, somewhere between the two responses of apoptosis and necrosis.
It's called pyroptosis. It's a form of programmed cell death (in immune cells, e.g. macrophages), so it is similar to apoptosis. However, instead of a neat and tidy non-phlogistic (inflammatory) death as is the case in apoptosis, the cell purposefully upregulates inflammatory cytokines, swells, and bursts, releasing the cytokines and other inflammatory mediators out into the extracellular space.
It's a response to certain Pathogen Associated Molecular Patterns (PAMPs). These are patterns that are present on pathogens - in this case particular bacterial species - and trigger an immune response. Read more about them here. This pro-inflammatory response attracts other immune cells to the area, and helps to drive an immune response, containing and aiding in the elimination of the invading pathogens.
Edit: OP may also be interested to know that if an apoptotic cell is not cleared by a macrophage, eventually it will become "secondarily necrotic", meaning the membrane eventually falls apart and the cell releases it's contents (Source). This turns it from non-inflammatory to an inflammatory response. Neutrophils are particularly adept at keeping their membranes intact, due to the harmful nature of the cell contents. There is a pubmed entry here regarding it, but the actual book I've taken this information from isn't available without subscription.
Necrosis can be described as accidental cell death or damage, triggered possibly from external environmental factors such as exposure to radiation, toxins, excessive heat and etc...whereas, Apoptosis is a programmed form of a cell death mechanism. This process may be used to recycle unwanted cells in the body. Therefore, the particular stimulus that the cell receives may be a key determinant of the cell death mechanism observed.