Newsgroup: it.scienza.medicina
Titolo: Perchè ai drogati cadono i denti?

 Vorrei sapere perchè ai drogati e mi pare anche ai malati di Aids cadono i
denti.
Nelle persone che non sono nè malate di aids , nè drogate quale è il motivo
perchè cadono i denti con la radice intera a causa della manacanza di
nutrimento delle stesse?La causa cioè dovrebbe essere l'occlusione delle
arteriole che nutrono il dente ma a sua volta coda determina cio'?

 il motivo perchč cadono i denti
Per quel che ne so io, il motivo piů comune (che puň interessare tutte
le categorie) č la parodontite da Actinobacillus actinomycetemcomitans
(ed eventualmente anche da Porphyromonas gingivalis).  Vedi ad es. la [2].
Bye,
  -= Ginzo =-
  [1] Minerva Stomatol 1999 Oct;48(10):485-92
 [The effects of drugs on the oral cavity]. [Article in Italian]
 Fazzi M, Vescovi P, Savi A, Manfredi M, Peracchia M
 Istituto di Clinica Odontoiatrica, Universita degli Studi, Parma.
  As shown by the growing numbers of users attending the public drug
 addiction services, drug abuse is a phenomenon that is constantly spreading.
 It is important that dentists are aware of the oral problems linked to
 drug abuse. This study examines the general effects and oral implications
 of the illegal substances used by the majority of drug addicts. The main
 dental complications of cannabinoids are the increased incidence of squamous
 cell carcinomas of the oral cavity, the presence of xerostomia and severe
 gingivitis. Depending on how it is taken, cocaine may cause ischemic
 necrosis of the palate, inflammation, ulceration and gingival retraction,
 as well as an increased incidence of bruxism. Hallucinogens have few direct
 oral effects, but among these it is worth recalling xerostomia, increased
 bruxism and oral problems linked to malnutrition caused by ecstasy. Turning
 to the opioids, heroin is the drug primarily used by the majority of drug
 addicts. Its oral effects mainly take the form of dental decay, showing
 a particular form and extent linked either directly or indirectly to heroin
 use. This results in "typical" or "atypical" caries pathologies directly
 linked to the effects of heroin. Given the extent of this phenomenon, it is
 important that dentists are aware of the problems linked to drug abuse
 that they may have to treat.
 PMID: 10726452, UI: 20190651
  [2] Periodontol 2000 1999 Jun;20:136-67
 Virulence factors of Actinobacillus actinomycetemcomitans.
 Fives-Taylor PM, Meyer DH, Mintz KP, Brissette C
 Department of Microbiology & Molecular Genetics, University of Vermont,
 Burlington, USA.
  A. actinomycetemcomitans has clearly adapted well to its environs; its
 armamentarium of virulence factors (Table 2) ensures its survival in the
 oral cavity and enables it to promote disease. Factors that promote A.
 actinomycetemcomitans colonization and persistence in the oral cavity
 include adhesins, bacteriocins, invasins and antibiotic resistance. It can
 interact with and adhere to all components of the oral cavity (the tooth
 surface, other oral bacteria, epithelial cells or the extracellular matrix).
 The adherence is mediated by a number of distinct adhesins that are
 elements of the cell surface (outer membrane proteins, vesicles, fimbriae
 or amorphous material). A. actinomycetemcomitans enhances its chance of
 colonization by producing actinobacillin, an antibiotic that is active
 against both streptococci and Actinomyces, primary colonizers of the tooth
 surface. The fact that A. actinomycetemcomitans resistance to tetracyclines,
 a drug often used in the treatment of periodontal disease, is on the rise
 is an added weapon. Periodontal pathogens or their pathogenic products
 must be able to pass through the epithelial cell barrier in order to reach
 and cause destruction to underlying tissues (the gingiva, cementum,
 periodontal ligament and alveolar bone). A. actinomycetemcomitans is able
 to elicit its own uptake into epithelial cells and its spread to adjacent
 cells by usurping normal epithelial cell function. A. actinomycetemcomitans
 may utilize these remarkable mechanisms for host cell infection and
 migration to deeper tissues. A. actinomycetemcomitans also orchestrates its
 own survival by elaborating factors that interfere with the host's defense
 system (such as factors that kill phagocytes and impair lymphocyte activity,
 inhibit phagocytosis and phagocyte chemotaxis or interfere with antibody
 production). Once the organisms are firmly established in the gingiva,
 the host responds to the bacterial onslaught, especially to the bacterial
 lipopolysaccharide, by a marked and continual inflammatory response,
 which results in the destruction of the periodontal tissues. A. actino-
 mycetemcomitans has at least three individual factors that cause bone
 resorption (lipopolysaccharide, proteolysis-sensitive factor and GroEL),
 as well as a number of activities (collagenase, fibroblast cytotoxin, etc.)
 that elicit detrimental effects on connective tissue and the extracellular
 matrix. It is of considerable interest to know that A. actinomycetemcomitans
 possesses so many virulence factors but unfortunate that only a few have
 been extensively studied. If we hope to understand and eradicate this
 pathogen, it is critical that in-depth investigations into the biochemistry,
 genetic expression, regulation and mechanisms of action of these factors
 be initiated.
 PMID: 10522226, UI: 99451724
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arteriole che nutrono il dente ma a sua volta coda determina cio'?
Istologicamente avviene un fenomeno di questo tipo, ma il colpevole
non e' l' arteriola che non nutre.
ciao
Riccardo Poli (RP)
ske...@lycosmail.com