We can define gingivitis more easily by contradicting what is wrongly thought.
New diagnostic studies from 2017 say: “The initial changes from health to plaque-induced gingivitis may not be detectable clinically, raising important debates concerning clinical thresholds for defining physiologic vs pathologic inflammation”.
… This is a completely false assertion as, looking at a microscopic view of plaque sulcus, we clearly see less than 1% spirochete presence, or even no spirochetes at all. This figure then increases from 1% to 10% to 45% etc. It is a continuous bacterial progression until the neutrophils come in at about 10% pathogen bacterial load and after 3 to 4 days without brushing, from one, to tens, to hundreds of neutrophils present. It is a very progressive and evaluable condition on a microscopic and has a medical basis. Refer to Newman and Nisengard’s Oral Microbiology and Immunology book adapted from Savitt and Socransky’s dark-field microscopy to gain an easy understanding of it.
It is currently said: “If Patients may notice symptoms that include bleeding with tooth brushing, blood in saliva, gingival swelling and redness, and halitosis in the case of established forms”.
… dentists accustomed to using microscopes clearly see spirochetes (red complex) and vibrios (red complex again) building up progressively. Of course this progression is concurrent to the common clinical signs of plaque-induced gingivitis. It can be measured in the same way a laboratory would measure WBC in a blood test. The number of pathogen bacteria can be measured and the number of neutrophils can be measured too. A microscope will give you a sufficient number relative to the specific condition.
It is said “Although recent studies suggest that bacterial phylotypes associated with gingivitis are distinct from those associated with health (…for sure) or periodontitis, further studies are needed to clearly define the microbial community of gingivitis”.
…from a microscopic point of view, those are already well defined. Gingivitis biofilm is specific, either microbially or on an inflammatory basis. Periodontitis is different, as we will later see.
It is said that “sub gingival restauration: prominent subgingival restoration margins promote gingivitis by increasing the local accumulation of bacterial plaque”.
…this may be right, but expert microbiologists will see neutrophils appearing first, and usually before bacteria appears as this is a mechanical aggression to living tissues.
It is also said that “Although the clinical signs of gingival inflammation that do occur may be statistically significant, the signs are not clinically significant and therefore not clinically evident to the dentist”.
…this assertion may be applicable to the any dentist not accustomed to working with a microscope. For dentists who do use this equipment, signs of bacterial infection and neutrophil invasion are completely visible even before clinical signs appear. It is just a matter of progression that can be mathematically calculated. Gingivitis or Periodontitis should not be measured by the length or width of tissues, but measured by microbiological criteria and inflammatory conditions. Microbiology and inflammation are specific to health, gingivitis, periodontitis and necrotising periodontitis, to mucositis and periimplantitis. All are characterised by different microbiota and dysbiosis level.
It is currently said: “Although different types of inflammation may be features of a specific diagnosis, possibly inflammation per se is not a diagnosis in itself. More specifically, the clinical presence or absence of an inflammatory response should not necessarily be considered a sign of disease or health”.
…This is a completely false assertion as perfect health from within the sulcus, as can be observed on healthy dentists and hygienists and completely cured patient from a microscopic sulcus point of view, shows a total lack of inflammatory cells. This is attainable for patients who are cured too.
It is said: “At the other end of the spectrum, the absence of clinical signs of inflammation may not exclude the presence of an ongoing inflammatory process evident at a histologic level”.
…This is exactly why the microscopic evaluation of microbiota sulcus will indicate to the dental professional that there is an onset of gingivitis.
It is said: “longitudinal studies examining the natural history of periodontal disease failed to show complete conversion of long-standing gingival inflammation to periodontitis”.
…This is the big problem behind dentists not having access to a microscope. We can see typical microbes related to periodontitis appearing. It is a form of microbial evidence. But one has to look through a microscope to understand it. It is not an opinion based concept. It is a medical fact.
It is said: “Gingival inflammation is associated with progression to periodontitis; however, the presence of gingival inflammation does not mean that all affected sites are destined to progress to destructive forms of periodontal disease”.
…Effectively, this is right and, as we will later explain within our periodontitis definition, only sites infected with parasites will be subject to periodontitis. (As already described by Kofoid, Keyes and Lyons in scientific literature…)
It is said: “consistent with all complex diseases, gingival inflammation may be a sufficient cause for destruction of the periodontium but insufficient on its own to cause the disease in all people. More specifically, how can it be determined which inflamed sites within particular individuals are susceptible to conversion to periodontitis? Presently, no one knows the answer to this question, but there has been an awareness that differences in the inflammatory responsiveness of dental plaque cannot be fully accounted for by the quantity or quality of the biofilm. In other words, the predilection for attachment loss at inflamed gingival sites may be dependent on the susceptibility and responsiveness of the individual to the inflammatory insult”.