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Hyperplasia

Accelerated growth in cell-numbers, which seems to be a survival-strategy primarily in two situations. The first being oxygen-starvation, where cells are seen to multiply faster than when normal amounts are present. This might be because less oxygen is required for anabolic than catabolic processes and that mitosis produces two cells with smaller energetic needs but at the expense of lowered cellular function and resilience to stress.

Figure illustrating the pro-survival function of hyperplasia where hypoxic stress leads to a mitotic response resulting in two daughter-cells with less energetic need but with lower function and resilience.

The second situation that stimulates cellular hyperplasia is exposure to a noxious stimulus, such as molecular signals of nearby pathogens. This is most readily observed on epithelial cell-sheets, the surfaces where the body is exposed to the external environment, and cellular proliferation here creates a counterflow that complicates the movement of intracellular microorganisms towards the underlying stem-cell layer and the blood-stream.

Figure illustrating the anti-microbial function of hyperplasia (spaced lines) that counteracts microbial penetration by increasing microbial migration-distance to the stem-cells as well as mitotic rate and speed.

Supporting Evidence

  • Cells are seen to proliferate more rapidly when less oxygen was available.1)https://www.ncbi.nlm.nih.gov/pubmed/6311421
  • Direct infection cause reactive hyperplasia2)https://www.ncbi.nlm.nih.gov/pubmed/17075821
  • Stimulation of cells with bacterial lipopolysaccharide cause hyperplasia in vitro3)https://www.ncbi.nlm.nih.gov/pubmed/29298445
  • Conventionally raised mice have twice the rate of epithelial turnover compareed with germ-free mice.4)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996021/
  • The proliferative capacity and phenotypic plasticity of stem-cells make them attractive targets for pathogens5)https://www.ncbi.nlm.nih.gov/pubmed/30649285

Association with Disease

  • Synovial hyperplasia and hypoxia occurs in OA and RA6)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383490/7)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3372675/8)https://arthritis-research.biomedcentral.com/articles/10.1186/ar42919)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5244982/10)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946116/
  • Increased number of tenocytes and evidence of tissue-hypoxia in tendinopathy11)https://bjsm.bmj.com/content/48/21/155312)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6923943/
  • Hyperplasia is seen to occur in early stages of atherosclerosis, before lipid-accumulation13)https://www.sciencedirect.com/science/article/pii/S1359644616301921

 

References   [ + ]

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