Zapalenie dziąseł
Patofizjologia i mechanizm

Zapalenie dziąseł (gingivitis) to odwracalny stan zapalny tkanki dziąsłowej wywołany głównie przez biofilm bakteryjny, w którym dominują gatunki takie jak Streptococcus, Fusobacterium, Actinomyces, Veillonella i Treponema. Patogeneza obejmuje progresję od prostych społeczności bakteryjnych do bardziej złożonych, z przewagą bakterii beztlenowych Gram-ujemnych, np. Porphyromonas gingivalis, które wytwarzają toksyny indukujące odpowiedź immunologiczną i uszkodzenie tkanek. Proces zapalny przebiega przez cztery stadia: początkowe (I) z ostrą odpowiedzią zapalną i migracją neutrofili, wczesne (II) z klinicznym zaczerwienieniem i naciekiem limfocytarnym, ustalone (III) z przewlekłym zapaleniem i dominacją komórek plazmatycznych oraz zaawansowane (IV) – zapalenie przyzębia z nieodwracalną utratą przyczepu łącznotkankowego i resorpcją kości wyrostka zębodołowego. Kluczową rolę odgrywają cytokiny prozapalne, takie jak IL-1β, IL-6 i TNF-α, oraz metaloproteinazy macierzy (MMP), które prowadzą do degradacji tkanek przyzębia.

Definicja i charakterystyka zapalenia dziąseł

Zapalenie dziąseł (gingivitis) to stan zapalny tkanki dziąsłowej, najczęściej spowodowany zakażeniem bakteryjnym. Jest to nieniszcząca choroba charakteryzująca się zapaleniem dziąseł wokół podstawy zębów12. Zapalenie dziąseł jest najczęstszą postacią łagodnej choroby przyzębia, a główną przyczyną tego stanu jest gromadzenie się płytki bakteryjnej (biofilmu) na powierzchniach zębów w pobliżu lub w rowku dziąsłowym34.

Gingivitis jest stanem odwracalnym, jednak nieleczone może prowadzić do bardziej zaawansowanej formy choroby przyzębia – zapalenia przyzębia (periodontitis), które charakteryzuje się nieodwracalną utratą przyczepu łącznotkankowego i kości wyrostka zębodołowego56. Z tego względu zrozumienie patogenezy gingivitis ma kluczowe znaczenie dla opracowania skutecznych strategii zapobiegania i leczenia chorób przyzębia7.

Czynniki etiologiczne zapalenia dziąseł

Głównym czynnikiem etiologicznym zapalenia dziąseł jest płytka bakteryjna. Płytka to lepka, bezbarwna warstwa składająca się głównie z bakterii, która przylega do powierzchni zębów i linii dziąseł89. Mikroorganizmy najsilniej związane z etiologią zapalenia dziąseł należą do gatunków Streptococcus, Fusobacterium, Actinomyces, Veillonella i Treponema1011.

Podczas gdy wczesna płytka w zdrowych warunkach składa się ze stosunkowo prostej społeczności bakteryjnej zdominowanej przez Gram-dodatnie ziarenkowce i pałeczki, w miarę dojrzewania płytki i rozwoju zapalenia dziąseł społeczności bakteryjne stają się coraz bardziej złożone, z wyższym odsetkiem Gram-ujemnych pałeczek, fusiformów, nitkowców, spirilli i krętków12. Wśród taksonów związanych z zapaleniem dziąseł wymienia się Fusobacterium nucleatum subspecies polymorphum, Lachnospiraceae species HOT100, Lautropia species HOTA94 i Prevotella oulorum13.

Szczególną rolę w patogenezie zapalenia dziąseł przypisuje się bakteriom beztlenowym Gram-ujemnym, takim jak Porphyromonas gingivalis, Prevotella intermedia i Tannerella forsythia. Bakterie te rozwijają się w środowisku pozbawionym tlenu pod linią dziąseł i wytwarzają toksyny, które wywołują odpowiedź immunologiczną, prowadząc do uszkodzenia tkanek i zapalenia14.

Biofilm bakteryjny i jego rola

Zdolność bakterii do tworzenia biofilmów odgrywa kluczową rolę w patogenezie zapalenia dziąseł15. W strukturze biofilmu bakterie są bardziej odporne na środki przeciwbakteryjne i odpowiedź immunologiczną gospodarza, co pozwala im przetrwać i namnażać się na powierzchniach zębów i pod dziąsłami16. Ta trwałość biofilmów bakteryjnych przyczynia się do przewlekłego charakteru zapalenia dziąseł i podkreśla znaczenie ukierunkowanych interwencji w skutecznym leczeniu17.

Biofilm bakteryjny na powierzchni korony zębu stale prezentuje antygen dla dziąsła brzeżnego, stymulując odpowiedź zapalną, co prowadzi do zapalenia dziąseł18. Z kolei zapalenie przyzębia jest wywoływane przez odpowiedź gospodarza na płytkę poddziąsłową19.

Patogeneza zapalenia dziąseł

Patogeneza zapalenia dziąseł jest najlepiej wyjaśniona poprzez opisanie zdarzeń histologicznych i ich powiązanie z objawami klinicznymi. Rozwój zapalenia dziąsłowego został podzielony na trzy odrębne stadia: początkowe, wczesne i ustalone, a zapalenie przyzębia jest określane jako stadium zaawansowane2021.

Stadium początkowe zapalenia dziąseł

Początkowe stadium zapalenia dziąseł (stadium I) pojawia się w ciągu pierwszych kilku dni kontaktu płytki bakteryjnej z tkankami dziąsłowymi22. Charakteryzuje się ostrą odpowiedzią zapalną z rozszerzeniem naczyń krwionośnych i zwiększonym przepływem krwi23. Na poziomie histologicznym obserwuje się zwiększony przepływ płynu dziąsłowego i migrację neutrofilów z naczyń krwionośnych splotu poddziąsłowego zlokalizowanego w tkance łącznej dziąsła do rowka dziąsłowego24.

Podczas stadium początkowego zapalenia dziąseł dochodzi do niszczenia kolagenu przez kolagenazę i inne enzymy wydzielane przez neutrofile25. Ten etap jest widoczny po około 4-5 dniach od rozpoczęcia gromadzenia się płytki nazębnej2627.

Wczesne stadium zapalenia dziąseł

Wczesne stadium zapalenia dziąseł (stadium II) pojawia się zwykle po tygodniu od rozpoczęcia odkładania się płytki28. Jest to pierwszy kliniczny dowód zapalenia dziąseł, który może trwać 21 dni lub dłużej29. To stadium jest zgodne z opóźnioną nadwrażliwością3031.

Charakterystyczne dla tego stadium jest zwiększenie aktywności kolagenolitycznej wraz ze wzrostem liczby makrofagów, komórek plazmatycznych oraz limfocytów T i B32. Na poziomie klinicznym dziąsła mają zaczerwieniony wygląd z powodu proliferacji naczyń włosowatych i rozszerzenia naczyń33.

Przejście do wczesnych zmian po około tygodniu charakteryzuje się zmianą na przeważająco limfocytarny naciek. Mogą być również obecne monocyty i komórki plazmatyczne34.

Ustalone stadium zapalenia dziąseł

Po 15-21 dniach zapalenie dziąseł osiąga stadium ustalone, nazywane stadium III35. W tym stadium obserwuje się wyraźną zmianę w rodzaju białych krwinek widocznych w preparatach histologicznych36. Ustalone zapalenie dziąseł odpowiada wyglądowi klinicznemu określanemu jako przewlekłe zapalenie dziąseł i zależy od wielu czynników, takich jak skład i ilość biofilmu płytki, czynniki podatności gospodarza oraz lokalne i ogólnoustrojowe czynniki ryzyka37.

W tym stadium dominują komórki plazmatyczne3839. Nabłonek łączący zostaje zastąpiony nabłonkiem kieszonki, który nie jest przytwierdzony do powierzchni zęba. Umożliwia to dalszą migrację biofilmu w kierunku szczytu40.

Ustalone zapalenie dziąseł może albo pozostać stabilne przez miesiące lub lata, albo postępować do bardziej destrukcyjnych zmian, co wydaje się być związane ze zmianą flory mikrobiologicznej lub zakażeniem dziąseł41. Stan ten jest odwracalny w przypadku regularnego usuwania płytki nazębnej, co pozwala tkankom powrócić do normy42.

Zaawansowane stadium zapalenia dziąseł – przejście do zapalenia przyzębia

Stadium IV zapalenia dziąseł to zaawansowane stadium, w którym procesy zapalne rozprzestrzeniają się poza dziąsła i wnikają w inne tkanki przyzębia43. To stadium oznacza przejście do zapalenia przyzębia i charakteryzuje się utratą przyczepu łącznotkankowego, która jest nieodwracalna4445.

Zaawansowana zmiana ma wiele cech zmiany ustalonej, ale różni się istotnie tym, że dochodzi do utraty przyczepu tkanki łącznej i kości wyrostka zębodołowego46. Przejście od ustalonego zapalenia dziąseł do zapalenia przyzębia jest w dużej mierze zdominowane przez limfocyty T i B47.

Najbardziej charakterystyczną cechą zaawansowanej zmiany jest owrzodzenie nabłonka, które było najbardziej zauważalną i stałą zmianą obserwowaną w związku z przekształceniem zmiany ustalonej w zmianę zaawansowaną. Przerwanie bariery nabłonkowej wraz z jednoczesnym wnikaniem bakterii i ich toksycznych produktów było najważniejsze dla przekształcenia zmiany ustalonej w zmianę agresywną48.

Mechanizmy molekularne w patogenezie zapalenia dziąseł

Cząsteczki odgrywające rolę w patogenezie zapalenia dziąseł dzielą się na dwie główne grupy: pochodzące z mikrobioty poddziąsłowej (tj. czynniki wirulencji drobnoustrojów) oraz pochodzące z immunologiczno-zapalnej odpowiedzi gospodarza4950.

Bakteryjne czynniki wirulencji

Bakterie obecne w biofilmie płytki nazębnej są rozpoznawane przez komórki odporności wrodzonej poprzez określone wzorce molekularne zwane patogen-associated molecular patterns (PAMPs), które obejmują lipopolisacharyd (LPS), peptydoglikany i kwasy lipotejchojowe, N-formylometioninę i lipoproteiny51.

Lipopolisacharyd bakterii Gram-ujemnych może aktywować kaskadę dopełniacza poprzez alternatywną drogę52. Lipopolisacharyd nie aktywuje ekspresji E-selektyny w komórkach śródbłonka naczyniowego, co blokuje lokalną odpowiedź neutrofilów na niego i inne mikroorganizmy w płytce nazębnej53.

Bakterie w płytce nazębnej wytwarzają chemikalia, takie jak enzymy degradacyjne i toksyny, np. lipopolisacharyd (LPS, znany również jako endotoksyna) lub kwas lipotejchojowy (LTA), które promują odpowiedź zapalną w tkance dziąsłowej54.

Odpowiedź immunologiczna gospodarza

Odpowiedź immunologiczna gospodarza na zapalenie dziąseł obejmuje zarówno mechanizmy odporności wrodzonej, jak i nabytej. Rozpoznanie patogennych mikroorganizmów i rekrutacja komórek efektorowych (np. neutrofilów) oraz cząsteczek (np. układu dopełniacza) są kluczowe dla skutecznej odporności wrodzonej55.

Neutrofile (leukocyty wielojądrzaste, PMN) stanowią pierwszą linię obrony przed bakteriami, a prawidłowa funkcja PMN jest niezbędna do ochrony integralności przyzębia56. Rozwój zapalenia dziąseł polega głównie na infiltracji tkanek łącznych przez liczne komórki obronne, w szczególności neutrofile, makrofagi, komórki plazmatyczne i limfocyty57.

Jeśli zapalenie dziąseł utrzymuje się bez rozwiązania, antygeny bakteryjne są wytwarzane przez limfocyty, makrofagi i komórki dendrytyczne58. Odporność adaptacyjna zapewnia bardziej ukierunkowaną obronę przed infekcjami niż odpowiedzi immunologiczne wrodzone, która jest wolniejsza i zależna od złożonych interakcji między komórkami prezentującymi antygen (APC) a limfocytami T i B, w szczególności cytotoksycznymi komórkami T i przeciwciałami59.

Cytokiny i mediatory zapalne

Cytokiny są kluczowymi mediatorami zapalnymi w patogenezie zapalenia dziąseł i przyzębia6061. Odpowiedź immunologiczna na mikroorganizmy jamy ustnej indukuje kaskadę zapalną, która promuje uwalnianie prozapalnych cytokin, takich jak interleukina (IL)-1β, IL-6 i czynnik martwicy nowotworów alfa (TNF-α), w tkance dziąsłowej62.

Niepanująca odpowiedź zapalna w dziąśle może prowadzić do nasilenia i zniszczenia tkanek przyzębia, a utrata przyczepu może zależeć od reaktywności gospodarza na agresję zapalną w miejscach dziąsłowych63. TNF-α jest cytokiną o wielu funkcjach, która może indukować destrukcję tkanek i resorpcję kości wyrostka zębodołowego64.

Przedłużone i nadmierne uwalnianie dużych ilości metaloproteinaz macierzy (MMP) w przyzębiu prowadzi do znacznego rozkładu strukturalnych składników tkanek łącznych, przyczyniając się do klinicznych objawów choroby65.

Czynniki wpływające na patogenezę zapalenia dziąseł

Chociaż bakterie są centralne dla rozwoju zapalenia dziąseł, czynniki gospodarza odgrywają również znaczącą rolę w określaniu indywidualnej podatności na chorobę66.

Czynniki związane z gospodarzem

Rozwój zapalenia przyzębia jest również zależny od innych czynników wewnętrznych (np. genetycznych, stłoczenia zębów, cienkiej kości wyrostka zębodołowego, wieku) i zewnętrznych (np. diety, stresu, chorób współistniejących, higieny jamy ustnej)67. Podatność na zapalenie przyzębia sugeruje, że osoby bardziej podatne na chorobę wykazują nadmierną lub dysregulowaną odpowiedź immunologiczno-zapalną na dane wyzwanie bakteryjne, co prowadzi do zwiększonego niszczenia tkanek w porównaniu z osobami o bardziej normalnej odpowiedzi zapalnej68.

Genetycznie kontrolowane mechanizmy wpływają na produkcję i aktywność biologiczną TNF-α. Polimorfizmy pojedynczego nukleotydu (SNP) zostały zidentyfikowane w regionie promotora genu TNF-α, a przejście z G na A w pozycji -308 zwiększa poziom produkcji cytokin69.

Zmiany hormonalne

Podczas ciąży występują nie tylko zmiany poziomu hormonów, ale także większa predyspozycja do rozszerzania naczyń krwionośnych. Czynniki te przyczyniają się do nasilonej odpowiedzi zapalnej tkanek dziąsłowych nawet na niewielką ilość nagromadzonej płytki nazębnej70.

Zmiany hormonalne występujące w okresie dojrzewania wpływają na sposób, w jaki tkanka dziąsłowa reaguje na gromadzenie się płytki nazębnej, powodując tzw. zapalenie dziąseł okresu dojrzewania71.

Wpływ stylu życia i diety

Styl życia ma znaczący wpływ na nasycenie fosforanem wapnia i kolonizację bakteryjną. Palenie tytoniu powoduje wyższe stężenie wapnia w ślinie, co zwiększa tworzenie się kamienia nazębnego72.

Dieta zdominowana przez węglowodany może indukować zapalenie dziąseł poprzez promowanie kolonizacji bakteryjnej na płytce nazębnej73. Mechanizm, w jaki węglowodany o wysokim indeksie glikemicznym promują proces zapalny, polega na aktywacji NFkB i stresu oksydacyjnego74.

Związek między zapaleniem dziąseł a chorobami ogólnoustrojowymi

Zapalenie przyzębia zwiększa ryzyko wystąpienia różnych chorób ogólnoustrojowych, w tym miażdżycy, choroby wieńcowej serca, udaru mózgu i niskiej masy urodzeniowej niemowląt75.

Badania sugerują związek między chorobą dziąseł a rozwojem choroby Alzheimera. Bakterie zaangażowane w zapalenie przyzębia, zwane gingipainami, były obecne w mózgach osób z chorobą Alzheimera i istotnie korelowały z diagnozą choroby Alzheimera z nasilającą się patologią tau i ubikwityny76.

Związek między zapaleniem dziąseł a innymi stanami zapalnymi, takimi jak choroba serca i cukrzyca, został od dawna ustalony, ale mechanizm leżący u podstaw tego związku pozostawał tajemnicą. Nowsze badania sugerują, że aktywność komórek immunologicznych neutrofilów jest brakującym ogniwem łączącym chorobę przyzębia z chorobą serca, rakiem i innymi stanami zapalnymi77.

Podsumowanie patogenezy zapalenia dziąseł

Zapalenie dziąseł jest wynikiem złożonej interakcji między biofilmem bakteryjnym a odpowiedzią immunologiczną gospodarza78. Chociaż bakterie periopatogenne są nadal uważane za główne czynniki inicjujące, immunologiczno-zapalna odpowiedź gospodarza na te patogeny odgrywa ważną rolę w patogenezie choroby przyzębia79.

Biofilm płytki nazębnej powoduje większość uszkodzeń tkanki przyzębia poprzez mechanizmy pośrednie zależne od inicjacji i rozprzestrzeniania się zapalnych reakcji tkankowych gospodarza80. W gingivitis płytka bakteryjna i jej komponenty, takie jak lipopolisacharydy, wywołują stan zapalny ograniczony do tkanki miękkiej dziąsła81.

Jeśli zapalenie dziąseł nie zostanie wyleczone, może przejść w zapalenie przyzębia, które charakteryzuje się destrukcją tkanek podporowych zęba i kości wyrostka zębodołowego u osób podatnych, co ostatecznie prowadzi do utraty zębów i zwiększonego ryzyka chorób ogólnoustrojowych, takich jak cukrzyca i choroby sercowo-naczyniowe82.

Stadium zapalenia dziąseł Charakterystyka kliniczna Zmiany histopatologiczne Dominujące komórki zapalne
Stadium początkowe (I) Subkliniczne, brak widocznych objawów Ostra odpowiedź zapalna, zwiększony przepływ płynu dziąsłowego, destrukcja kolagenu Neutrofile
Stadium wczesne (II) Zaczerwienienie, obrzęk, krwawienie przy sondowaniu Proliferacja naczyń włosowatych, rozszerzenie naczyń Limfocyty, monocyty, pojedyncze komórki plazmatyczne
Stadium ustalone (III) Przewlekłe zapalenie dziąseł, nasilone zaczerwienienie, obrzęk, krwawienie Zastąpienie nabłonka łączącego nabłonkiem kieszonki, początek tworzenia kieszonek Komórki plazmatyczne, limfocyty B
Stadium zaawansowane (IV) Utrata przyczepu, pogłębienie kieszonek, możliwa utrata kości Owrzodzenie nabłonka, utrata przyczepu łącznotkankowego, resorpcja kości Komórki plazmatyczne, limfocyty T i B

Zrozumienie mechanizmów patogenezy zapalenia dziąseł ma kluczowe znaczenie dla opracowania skutecznych strategii zapobiegania i leczenia. Wczesna interwencja może zapobiec progresji do zapalenia przyzębia, co czyni profilaktykę i leczenie zapalenia dziąseł kluczowym elementem opieki stomatologicznej8384.

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  1. 11.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Gingivitis – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Immunology/Gingivitis/
    Gingivitis is a condition characterized by inflammation of the gums, which is caused by the presence of plaque and bacterial components such as lipopolysaccharides. Symptoms of gingivitis include redness, swelling, tenderness, and bleeding of the gums, which result from plaque buildup. […] Gingivitis is the most common form of mild periodontal disease. It causes inflammation, redness, and swelling of the gingiva, or part of the gum, around the base of the teeth. Bleeding gums are a sign of gingivitis, or inflammation of the gums. It is a common and mild form of gum disease caused by a buildup of plaque at the gum-line. The goal of treatment is to reverse the damage from gingivitis and to prevent progression to periodontitis because gum disease is the leading cause of tooth loss in adults.
  • #2 Gingivitis: Causes, symptoms, and treatment
    https://www.medicalnewstoday.com/articles/241721
    Gingivitis is a common condition that affects most adults at some point in their life. […] The most common cause of gingivitis is the accumulation of bacterial plaque between and around the teeth. […] Buildup of plaque and tartar can trigger immune responses that lead to gingival or gum tissue destruction. […] There are two main types of gingivitis. Dental plaque-induced gingivitis occurs when plaque buildup irritates a persons gums, resulting in inflammation, discoloration, and pain. […] In contrast, nonplaque-induced gingival lesions can result from a bacterial, viral, or fungal infection. […] Both types of gingivitis can progress to periodontitis if a person does not treat them adequately. Periodontitis is a more severe condition and can lead to further complications, such as loss of teeth.
  • #3 Gingivitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/sites/books/n/statpearls/article-22251/
    Gingivitis is an inflammatory condition of the gingival tissue most commonly caused by bacterial infection. […] This activity describes the evaluation and management of gingivitis and highlights the role of the interprofessional team in managing patients with this condition. […] Describe the etiology and pathogenesis of gingivitis. […] Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] This stage is characterized by an acute exudative inflammatory response, a raised gingival fluid flow, and the migration of neutrophils from the blood vessel of the subgingival plexus located in the gingival connective tissue to the gingival sulcus.
  • #4 Gingivitis – Wikipedia
    https://en.wikipedia.org/wiki/Gingivitis
    Gingivitis is a non-destructive disease that causes inflammation of the gums; ulitis is an alternative term. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms (also called plaque) that are attached to tooth surfaces, termed plaque-induced gingivitis. Most forms of gingivitis are plaque-induced. […] The cause of plaque-induced gingivitis is bacterial plaque, which acts to initiate the body’s host response. This, in turn, can lead to destruction of the gingival tissues, which may progress to destruction of the periodontal attachment apparatus. The plaque accumulates in the small gaps between teeth, in the gingival grooves and in areas known as plaque traps: locations that serve to accumulate and maintain plaque.
  • #5 Pathogenesis of Periodontal Disease | IntechOpen
    https://www.intechopen.com/chapters/67314
    The primary features of periodontitis include the loss of periodontal tissue support, manifested through clinical attachment loss and radiographically assessed alveolar bone loss, presence of periodontal pocketing, and gingival bleeding. […] The development of gingivitis and periodontitis can be divided into a series of stages: initial, early, established, and advanced lesions. […] The inflammatory immune response is triggered by the interaction of resident cells with the bacterial biofilm attached to the tooth surface. […] The junctional epithelium is the first periodontal structure to face the bacterial challenge. […] The most important characteristic of periodontitis is the inflammatory reabsorption of the tooth-supporting alveolar bone due to the uncontrolled host immune response against periodontal infection, since the destructive events, which lead to the irreversible phenotype of periodontal disease, are the result of the persistence of a chronic and exacerbated inflammatory immune response.
  • #6 Gingivitis: Causes, symptoms, and treatment
    https://www.medicalnewstoday.com/articles/241721
    Gingivitis is a common condition that affects most adults at some point in their life. […] The most common cause of gingivitis is the accumulation of bacterial plaque between and around the teeth. […] Buildup of plaque and tartar can trigger immune responses that lead to gingival or gum tissue destruction. […] There are two main types of gingivitis. Dental plaque-induced gingivitis occurs when plaque buildup irritates a persons gums, resulting in inflammation, discoloration, and pain. […] In contrast, nonplaque-induced gingival lesions can result from a bacterial, viral, or fungal infection. […] Both types of gingivitis can progress to periodontitis if a person does not treat them adequately. Periodontitis is a more severe condition and can lead to further complications, such as loss of teeth.
  • #7 Pathogenesis of Gingivitis – CORE
    https://core.ac.uk/works/10922453/
    The molecules that play a role in the pathogenesis are divided into two main groups: those derived from the subgingival microbiota (i.e., microbial virulence factors) and those derived from the host immune-inflammatory response. […] Understanding the disease processes is important for the development of improved treatment strategies.
  • #8 Gingivitis – Wikipedia
    https://en.wikipedia.org/wiki/Gingivitis
    Gingivitis is a non-destructive disease that causes inflammation of the gums; ulitis is an alternative term. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms (also called plaque) that are attached to tooth surfaces, termed plaque-induced gingivitis. Most forms of gingivitis are plaque-induced. […] The cause of plaque-induced gingivitis is bacterial plaque, which acts to initiate the body’s host response. This, in turn, can lead to destruction of the gingival tissues, which may progress to destruction of the periodontal attachment apparatus. The plaque accumulates in the small gaps between teeth, in the gingival grooves and in areas known as plaque traps: locations that serve to accumulate and maintain plaque.
  • #9 Gingivitis: Causes, symptoms, and treatment
    https://www.medicalnewstoday.com/articles/241721
    Gingivitis is a common condition that affects most adults at some point in their life. […] The most common cause of gingivitis is the accumulation of bacterial plaque between and around the teeth. […] Buildup of plaque and tartar can trigger immune responses that lead to gingival or gum tissue destruction. […] There are two main types of gingivitis. Dental plaque-induced gingivitis occurs when plaque buildup irritates a persons gums, resulting in inflammation, discoloration, and pain. […] In contrast, nonplaque-induced gingival lesions can result from a bacterial, viral, or fungal infection. […] Both types of gingivitis can progress to periodontitis if a person does not treat them adequately. Periodontitis is a more severe condition and can lead to further complications, such as loss of teeth.
  • #10 Gingivitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/sites/books/n/statpearls/article-22251/
    Gingivitis is an inflammatory condition of the gingival tissue most commonly caused by bacterial infection. […] This activity describes the evaluation and management of gingivitis and highlights the role of the interprofessional team in managing patients with this condition. […] Describe the etiology and pathogenesis of gingivitis. […] Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] This stage is characterized by an acute exudative inflammatory response, a raised gingival fluid flow, and the migration of neutrophils from the blood vessel of the subgingival plexus located in the gingival connective tissue to the gingival sulcus.
  • #11 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] The mechanism by which carbohydrates with a high glycemic index promote the inflammatory process is through activation of NFkB and oxidative stress. […] During pregnancy, there are not only changes in hormone levels but also a greater predisposition to dilating blood vessels. These factors contribute to an exaggerated inflammatory response by the gingival tissues even to a minor quantity of plaque accumulation. […] The hormonal alterations that occurred during puberty influence how the gingival tissue reacts to plaque accumulation causing what is known as puberty gingivitis.
  • #12 Gingivitis – Wikipedia
    https://en.wikipedia.org/wiki/Gingivitis
    Although these accumulations may be tiny, the bacteria in them produce chemicals, such as degradative enzymes, and toxins, such as lipopolysaccharide (LPS, otherwise known as endotoxin) or lipoteichoic acid (LTA), that promote an inflammatory response in the gum tissue. This inflammation can cause an enlargement of the gingiva and subsequent formation. Early plaque in health consists of a relatively simple bacterial community dominated by Gram-positive cocci and rods. As plaque matures and gingivitis develops, the communities become increasingly complex with higher proportions of Gram-negative rods, fusiforms, filaments, spirilla and spirochetes. Later experimental gingivitis studies, using culture, provided more information regarding the specific bacterial species present in plaque. Taxa associated with gingivitis included Fusobacterium nucleatum subspecies polymorphum, Lachnospiraceae species HOT100, Lautropia species HOTA94, and Prevotella oulorum (a species of Prevotella bacterium), whilst Rothia dentocariosa was associated with periodontal health. Further study of these taxa is warranted and may lead to new therapeutic approaches to prevent periodontal disease including systemic health.
  • #13 Gingivitis – Wikipedia
    https://en.wikipedia.org/wiki/Gingivitis
    Although these accumulations may be tiny, the bacteria in them produce chemicals, such as degradative enzymes, and toxins, such as lipopolysaccharide (LPS, otherwise known as endotoxin) or lipoteichoic acid (LTA), that promote an inflammatory response in the gum tissue. This inflammation can cause an enlargement of the gingiva and subsequent formation. Early plaque in health consists of a relatively simple bacterial community dominated by Gram-positive cocci and rods. As plaque matures and gingivitis develops, the communities become increasingly complex with higher proportions of Gram-negative rods, fusiforms, filaments, spirilla and spirochetes. Later experimental gingivitis studies, using culture, provided more information regarding the specific bacterial species present in plaque. Taxa associated with gingivitis included Fusobacterium nucleatum subspecies polymorphum, Lachnospiraceae species HOT100, Lautropia species HOTA94, and Prevotella oulorum (a species of Prevotella bacterium), whilst Rothia dentocariosa was associated with periodontal health. Further study of these taxa is warranted and may lead to new therapeutic approaches to prevent periodontal disease including systemic health.
  • #14 The Role of Microorganisms in Gingivitis Pathogenesis and Periodo
    https://www.longdom.org/open-access/the-role-of-microorganisms-in-gingivitis-pathogenesis-and-periodontal-disease-106569.html
    Gingivitis, a common oral health ailment, often serves as a precursor to more severe periodontal diseases if left untreated. […] Recent research has shed light on the significant role of bacteria in gingivitis development. […] Bacteria play a pivotal role in the initiation and progression of gingivitis. […] One such group is the Gram-negative anaerobic bacteria, including Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia. […] These bacteria thrive in the oxygen-deprived environment beneath the gum line and produce toxins that trigger an immune response, leading to tissue damage and inflammation. […] The ability of bacteria to form biofilms plays a crucial role in gingivitis pathogenesis. […] Within these biofilms, bacteria are more resistant to antimicrobial agents and host immune responses, allowing them to persist and proliferate on tooth surfaces and beneath the gums.
  • #15 The Role of Microorganisms in Gingivitis Pathogenesis and Periodo
    https://www.longdom.org/open-access/the-role-of-microorganisms-in-gingivitis-pathogenesis-and-periodontal-disease-106569.html
    Gingivitis, a common oral health ailment, often serves as a precursor to more severe periodontal diseases if left untreated. […] Recent research has shed light on the significant role of bacteria in gingivitis development. […] Bacteria play a pivotal role in the initiation and progression of gingivitis. […] One such group is the Gram-negative anaerobic bacteria, including Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia. […] These bacteria thrive in the oxygen-deprived environment beneath the gum line and produce toxins that trigger an immune response, leading to tissue damage and inflammation. […] The ability of bacteria to form biofilms plays a crucial role in gingivitis pathogenesis. […] Within these biofilms, bacteria are more resistant to antimicrobial agents and host immune responses, allowing them to persist and proliferate on tooth surfaces and beneath the gums.
  • #16 The Role of Microorganisms in Gingivitis Pathogenesis and Periodo
    https://www.longdom.org/open-access/the-role-of-microorganisms-in-gingivitis-pathogenesis-and-periodontal-disease-106569.html
    Gingivitis, a common oral health ailment, often serves as a precursor to more severe periodontal diseases if left untreated. […] Recent research has shed light on the significant role of bacteria in gingivitis development. […] Bacteria play a pivotal role in the initiation and progression of gingivitis. […] One such group is the Gram-negative anaerobic bacteria, including Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia. […] These bacteria thrive in the oxygen-deprived environment beneath the gum line and produce toxins that trigger an immune response, leading to tissue damage and inflammation. […] The ability of bacteria to form biofilms plays a crucial role in gingivitis pathogenesis. […] Within these biofilms, bacteria are more resistant to antimicrobial agents and host immune responses, allowing them to persist and proliferate on tooth surfaces and beneath the gums.
  • #17 The Role of Microorganisms in Gingivitis Pathogenesis and Periodo
    https://www.longdom.org/open-access/the-role-of-microorganisms-in-gingivitis-pathogenesis-and-periodontal-disease-106569.html
    This persistence of bacterial biofilms contributes to the chronic nature of gingivitis and underscores the importance of targeted interventions for effective management. […] While bacteria are central to gingivitis development, host factors also play a significant role in determining individual susceptibility to the disease. […] Gingivitis is a prevalent oral health condition influenced by a complex interplay of bacteria, host factors, and environmental influences. […] While bacteria, particularly those forming biofilms, are central to its pathogenesis, individual susceptibility varies based on genetic, systemic, and behavioral factors.
  • #18 Periodontal Disease in Small Animals – Digestive System – Merck Veterinary Manual
    https://www.merckvetmanual.com/digestive-system/dentistry-in-small-animals/periodontal-disease-in-small-animals
    Periodontal disease is caused by plaque bacteria accumulating on the tooth surface and eliciting a host response to the bacterial insult. The accumulation of plaque, the biodiversity of microbiota, and the host immune system are factors in the pathogenesis of periodontal disease. […] Bacterial plaque on the crown surface of a tooth constantly presents antigen to the marginal gingiva, stimulating an inflammatory response, resulting in gingivitis. […] Periodontitis is caused by the host’s response to subgingival plaque. […] Inflammatory mediators produced by the host directly result in bone and tissue damage around the root. The bacteria themselves and their metabolic products also contribute to bone damage. […] Development of periodontitis is also affected by other intrinsic (eg, genetics, tooth crowding, thin alveolar bone, age) and extrinsic (eg, diet, stress, concurrent disease, oral hygiene) factors.
  • #19 Periodontal Disease in Small Animals – Digestive System – Merck Veterinary Manual
    https://www.merckvetmanual.com/digestive-system/dentistry-in-small-animals/periodontal-disease-in-small-animals
    Periodontal disease is caused by plaque bacteria accumulating on the tooth surface and eliciting a host response to the bacterial insult. The accumulation of plaque, the biodiversity of microbiota, and the host immune system are factors in the pathogenesis of periodontal disease. […] Bacterial plaque on the crown surface of a tooth constantly presents antigen to the marginal gingiva, stimulating an inflammatory response, resulting in gingivitis. […] Periodontitis is caused by the host’s response to subgingival plaque. […] Inflammatory mediators produced by the host directly result in bone and tissue damage around the root. The bacteria themselves and their metabolic products also contribute to bone damage. […] Development of periodontitis is also affected by other intrinsic (eg, genetics, tooth crowding, thin alveolar bone, age) and extrinsic (eg, diet, stress, concurrent disease, oral hygiene) factors.
  • #20 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Pathogenesis refers to the events in the development and progression of a disease. The pathogenesis of gingivitis is best explained by describing the histologic events as they relate to clinical signs. Extensive research on the pathogenesis of gingivitis, obtained by observing people and animals when bacterial plaque was allowed to accumulate, has explained most of the events in the development of gingival inflammation. With this knowledge, scientists have classified the development of gingival inflammation into three separate stages: […] Research has also defined a fourth stage, characterized by the extension of inflammation into the alveolar bone, which is the stage of periodontal breakdown, or advanced stage. […] It is critical to treat gingivitis because it can progress to periodontal disease.
  • #21 Gingivitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/sites/books/n/statpearls/article-22251/
    Gingivitis is an inflammatory condition of the gingival tissue most commonly caused by bacterial infection. […] This activity describes the evaluation and management of gingivitis and highlights the role of the interprofessional team in managing patients with this condition. […] Describe the etiology and pathogenesis of gingivitis. […] Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] This stage is characterized by an acute exudative inflammatory response, a raised gingival fluid flow, and the migration of neutrophils from the blood vessel of the subgingival plexus located in the gingival connective tissue to the gingival sulcus.
  • #22 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Stage I gingivitis, the initial stage, occurs in the first few days of contact between microbial plaque and the gingival tissues. This stage is an acute inflammatory response that is characterized by dilation of the blood vessels and increased blood flow. […] The early stage of gingivitis may continue for 21 days or longer. It is the earliest clinical evidence of gingivitis. […] After 15 to 21 days, the gingival inflammation reaches the established stage, called stage III gingivitis. […] In established gingivitis, there is a distinct change in the type of white blood cells seen in histologic specimens. […] The established gingivitis lesion may persist unchanged for months or years. The condition is reversible when plaque is regularly removed, permitting the tissues to return to normal.
  • #23 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Stage I gingivitis, the initial stage, occurs in the first few days of contact between microbial plaque and the gingival tissues. This stage is an acute inflammatory response that is characterized by dilation of the blood vessels and increased blood flow. […] The early stage of gingivitis may continue for 21 days or longer. It is the earliest clinical evidence of gingivitis. […] After 15 to 21 days, the gingival inflammation reaches the established stage, called stage III gingivitis. […] In established gingivitis, there is a distinct change in the type of white blood cells seen in histologic specimens. […] The established gingivitis lesion may persist unchanged for months or years. The condition is reversible when plaque is regularly removed, permitting the tissues to return to normal.
  • #24 Gingivitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/sites/books/n/statpearls/article-22251/
    Gingivitis is an inflammatory condition of the gingival tissue most commonly caused by bacterial infection. […] This activity describes the evaluation and management of gingivitis and highlights the role of the interprofessional team in managing patients with this condition. […] Describe the etiology and pathogenesis of gingivitis. […] Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] This stage is characterized by an acute exudative inflammatory response, a raised gingival fluid flow, and the migration of neutrophils from the blood vessel of the subgingival plexus located in the gingival connective tissue to the gingival sulcus.
  • #25 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] The initial lesion is seen within four days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. […] The early lesion is consistent with delayed hypersensitivity. It usually appears after one week from the beginning of plaque deposition. […] The established lesion may follow two paths, it can either remain stable for months or years; or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #26 Gingivitis: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/763801-overview
    The most common type of gingivitis involves the marginal gingiva and is brought on by the accumulation of microbial plaques in persons with inadequate oral hygiene. Gingivitis proceeds through an initial stage to produce early lesions, which then progress to advanced disease. […] The initial stage of an acute exudative inflammatory response begins within 4 or 5 days of plaque accumulation. Both gingival fluid and transmigration of neutrophils increase. Deposition of fibrin and destruction of collagen can be noted in the initial stage. At approximately 1 week, transition to early lesions is marked by the change to predominately lymphocytic infiltrates. Monocytes and plasma cells also may be present. With time, lesions become chronic and are characterized by the presence of plasma cells and B lymphocytes. As chronic local inflammation progresses, pockets develop where the gingiva separates from the tooth. These pockets deepen and may bleed during tooth brushing, flossing, and even normal chewing. As this persistent inflammation continues, periodontal ligaments break down and destruction of the local alveolar bone occurs. Teeth loosen and eventually fall out.
  • #27 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] The initial lesion is seen within four days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. […] The early lesion is consistent with delayed hypersensitivity. It usually appears after one week from the beginning of plaque deposition. […] The established lesion may follow two paths, it can either remain stable for months or years; or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #28 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] The initial lesion is seen within four days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. […] The early lesion is consistent with delayed hypersensitivity. It usually appears after one week from the beginning of plaque deposition. […] The established lesion may follow two paths, it can either remain stable for months or years; or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #29 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Stage I gingivitis, the initial stage, occurs in the first few days of contact between microbial plaque and the gingival tissues. This stage is an acute inflammatory response that is characterized by dilation of the blood vessels and increased blood flow. […] The early stage of gingivitis may continue for 21 days or longer. It is the earliest clinical evidence of gingivitis. […] After 15 to 21 days, the gingival inflammation reaches the established stage, called stage III gingivitis. […] In established gingivitis, there is a distinct change in the type of white blood cells seen in histologic specimens. […] The established gingivitis lesion may persist unchanged for months or years. The condition is reversible when plaque is regularly removed, permitting the tissues to return to normal.
  • #30 Gingivitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/sites/books/n/statpearls/article-22251/
    The early lesion is consistent with delayed hypersensitivity. […] There is increased collagenolytic activity in this stage along with a rise in the number of macrophages, plasma cells, T and B lymphocytes. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #31 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] The initial lesion is seen within four days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. […] The early lesion is consistent with delayed hypersensitivity. It usually appears after one week from the beginning of plaque deposition. […] The established lesion may follow two paths, it can either remain stable for months or years; or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #32 Gingivitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/sites/books/n/statpearls/article-22251/
    The early lesion is consistent with delayed hypersensitivity. […] There is increased collagenolytic activity in this stage along with a rise in the number of macrophages, plasma cells, T and B lymphocytes. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #33 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The development of gingivitis is mainly the infiltration of the connective tissues by numerous defense cells, particularly neutrophils, macrophages, plasma cells, and lymphocytes. […] The classic studies of Page and Schroeder described the basic understanding of histologic changes that occur in the gingival tissues as the initial, early, established, and advanced gingival lesions. […] The initial lesion develops within 24 days of the accumulation of plaque at a site free of plaque biofilm, which is evident microscopically since the gingival tissues always have characteristics of a low-grade chronic inflammatory response as a result of the continual presence of the subgingival biofilm. […] The early lesion corresponds to the early clinical signs of gingivitis and characterized by erythematous clinical appearance of gingiva due to proliferation of capillaries and vasodilatation.
  • #34 Gingivitis: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/763801-overview
    The most common type of gingivitis involves the marginal gingiva and is brought on by the accumulation of microbial plaques in persons with inadequate oral hygiene. Gingivitis proceeds through an initial stage to produce early lesions, which then progress to advanced disease. […] The initial stage of an acute exudative inflammatory response begins within 4 or 5 days of plaque accumulation. Both gingival fluid and transmigration of neutrophils increase. Deposition of fibrin and destruction of collagen can be noted in the initial stage. At approximately 1 week, transition to early lesions is marked by the change to predominately lymphocytic infiltrates. Monocytes and plasma cells also may be present. With time, lesions become chronic and are characterized by the presence of plasma cells and B lymphocytes. As chronic local inflammation progresses, pockets develop where the gingiva separates from the tooth. These pockets deepen and may bleed during tooth brushing, flossing, and even normal chewing. As this persistent inflammation continues, periodontal ligaments break down and destruction of the local alveolar bone occurs. Teeth loosen and eventually fall out.
  • #35 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Stage I gingivitis, the initial stage, occurs in the first few days of contact between microbial plaque and the gingival tissues. This stage is an acute inflammatory response that is characterized by dilation of the blood vessels and increased blood flow. […] The early stage of gingivitis may continue for 21 days or longer. It is the earliest clinical evidence of gingivitis. […] After 15 to 21 days, the gingival inflammation reaches the established stage, called stage III gingivitis. […] In established gingivitis, there is a distinct change in the type of white blood cells seen in histologic specimens. […] The established gingivitis lesion may persist unchanged for months or years. The condition is reversible when plaque is regularly removed, permitting the tissues to return to normal.
  • #36 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Stage I gingivitis, the initial stage, occurs in the first few days of contact between microbial plaque and the gingival tissues. This stage is an acute inflammatory response that is characterized by dilation of the blood vessels and increased blood flow. […] The early stage of gingivitis may continue for 21 days or longer. It is the earliest clinical evidence of gingivitis. […] After 15 to 21 days, the gingival inflammation reaches the established stage, called stage III gingivitis. […] In established gingivitis, there is a distinct change in the type of white blood cells seen in histologic specimens. […] The established gingivitis lesion may persist unchanged for months or years. The condition is reversible when plaque is regularly removed, permitting the tissues to return to normal.
  • #37 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The established lesion corresponds to clinical appearance referred to as chronic gingivitis and depends on many factors, such as composition and quantity of the plaque biofilm, host susceptibility factors, local and systemic risk factors. […] The advanced lesion, as described by Page and Schroeder, marks the transition from gingivitis to periodontitis which is determined by many factors, such as composition and quantity of the biofilm, the host inflammatory response, and environmental and genetic risk factors. […] The inflammatory infiltrate of periodontal disease (gingivitis and periodontitis) is characterized by polymorphonuclear leukocytes (PMNs), macrophages, lymphocytes, plasma cells. […] The interactions between these components determine the nature of periodontal disease activity, whether gingivitis or periodontitis.
  • #38 Gingivitis | PPT
    https://www.slideshare.net/slideshow/gingivitis-249410663/249410663
    The character and intensity of the host response determine whether this initial lesion resolves rapidly, with the restoration of the tissue to a normal state or evolves into a chronic inflammatory lesion. If the latter occurs, an infiltrate of macrophages and lymphoid cells appears within a few days. […] The established lesion evolves characterized by a predominance of plasma cells B lymphocytes in conjunction with the creation of a small gingival pocket lined with a pocket epithelium. […] In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of plaque accumulation, blood vessels are engorged and congested, venous return is impaired, and blood flow is sluggish. […] The predominance of plasma cells is thought to be a primary characteristic of the established lesion. […] The junctional epithelium is substituted by a pocket epithelium that is not attached to the tooth surface. This allows for a further apical migration of the biofilm.
  • #39 22. Pathogenesis / Disease Activity: Pathogenesis and Inflammation
    https://spindlerperio.net/protected/lit/LR22.html
    The presence of different areas may also suggest the theory that periods of quiescence or exacerbation within a pocket may be the cumulative effect of all the activities within the pocket wall. […] The presence of plasma cell lesion, which is accompanied by extensive bone resorption even though the site of infiltration is some distance from the bone surface. […] The advanced lesion is predominated by plasma cells. […] The advanced lesion is characterized by the periodontal pocket, bone loss and eventually tooth loss. […] Periodontitis is not a single homogenous disease but rather consists of a family of closely related diseases each of which may vary somewhat in etiology, natural history and response to therapy. […] The severity and rate of progression of disease feedback to influence the nature and magnitude of the microbial challenge by, for example, influencing the pH and availability of oxygen and various nutrients in the periodontal pocket.
  • #40 Gingivitis | PPT
    https://www.slideshare.net/slideshow/gingivitis-249410663/249410663
    The character and intensity of the host response determine whether this initial lesion resolves rapidly, with the restoration of the tissue to a normal state or evolves into a chronic inflammatory lesion. If the latter occurs, an infiltrate of macrophages and lymphoid cells appears within a few days. […] The established lesion evolves characterized by a predominance of plasma cells B lymphocytes in conjunction with the creation of a small gingival pocket lined with a pocket epithelium. […] In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of plaque accumulation, blood vessels are engorged and congested, venous return is impaired, and blood flow is sluggish. […] The predominance of plasma cells is thought to be a primary characteristic of the established lesion. […] The junctional epithelium is substituted by a pocket epithelium that is not attached to the tooth surface. This allows for a further apical migration of the biofilm.
  • #41 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] The initial lesion is seen within four days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. […] The early lesion is consistent with delayed hypersensitivity. It usually appears after one week from the beginning of plaque deposition. […] The established lesion may follow two paths, it can either remain stable for months or years; or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #42 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Stage I gingivitis, the initial stage, occurs in the first few days of contact between microbial plaque and the gingival tissues. This stage is an acute inflammatory response that is characterized by dilation of the blood vessels and increased blood flow. […] The early stage of gingivitis may continue for 21 days or longer. It is the earliest clinical evidence of gingivitis. […] After 15 to 21 days, the gingival inflammation reaches the established stage, called stage III gingivitis. […] In established gingivitis, there is a distinct change in the type of white blood cells seen in histologic specimens. […] The established gingivitis lesion may persist unchanged for months or years. The condition is reversible when plaque is regularly removed, permitting the tissues to return to normal.
  • #43 6: Gingival Diseases | Pocket Dentistry
    https://pocketdentistry.com/6-gingival-diseases/
    Stage IV gingivitis is the advanced stage of gingivitis. The inflammatory processes have extended beyond the gingiva and into the other periodontal tissues. […] The pathogenesis of the stages of gingivitis is summarized in Table 6-1. […] The sequence of healing events is the reverse of those described for the pathogenesis. Healing of gingivitis begins in the connective tissues.
  • #44 Gingivitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/sites/books/n/statpearls/article-22251/
    The early lesion is consistent with delayed hypersensitivity. […] There is increased collagenolytic activity in this stage along with a rise in the number of macrophages, plasma cells, T and B lymphocytes. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #45 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. […] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. […] The initial lesion is seen within four days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. […] The early lesion is consistent with delayed hypersensitivity. It usually appears after one week from the beginning of plaque deposition. […] The established lesion may follow two paths, it can either remain stable for months or years; or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. […] This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible.
  • #46 Gingivitis | PPT
    https://www.slideshare.net/slideshow/gingivitis-249410663/249410663
    The advanced lesion has many of the characteristics of the established lesion but differs importantly in that loss of connective tissue attachment and alveolar bone occurs. […] The two earliest signs of gingival inflammation preceding established gingivitis are (1) Increased gingival crevicular fluid production rate (2) Bleeding from the gingival sulcus on gentle probing. […] Persistent gingivitis can be considered as a risk factor for periodontal attachment loss that may lead to tooth loss.
  • #47 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The transition from the established gingivitis lesion to periodontitis is mainly dominated by T and B cells. […] The key proinflammatory mediators in periodontal disease pathogenesis are as follows. […] Cytokines are key inflammatory mediators in periodontal disease. […] The prolonged and excessive release of large quantities of MMPs in the periodontium leads to the significant breakdown of structural components of the connective tissues, thereby contributing to the clinical signs of disease.
  • #48 22. Pathogenesis / Disease Activity: Pathogenesis and Inflammation | GeauxPerio
    https://spindlerperio.net/lr22/
    Bacteria are essential but insufficient to cause disease, host factors are equally important. […] The host response results in production of cytokines, eicosanoids, other inflammatory mediators such as the kinins, complement activation products and matrix metalloproteinases, which perpetuate the response and mediate connective tissue and bone destruction. […] The mechanisms that force the transition from one condition to the other are not completely known. […] The advanced lesion is predominated by plasma cells. […] Epithelial ulceration was the most remarkable and constant change observed in relation to conversion of established to advanced lesion. […] The disruption of the epithelial barrier along with the concomitant penetration of bacteria and their toxic products was most important to convert an established lesion into an aggressive lesion.
  • #49 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Condition identified the gingivitis case by the presence of gingival inflammation at one or more sites and agreed upon bleeding on probing as the primary parameter for diagnosis of gingivitis. […] The molecules that play a role in the pathogenesis are divided into two main groups: those derived from the subgingival microbiota (i.e., microbial virulence factors) and those derived from the host immune-inflammatory response. […] Even though periopathogenic bacteria are still regarded as the main initiating agents, immune-inflammatory response of the host to these pathogens plays an important role in the pathogenesis of PD. […] The plaque biofilm causes most of the injury to the periodontal tissue through indirect mechanisms dependent on initiation and propagation of inflammatory host tissue reactions.
  • #50 Pathogenesis of Gingivitis – CORE
    https://core.ac.uk/works/10922453/
    The molecules that play a role in the pathogenesis are divided into two main groups: those derived from the subgingival microbiota (i.e., microbial virulence factors) and those derived from the host immune-inflammatory response. […] Understanding the disease processes is important for the development of improved treatment strategies.
  • #51 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The biofilm microbes on the tooth surfaces are recognized by the cells from the innate immunity through certain molecular patterns called pathogen-associated molecular patterns (PAMPs) which include lipopolysaccharide (LPS), peptidoglycans and lipoteichoic acids, N-formylmethionine, and lipoproteins. […] The two major families of PRRs that have been most extensively studied in the periodontium are the Toll-like receptor (TLRs) and the Nod-like receptors (NLRs). […] If gingivitis persists without resolution, bacterial antigens are produced by lymphocytes, macrophages, and dendritic cells. […] Adaptive immunity provides a more focused defense against infections than innate immune responses, which is slower and dependent on complex interactions between antigen-presenting cells (APCs) and T and B lymphocytes, specifically cytotoxic T cells and antibodies.
  • #52 22. Pathogenesis / Disease Activity: Pathogenesis and Inflammation
    https://spindlerperio.net/protected/lit/LR22.html
    The host response results in production of cytokines, eicosanoids, other inflammatory mediators such as the kinins, complement activation products and matrix metalloproteinases, which perpetuate the response and mediate connective tissue and bone destruction. […] The mechanisms that force the transition from one condition to the other are not completely known. […] The lipoteichoic acid and lipopolysaccharides of the gram-negative cell wall are able to activate the complement cascade through the alternative pathway. […] Periodontitis enhances the risk for various systemic diseases, including atherosclerosis, coronary heart disease, stroke and infants with low birth weight. […] The periodontal ligament has the fastest turnover of collagenous proteins. […] The metabolism of collagens in the PDL has to have a precise balance between synthesis and degradation of collagen.
  • #53 22. Pathogenesis / Disease Activity: Pathogenesis and Inflammation | GeauxPerio
    https://spindlerperio.net/lr22/
    The major developments since the 1976 article by Page Schroeder have been the discovery of the pathways through which bacteria activate host cells and systems in a manner that tissue destruction ensues. […] The expression of bacterial virulence requires participation from the dental plaque biofilm. […] The presence of different areas may also suggest the theory that periods of quiescence or exacerbation within a pocket may be the cumulative effect of all the activities within the pocket wall. […] The clinical picture observed is a result of the sum of these events. […] The lipopolysaccharide does not activate the expression of E-selectin in vascular endothelial cells, therefore blocking the local neutrophil response to itself and other microorganisms in the plaque. […] The cytokine-induced reservoir of latent collagenase in the extracellular matrix is a possible mechanism for a burst of periodontal breakdown.
  • #54 Gingivitis – Wikipedia
    https://en.wikipedia.org/wiki/Gingivitis
    Although these accumulations may be tiny, the bacteria in them produce chemicals, such as degradative enzymes, and toxins, such as lipopolysaccharide (LPS, otherwise known as endotoxin) or lipoteichoic acid (LTA), that promote an inflammatory response in the gum tissue. This inflammation can cause an enlargement of the gingiva and subsequent formation. Early plaque in health consists of a relatively simple bacterial community dominated by Gram-positive cocci and rods. As plaque matures and gingivitis develops, the communities become increasingly complex with higher proportions of Gram-negative rods, fusiforms, filaments, spirilla and spirochetes. Later experimental gingivitis studies, using culture, provided more information regarding the specific bacterial species present in plaque. Taxa associated with gingivitis included Fusobacterium nucleatum subspecies polymorphum, Lachnospiraceae species HOT100, Lautropia species HOTA94, and Prevotella oulorum (a species of Prevotella bacterium), whilst Rothia dentocariosa was associated with periodontal health. Further study of these taxa is warranted and may lead to new therapeutic approaches to prevent periodontal disease including systemic health.
  • #55 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    Polymorphonuclear leukocytes (PMNs) are the first line of defense against bacteria, and proper PMN functionality is essential for protecting the integrity of the periodontium. […] The recognition of pathogenic microorganisms and the recruitment of effector cells (e.g., neutrophils) and molecules (e.g., the complement system) are central to effective innate immunity. […] The combination of natural host defense mechanisms and oral hygiene practices of individuals helps to have a balanced coexistence of oral microbiota in a healthy oral cavity which can be disturbed by either quantitative (higher bacterial load) or qualitative (growth of pathogenic species) changes in the biofilm leading to early stages of gingivitis. […] The protective function of the gingival epithelium is enhanced by keratinization, which helps resist abrasion.
  • #56 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    Polymorphonuclear leukocytes (PMNs) are the first line of defense against bacteria, and proper PMN functionality is essential for protecting the integrity of the periodontium. […] The recognition of pathogenic microorganisms and the recruitment of effector cells (e.g., neutrophils) and molecules (e.g., the complement system) are central to effective innate immunity. […] The combination of natural host defense mechanisms and oral hygiene practices of individuals helps to have a balanced coexistence of oral microbiota in a healthy oral cavity which can be disturbed by either quantitative (higher bacterial load) or qualitative (growth of pathogenic species) changes in the biofilm leading to early stages of gingivitis. […] The protective function of the gingival epithelium is enhanced by keratinization, which helps resist abrasion.
  • #57 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The development of gingivitis is mainly the infiltration of the connective tissues by numerous defense cells, particularly neutrophils, macrophages, plasma cells, and lymphocytes. […] The classic studies of Page and Schroeder described the basic understanding of histologic changes that occur in the gingival tissues as the initial, early, established, and advanced gingival lesions. […] The initial lesion develops within 24 days of the accumulation of plaque at a site free of plaque biofilm, which is evident microscopically since the gingival tissues always have characteristics of a low-grade chronic inflammatory response as a result of the continual presence of the subgingival biofilm. […] The early lesion corresponds to the early clinical signs of gingivitis and characterized by erythematous clinical appearance of gingiva due to proliferation of capillaries and vasodilatation.
  • #58 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The biofilm microbes on the tooth surfaces are recognized by the cells from the innate immunity through certain molecular patterns called pathogen-associated molecular patterns (PAMPs) which include lipopolysaccharide (LPS), peptidoglycans and lipoteichoic acids, N-formylmethionine, and lipoproteins. […] The two major families of PRRs that have been most extensively studied in the periodontium are the Toll-like receptor (TLRs) and the Nod-like receptors (NLRs). […] If gingivitis persists without resolution, bacterial antigens are produced by lymphocytes, macrophages, and dendritic cells. […] Adaptive immunity provides a more focused defense against infections than innate immune responses, which is slower and dependent on complex interactions between antigen-presenting cells (APCs) and T and B lymphocytes, specifically cytotoxic T cells and antibodies.
  • #59 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The biofilm microbes on the tooth surfaces are recognized by the cells from the innate immunity through certain molecular patterns called pathogen-associated molecular patterns (PAMPs) which include lipopolysaccharide (LPS), peptidoglycans and lipoteichoic acids, N-formylmethionine, and lipoproteins. […] The two major families of PRRs that have been most extensively studied in the periodontium are the Toll-like receptor (TLRs) and the Nod-like receptors (NLRs). […] If gingivitis persists without resolution, bacterial antigens are produced by lymphocytes, macrophages, and dendritic cells. […] Adaptive immunity provides a more focused defense against infections than innate immune responses, which is slower and dependent on complex interactions between antigen-presenting cells (APCs) and T and B lymphocytes, specifically cytotoxic T cells and antibodies.
  • #60 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The transition from the established gingivitis lesion to periodontitis is mainly dominated by T and B cells. […] The key proinflammatory mediators in periodontal disease pathogenesis are as follows. […] Cytokines are key inflammatory mediators in periodontal disease. […] The prolonged and excessive release of large quantities of MMPs in the periodontium leads to the significant breakdown of structural components of the connective tissues, thereby contributing to the clinical signs of disease.
  • #61 Cytokines in gingivitis and periodontitis: from pathogenesis to therapeutic targets
    https://ouci.dntb.gov.ua/en/works/9QxnbANl/
    Chronic inflammatory processes in the oral mucosa and periodontitis are common disorders caused by microflora and microbial biofilms. […] Cytokines are known to play a crucial role in the pathogenesis of gingivitis and periodontitis and have been proposed as biomarkers for diagnosis and follow-up of these diseases. […] They can activate immune and stromal cells, leading to local inflammation and tissue damage. This damage can include destruction of the periodontal ligaments, gingiva, and alveolar bone. […] In experimental models of periodontitis, TNF and the IL-23/IL-17 axis play a pivotal role in disease pathogenesis. […] This review discusses the role of cytokines in gingivitis and periodontitis, with particular emphasis on their role in mediating inflammation and tissue destruction.
  • #62 Gingivitis – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Immunology/Gingivitis/
    Gingivitis is an inflammatory lesion that remains confined to the gingiva, but which may, in susceptible people, progress to a more severe and destructive form, periodontitis. […] Gingivitis is caused by bacterial components such as lipopolysaccharides, which induce an inflammatory response in the host. The immune response to oral microorganisms induces an inflammatory cascade that promotes the release of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumour necrosis factor-alpha (TNF-α), in gingival tissue. Uncontrolled inflammation in the gingiva can cause the aggravation and destruction of the periodontal tissues, and the attachment loss may depend on the host’s responsiveness to inflammatory aggression at the gingival sites. TNF-α is a cytokine with multiple functions that can induce tissue destruction and alveolar bone resorption. The production and biological activity of TNF-α depends on genetically controlled mechanisms. Single-nucleotide polymorphisms (SNPs) have been identified in the TNF-α gene promoter region, and the transition from G to A at position -308 has been shown to increase cytokine production levels.
  • #63 Gingivitis – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Immunology/Gingivitis/
    Gingivitis is an inflammatory lesion that remains confined to the gingiva, but which may, in susceptible people, progress to a more severe and destructive form, periodontitis. […] Gingivitis is caused by bacterial components such as lipopolysaccharides, which induce an inflammatory response in the host. The immune response to oral microorganisms induces an inflammatory cascade that promotes the release of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumour necrosis factor-alpha (TNF-α), in gingival tissue. Uncontrolled inflammation in the gingiva can cause the aggravation and destruction of the periodontal tissues, and the attachment loss may depend on the host’s responsiveness to inflammatory aggression at the gingival sites. TNF-α is a cytokine with multiple functions that can induce tissue destruction and alveolar bone resorption. The production and biological activity of TNF-α depends on genetically controlled mechanisms. Single-nucleotide polymorphisms (SNPs) have been identified in the TNF-α gene promoter region, and the transition from G to A at position -308 has been shown to increase cytokine production levels.
  • #64 Gingivitis – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Immunology/Gingivitis/
    Gingivitis is an inflammatory lesion that remains confined to the gingiva, but which may, in susceptible people, progress to a more severe and destructive form, periodontitis. […] Gingivitis is caused by bacterial components such as lipopolysaccharides, which induce an inflammatory response in the host. The immune response to oral microorganisms induces an inflammatory cascade that promotes the release of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumour necrosis factor-alpha (TNF-α), in gingival tissue. Uncontrolled inflammation in the gingiva can cause the aggravation and destruction of the periodontal tissues, and the attachment loss may depend on the host’s responsiveness to inflammatory aggression at the gingival sites. TNF-α is a cytokine with multiple functions that can induce tissue destruction and alveolar bone resorption. The production and biological activity of TNF-α depends on genetically controlled mechanisms. Single-nucleotide polymorphisms (SNPs) have been identified in the TNF-α gene promoter region, and the transition from G to A at position -308 has been shown to increase cytokine production levels.
  • #65 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The transition from the established gingivitis lesion to periodontitis is mainly dominated by T and B cells. […] The key proinflammatory mediators in periodontal disease pathogenesis are as follows. […] Cytokines are key inflammatory mediators in periodontal disease. […] The prolonged and excessive release of large quantities of MMPs in the periodontium leads to the significant breakdown of structural components of the connective tissues, thereby contributing to the clinical signs of disease.
  • #66 The Role of Microorganisms in Gingivitis Pathogenesis and Periodo
    https://www.longdom.org/open-access/the-role-of-microorganisms-in-gingivitis-pathogenesis-and-periodontal-disease-106569.html
    This persistence of bacterial biofilms contributes to the chronic nature of gingivitis and underscores the importance of targeted interventions for effective management. […] While bacteria are central to gingivitis development, host factors also play a significant role in determining individual susceptibility to the disease. […] Gingivitis is a prevalent oral health condition influenced by a complex interplay of bacteria, host factors, and environmental influences. […] While bacteria, particularly those forming biofilms, are central to its pathogenesis, individual susceptibility varies based on genetic, systemic, and behavioral factors.
  • #67 Periodontal Disease in Small Animals – Digestive System – Merck Veterinary Manual
    https://www.merckvetmanual.com/digestive-system/dentistry-in-small-animals/periodontal-disease-in-small-animals
    Periodontal disease is caused by plaque bacteria accumulating on the tooth surface and eliciting a host response to the bacterial insult. The accumulation of plaque, the biodiversity of microbiota, and the host immune system are factors in the pathogenesis of periodontal disease. […] Bacterial plaque on the crown surface of a tooth constantly presents antigen to the marginal gingiva, stimulating an inflammatory response, resulting in gingivitis. […] Periodontitis is caused by the host’s response to subgingival plaque. […] Inflammatory mediators produced by the host directly result in bone and tissue damage around the root. The bacteria themselves and their metabolic products also contribute to bone damage. […] Development of periodontitis is also affected by other intrinsic (eg, genetics, tooth crowding, thin alveolar bone, age) and extrinsic (eg, diet, stress, concurrent disease, oral hygiene) factors.
  • #68 Pathogenesis of plaque associated periodontal disease | PPT
    https://www.slideshare.net/slideshow/pathogenesis-of-plaque-associated-periodontal-disease/249410788
    Pathogenesis of plaque associated periodontal disease […] The etiologic role of plaque bacteria is clear in that the bacteria initiate and perpetuate the inflammatory responses that develop in the gingival tissues. However, the major determinants of susceptibility to disease is the nature of the immune- inflammatory responses themselves. […] Periodontal pocket is a favourable environment for the survival of many species that are considered important in periodontal pathogenesis. Many of the unique features of periodontitis derive from the anatomy of the periodontium Hard, non-shedding surface (tooth) Tooth is partly embedded within the body (within connective tissue) Crosses an epithelial surface Partly exposed to the outside world Bacteria that colonize this surface are effectively outside the body, yet the inflammatory response that develops is located within the body. […] Gingivitis and Periodontitis are inflammatory conditions of infectious nature. Gingivitis precedes the onset of Periodontitis; however, not all gingivitis cases develop into Periodontitis. The reason for this is that accumulation of plaque bacteria is necessary but not sufficient by itself for the development of Periodontitis: a susceptible host is necessary. A biofilm environment confers certain properties to bacteria that are not seen in the planktonic state. […] The initial lesion in the development of periodontitis is the inflammation of the gingiva in response to a bacterial challenge. […] Pocket formation starts as an inflammatory change in connective tissue wall of gingival sulcus Inflammatory exudate causes degeneration of surrounding connecting tissue including the gingival fibers Just apical to Junctional epithelium, collagen fibers are destroyed and area becomes occupied by inflammatory cells and edema. […] Susceptibility of periodontitis suggests that individuals who are more susceptible to the disease mount an excessive, or dysregulated, immune- inflammatory response for a given bacterial challenge, leading to increased tissue breakdown compared to those individuals who have a more normal inflammatory response. […] The ability of P. gingivalis to orchestrate inflammatory disease via community-wide effects, while being a minor constituent of this community, qualifies it as a keystone pathogen. […] The dysbiosis of the periodontal microbiota signifies a change in the relative abundance of individual components of the bacterial community compared to their abundance in health, leading to alterations in the host-microbe crosstalk sufficient to mediate destructive inflammation and bone loss.
  • #69 Gingivitis – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Immunology/Gingivitis/
    Gingivitis is an inflammatory lesion that remains confined to the gingiva, but which may, in susceptible people, progress to a more severe and destructive form, periodontitis. […] Gingivitis is caused by bacterial components such as lipopolysaccharides, which induce an inflammatory response in the host. The immune response to oral microorganisms induces an inflammatory cascade that promotes the release of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumour necrosis factor-alpha (TNF-α), in gingival tissue. Uncontrolled inflammation in the gingiva can cause the aggravation and destruction of the periodontal tissues, and the attachment loss may depend on the host’s responsiveness to inflammatory aggression at the gingival sites. TNF-α is a cytokine with multiple functions that can induce tissue destruction and alveolar bone resorption. The production and biological activity of TNF-α depends on genetically controlled mechanisms. Single-nucleotide polymorphisms (SNPs) have been identified in the TNF-α gene promoter region, and the transition from G to A at position -308 has been shown to increase cytokine production levels.
  • #70 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] The mechanism by which carbohydrates with a high glycemic index promote the inflammatory process is through activation of NFkB and oxidative stress. […] During pregnancy, there are not only changes in hormone levels but also a greater predisposition to dilating blood vessels. These factors contribute to an exaggerated inflammatory response by the gingival tissues even to a minor quantity of plaque accumulation. […] The hormonal alterations that occurred during puberty influence how the gingival tissue reacts to plaque accumulation causing what is known as puberty gingivitis.
  • #71 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] The mechanism by which carbohydrates with a high glycemic index promote the inflammatory process is through activation of NFkB and oxidative stress. […] During pregnancy, there are not only changes in hormone levels but also a greater predisposition to dilating blood vessels. These factors contribute to an exaggerated inflammatory response by the gingival tissues even to a minor quantity of plaque accumulation. […] The hormonal alterations that occurred during puberty influence how the gingival tissue reacts to plaque accumulation causing what is known as puberty gingivitis.
  • #72 Recent advances in the pathogenesis and prevention strategies of dental calculus | npj Biofilms and Microbiomes
    https://www.nature.com/articles/s41522-024-00529-1
    Lifestyles have significant effects on calcium phosphate saturation and bacterial colonization. Tobacco smoking induces higher salivary calcium contents which increase the formation of calculus. […] A carbohydrate-dominated diet may induce dental calculus by promoting bacterial colonization on the plaque.
  • #73 Recent advances in the pathogenesis and prevention strategies of dental calculus | npj Biofilms and Microbiomes
    https://www.nature.com/articles/s41522-024-00529-1
    Lifestyles have significant effects on calcium phosphate saturation and bacterial colonization. Tobacco smoking induces higher salivary calcium contents which increase the formation of calculus. […] A carbohydrate-dominated diet may induce dental calculus by promoting bacterial colonization on the plaque.
  • #74 Gingivitis | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/22251
    Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. […] The mechanism by which carbohydrates with a high glycemic index promote the inflammatory process is through activation of NFkB and oxidative stress. […] During pregnancy, there are not only changes in hormone levels but also a greater predisposition to dilating blood vessels. These factors contribute to an exaggerated inflammatory response by the gingival tissues even to a minor quantity of plaque accumulation. […] The hormonal alterations that occurred during puberty influence how the gingival tissue reacts to plaque accumulation causing what is known as puberty gingivitis.
  • #75 22. Pathogenesis / Disease Activity: Pathogenesis and Inflammation
    https://spindlerperio.net/protected/lit/LR22.html
    The host response results in production of cytokines, eicosanoids, other inflammatory mediators such as the kinins, complement activation products and matrix metalloproteinases, which perpetuate the response and mediate connective tissue and bone destruction. […] The mechanisms that force the transition from one condition to the other are not completely known. […] The lipoteichoic acid and lipopolysaccharides of the gram-negative cell wall are able to activate the complement cascade through the alternative pathway. […] Periodontitis enhances the risk for various systemic diseases, including atherosclerosis, coronary heart disease, stroke and infants with low birth weight. […] The periodontal ligament has the fastest turnover of collagenous proteins. […] The metabolism of collagens in the PDL has to have a precise balance between synthesis and degradation of collagen.
  • #76 Study suggests a link between gum disease and AD pathogenesis | Alzheimer Europe
    https://www.alzheimer-europe.org/news/study-suggests-link-between-gum-disease-and-ad-pathogenesis?language_content_entity=en
    On 23 January, researchers from Cortexyme – a clinical-stage pharmaceutical company developing novel treatments for altering the course of Alzheimers disease (AD) and other neurodegenerative disorders reported that periodontitis, often known as gum disease, may contribute to the development of AD. […] In the published study, the bacteria involved in periodontitis called gingipain was shown to be present in the brains of people with AD and to be significantly correlated with AD diagnosis with an increasing tau and ubiquitin pathology. […] In addition, gingipains were found to be neurotoxic in cell culture with detrimental and fragmented effects on tau. […] Additional tests on mouse models showed that gingipain infection led to an increased production of A in the brain. […] Scientists synthesised selective, brain-penetrant and small-molecules targeting gingipains namely COR286 and COR271. […] Using mouse models, they noted that gingipain inhibitors could reduce the load of gingipain in the mouse brain, decrease the neurodegeneration and block the A production.
  • #77 U of T researchers discover mechanism linking gum disease to heart disease, other conditions | University of Toronto
    https://www.utoronto.ca/news/u-t-researchers-discover-mechanism-linking-gum-disease-heart-disease-other-conditions
    Researchers at the University of Toronto have found evidence that neutrophil immune cell activity is the missing link connecting periodontal disease with heart disease, cancer and other inflammatory conditions possibly including COVID-19. […] The link between periodontal (gum) disease and other inflammatory conditions such as heart disease and diabetes has long been established, but the mechanism behind the association has, until now, remained a mystery. […] Now, a team of scientists and clinicians led by U of Ts Faculty of Dentistry say theyve found the reason why and its related to the bodys own hyperactive immune response. […] To find what links those conditions, the researchers focused on the behaviours of cells primarily activated by gum disease: neutrophils, which are cells of the innate immune system.
  • #78
    https://www.gov.uk/government/publications/delivering-better-oral-health-an-evidence-based-toolkit-for-prevention/chapter-5-periodontal-diseases
    Gingivitis is an inflammatory condition resulting from interactions between the dental plaque and the hosts immune response, which remains contained within the gingiva and does not extend to the periodontal attachment (cementum, periodontal ligament, and alveolar bone). Such inflammation is reversible by reducing levels of dental plaque at and below the gingival margin. […] A disruption in the balance (dysbiosis) between the plaque and persons immune system can lead to the initiation of gingivitis and progression to periodontitis. […] Periodontitis causes progressive destruction of the toothsupporting tissues. Signs of the disease include clinical attachment loss, manifested as interdental recession and/or periodontal pocketing and alveolar bone loss. This chronic and inflammatory disease is caused by a complex interplay of risk factors, with dental plaque being the most important.
  • #79 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Condition identified the gingivitis case by the presence of gingival inflammation at one or more sites and agreed upon bleeding on probing as the primary parameter for diagnosis of gingivitis. […] The molecules that play a role in the pathogenesis are divided into two main groups: those derived from the subgingival microbiota (i.e., microbial virulence factors) and those derived from the host immune-inflammatory response. […] Even though periopathogenic bacteria are still regarded as the main initiating agents, immune-inflammatory response of the host to these pathogens plays an important role in the pathogenesis of PD. […] The plaque biofilm causes most of the injury to the periodontal tissue through indirect mechanisms dependent on initiation and propagation of inflammatory host tissue reactions.
  • #80 Pathogenesis of Gingivitis | IntechOpen
    https://www.intechopen.com/chapters/71343
    The 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases and Condition identified the gingivitis case by the presence of gingival inflammation at one or more sites and agreed upon bleeding on probing as the primary parameter for diagnosis of gingivitis. […] The molecules that play a role in the pathogenesis are divided into two main groups: those derived from the subgingival microbiota (i.e., microbial virulence factors) and those derived from the host immune-inflammatory response. […] Even though periopathogenic bacteria are still regarded as the main initiating agents, immune-inflammatory response of the host to these pathogens plays an important role in the pathogenesis of PD. […] The plaque biofilm causes most of the injury to the periodontal tissue through indirect mechanisms dependent on initiation and propagation of inflammatory host tissue reactions.
  • #81
    https://www.vin.com/apputil/content/defaultadv1.aspx?id=3866564&pid=11268
    Periodontal disease is a collective term for a number of plaque-induced inflammatory lesions that affect the periodontium. The primary cause of gingivitis and periodontitis is accumulation of dental plaque on the tooth surfaces. […] The pathogenic mechanisms involved in periodontal disease include: 1. Direct injury by plaque microorganisms, and 2. Indirect injury by plaque microorganisms via inflammation. […] It is now well accepted that it is the host’s response to the plaque bacteria, rather than microbial virulence per se, that directly causes the tissue damage. […] In gingivitis, the plaque-induced inflammation is limited to the soft tissue of the gingiva. […] Disease progression is generally an episodic occurrence rather than a continuous process. […] Other conditions, such as physical or psychological stress and malnutrition may impair protective responses, such as the production of antioxidants and acute phase proteins, and can aggravate periodontitis but do not actually cause destructive tissue inflammation. […] Undisturbed plaque accumulation results in gingivitis. […] Consequently, the aim in periodontal disease prevention and treatment is to establish and maintain clinically healthy gingivae to prevent periodontitis.
  • #82 Longitudinal multi-omics along gingivitis development reveal a suboptimal-health gum state with periodontitis-like microbiome | bioRxiv
    https://www.biorxiv.org/content/10.1101/2020.09.26.315127v1.full-text
    Most adults experience episodes of gingivitis, which can progress to the irreversible, chronic state of periodontitis. However the mechanistic roles of plaque in gingivitis onset and progression to periodontitis remain elusive. […] It results from a dysregulated immuno-inflammatory response which is induced by dysbiotic plaque biofilm. […] Notably, this inflammatory lesion can be resolved (i.e., reversible) following appropriate professional care. Whereas, uncontrolled gingivitis can progress to the irreversible periodontitis, which is characterized by destruction of tooth-supporting tissues and alveolar bone in susceptible individuals, eventually leading to tooth loss and an increased risk of systemic diseases like diabetes and cardiovascular disease. […] However, how gingivitis is initiated remains elusive.
  • #83 Pathogenesis of Periodontal Disease | IntechOpen
    https://www.intechopen.com/chapters/67314
    The primary features of periodontitis include the loss of periodontal tissue support, manifested through clinical attachment loss and radiographically assessed alveolar bone loss, presence of periodontal pocketing, and gingival bleeding. […] The development of gingivitis and periodontitis can be divided into a series of stages: initial, early, established, and advanced lesions. […] The inflammatory immune response is triggered by the interaction of resident cells with the bacterial biofilm attached to the tooth surface. […] The junctional epithelium is the first periodontal structure to face the bacterial challenge. […] The most important characteristic of periodontitis is the inflammatory reabsorption of the tooth-supporting alveolar bone due to the uncontrolled host immune response against periodontal infection, since the destructive events, which lead to the irreversible phenotype of periodontal disease, are the result of the persistence of a chronic and exacerbated inflammatory immune response.
  • #84
    https://www.vin.com/apputil/content/defaultadv1.aspx?id=3866564&pid=11268
    Periodontal disease is a collective term for a number of plaque-induced inflammatory lesions that affect the periodontium. The primary cause of gingivitis and periodontitis is accumulation of dental plaque on the tooth surfaces. […] The pathogenic mechanisms involved in periodontal disease include: 1. Direct injury by plaque microorganisms, and 2. Indirect injury by plaque microorganisms via inflammation. […] It is now well accepted that it is the host’s response to the plaque bacteria, rather than microbial virulence per se, that directly causes the tissue damage. […] In gingivitis, the plaque-induced inflammation is limited to the soft tissue of the gingiva. […] Disease progression is generally an episodic occurrence rather than a continuous process. […] Other conditions, such as physical or psychological stress and malnutrition may impair protective responses, such as the production of antioxidants and acute phase proteins, and can aggravate periodontitis but do not actually cause destructive tissue inflammation. […] Undisturbed plaque accumulation results in gingivitis. […] Consequently, the aim in periodontal disease prevention and treatment is to establish and maintain clinically healthy gingivae to prevent periodontitis.