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Commentary: Periodontitis severity and progression are modified by various host and environmental factors.

Disease modifiers do not cause disease. But they can change the biology to increase or decrease the rate of progression of disease, thereby determining the age of clinical detection and the severity at a given age. Modifiers are like the volume control on a sound system. Nothing happens unless the on/off switch is activated, but once activated there may be a big difference between low and high amplification of the sound. In periodontitis there are some subtle distinctions between a disease risk factor and a disease modifier, but in most uses the terms can be interchangeable. Substantial evidence supports an essential bacterial role in the initiation and progression of periodontitis, and most of the non-bacterial risk factors for periodontitis, such as smoking, appear to operate as disease modifiers to differentially alter the clinical effects of a bacterial challenge. 
 
In the field of periodontology, much of the second half of the 20th century was devoted to unraveling the causes of periodontitis and determining how to use that information to more predictably prevent and treat the disease. Epidemiological studies using basic statistical models documented strong associations between plaque and periodontitis and showed that disease was primarily explainable by age and plaque. These observations, the generally poor state of oral hygiene at the time, and multiple theories of causation and treatment produced a prevalent mid-century view that periodontitis was inevitable with aging and that treatment outcomes were unpredictable.