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       #Post#: 12794--------------------------------------------------
       Dental Health
       By: AGelbert Date: July 5, 2019, 4:47 pm
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       [center]WHAT IS THE DIFFERENCE BETWEEN PLAQUE AND
       CALCULUS?[/center]
       Plaque is the sticky, colorless film that constantly forms on
       your teeth. Bacteria live in plaque and secrete acids that cause
       tooth decay and irritate gum tissue. This irritation causes an
       inflammatory reaction by your body that can eventually lead to
       gingivitis and periodontal disease. If plaque is not removed
       regularly by tooth brushing and flossing, it hardens to create
       calculus (also known as tartar). Calculus cannot be removed with
       a toothbrush; only a dental professional can remove it during an
       oral cleaning.
  HTML https://www.perio.org/consumer/difference-between-plaque-and-calculus
       Eur J Oral Sci. 1997 Oct;105(5 Pt 2):508-22.
       [center]Dental calculus: recent insights into occurrence,
       formation, prevention, removal and oral health effects of
       supragingival and subgingival deposits.[/center]
       SNIPPET:
       [quote]Subgingival calculus formation in these populations
       occurs coincident with periodontal disease (although the
       calculus itself appears to have little impact on attachment
       loss), the latter being correlated with dental plaque.
       Despite extensive research, a complete understanding of the
       etiologic significance of subgingival calculus to periodontal
       disease remains elusive, due to inability to clearly
       differentiate effects of calculus versus "plaque on calculus".
       As a result, we are not entirely sure whether subgingival
       calculus is the cause or result of periodontal inflammation.
       Research suggests that subgingival calculus, at a minimum, may
       expand the radius of plaque induced periodontal injury. Removal
       of subgingival plaque and calculus remains the cornerstone of
       periodontal therapy.
       Full Abstract.
  HTML https://www.ncbi.nlm.nih.gov/pubmed/9395117[/quote]
       Agelbert NOTE: The literal bottom line in regard to bacteria
       causing dental problems is the word, "SUBgingival". The reason
       for that is that the types of bacteria that live between the gum
       line and your teeth have anaerobic metabolism. That is, they
       function where there is not enough oxygen for the aerobic
       (oxygen using metabolism) types of bacteria, like those that
       live in the supragingival area (above the gum line).
       IOW, the pathogenic bacteria are out of sight, where they do
       their damage free from benign aerobic bacteria competition
       interference. Although the bad bacteria has been identified as
       "gram-negative", the key to the problem these critters cause in
       the periodontium is their metabolism. The "obligate" anaerobes
       must live where oxygen is not present because they die when it
       is present. The "facultative" anaerobes can use or not use
       oxygen, depending on the environment. The only two obligate
       anaerobe species associated with periodontal disease are in
       proportionately small percentages compared with the facultative
       anaerobes.
       [quote]Most of the periodontal pathogens are anaerobes but the
       biofilm can also harbour facultative aerobes, capnophiles and
       microaerophiles whose number depends on the environment in the
       developed biofilm and periodontal pocket. Most periodontal
       pathogens represent the true periodontal infection.
       Some bacterial species in the periodontal environment that are
       part of the commensal flora (Actinomyces, certain
       Streptococcusand Staphylococcus spp.) can provoke opportunistic
       infections in case of ecosystem disturbance.
       There is evidence that detection of certain enterobacteria,
       viruses and Saccharomyces spp. in the periodontal pockets could
       indicate superinfection associated with a periodontal
       destructive process.
       It has recently been generally recognized that periodontal
       diseases are mixed infections.
  HTML https://www.tandfonline.com/doi/pdf/10.5504/BBEQ.2013.0027[/quote]
       The point is that the bad action happens below (subgingival
       peridontium adjacent to the tooth). The pH, temperature and
       humidity above and below the gum line are almost identical at
       all times. It is below the gum line that the anaerobes can then
       create more acidic/corrosive conditions that enable other
       opportunistic bacteria to attack the area. It stands to reason
       that the lower your population of anaerobes, both of the
       obligate and the more abundant facutative species of bacteria,
       the better your mouth health. There is no way you can get rid of
       all of them due to the fact that you will always have some
       subgingival gum areas where only anaerobic metabolism bacteria
       can survive, so there is no danger of losing those types of
       bacteria altogether. Though they are gram-negative and are
       technically considered "pathogens", I'm sure the correct
       percentage of them, as is found in a healthy mouth (Normal
       Microbial Flora of Oral Cavity
  HTML https://pdfs.semanticscholar.org/8830/bfd2e396fc543131a02f94a922fde36b80ff.pdf),<br
       />is good for us.
       I am guilty of adding the bacteria graphics below. The
       scientists that participated in this study and wrote this
       excellent abstract are innocent of such frivolous levity.
       &#128512;
       J N Z Soc Periodontol. 2004;(87):7-21.
       [center]Dental plaque revisited: bacteria associated with
       periodontal disease.[/center]
       Lovegrove JM.
       Abstract
       Between 3-12 weeks after the beginning of supragingival plaque
       formation, a distinctive subgingival microflora predominantly
       made up of gram-negative, anaerobic bacteria and including some
       motile species, becomes established. In order to establish in a
       periodontal site, a species must be able to attach to one of
       several surfaces including the tooth (or host derived substances
       adhering to the tooth), the sulcular or pocket epithelium, or
       other bacterial species that are attached to these surfaces
       (Socransky and Haffajee 1991).
       Bacterial adhesion has demonstrated specificity in the
       mechanisms involved and studies have shown that there is a
       diversity of receptors on tooth surfaces, epithelial or other
       host cells and other bacteria. Recent studies have described
       bacterial complexes that are present in subgingival plaque and
       these studies are likely to help in current understanding of the
       complex ecology observed in dental plaque biofilm (Socransky,
       Haffajee et al. 1998). Bacterial interactions play important
       roles in species survival. Some interspecies relationships are
       favourable, in that one species produces growth factors for, or
       facilitates attachment of, another species. Other relationships
       are antagonistic due to competition for nutrients and binding
       sites, or to the production of substances that limit or prevent
       the growth of another species (Socransky and Haffajee 1991).
       A number of different bacterial interactions within plaque
       biofilm have been discussed. In the last 30-40 years, a vast
       amount of evidence has been published to suggest that bacteria
       are the primary aetiological agents of periodontal diseases.
       In the 1950s and early 1960s, periodontal treatment was based on
       the non-specific plaque hypothesis. However, the non-specific
       plaque hypothesis gave way after studies suggested that not all
       organisms in plaque are equally capable of causing destructive
       periodontal disease.
       Thus the concept of specificity re-emerged. Criteria for
       defining periodontal pathogens have been developed and include
       association, elimination, host response, virulence factors,
       animal studies and risk assessment (Haffajee and Socransky
       1994).
       Until recently there were few consensus periodontal pathogens
       and trying to discriminate pathogenic from non-pathogenic
       species has been a difficult task for dental researchers for a
       variety of reasons.
       A discussion of the specific microbiota associated with
       gingivitis, chronic and aggressive periodontitis, NUG,
       HIV-associated periodontitis and implantitis has been presented.
       The[img
       width=100]
  HTML https://thumbs.dreamstime.com/z/cartoon-virus-germ-bacteria-3234482.jpg[/img]<br
       />bacteria associated with periodontal diseases are predominantl
       y
       gram-negative anaerobic bacteria and may include:
       [img
       width=400]
  HTML https://render.fineartamerica.com/images/rendered/default/print/8.000/8.000/break/images-medium-5/cartoon-bacteria-collection-set-tigatelu.jpg[/img]
       A. actinomycetemcomitans,
       Porphyromonas (P.) gingivalis,  (obligate anaerobe)
       P. intermedia, (obligate anaerobe)
       [s]B. forsythus[/s] NEW NAME = Tannerella forsythia, (obligate
       anaerobe)
       C. rectus,
       E. nodatum,
       P. micros,
       S. intermedius and
       Treponema sp.
       The bacterial numbers associated with disease are up to 10(5)
       times larger than [img
       width=60]
  HTML http://www.clker.com/cliparts/2/4/c/b/15167389891021593515clipart-bacteria-cartoon.hi.png[/img]<br
       />those associated with health. &#128064;
       PMID: 15143484
       [Indexed for MEDLINE]
  HTML https://www.ncbi.nlm.nih.gov/pubmed/15143484
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