Bruksizm
Patofizjologia i mechanizm

Bruksizm to mimowolne, rytmiczne skurcze mięśni żwaczy, prowadzące do zgrzytania zębami lub zaciskania szczęk, występujące zarówno w stanie czuwania, jak i podczas snu (bruksizm nocny). Patofizjologia bruksizmu wiąże się z dysregulacją ośrodkowego układu nerwowego, zwłaszcza jąder podstawy i pnia mózgu, oraz zaburzeniami równowagi neuroprzekaźników, takich jak dopamina, serotonina, glutaminian i GABA. Bruksizm nocny jest klasyfikowany jako zaburzenie ruchowe związane ze snem, powiązane z aktywnością autonomiczną i mózgową, obejmującą sekwencję zdarzeń fizjologicznych poprzedzających epizody zgrzytania, w tym aktywację autonomicznego układu sercowego na około 4 minuty przed epizodem oraz wzrost napięcia mięśni otwierających szczękę i przyspieszenie tętna tuż przed zgrzytaniem. Częstość mikrowybudzeń i związanych z nimi rytmicznych ruchów mięśni żuchwy wynosi 8-14 na godzinę snu, a bruksizm może pełnić funkcję ochronną w zaburzeniach oddychania podczas snu, takich jak obturacyjny bezdech senny (OSA), występując u około 50% pacjentów z OSA.

Bruksizm – Patogeneza

Bruksizm to złożone, mimowolne, rytmiczne skurcze mięśni żwaczy prowadzące do zgrzytania zębami lub zaciskania szczęk, które mogą występować zarówno podczas snu (bruksizm nocny), jak i w stanie czuwania (bruksizm dzienny). Jest to aktywność parafunkcjonalna, niezwiązana z normalnymi funkcjami jak jedzenie czy mówienie, dotykająca ponad jedną trzecią populacji w pewnym momencie życia.123

Czynniki neurofizjologiczne

Patofizjologia bruksizmu jest powiązana z fazą dobową i regulowana przez ośrodkowy układ nerwowy. Bruksizm nocny, klasyfikowany jako zaburzenie ruchowe związane ze snem, wiąże się z aktywnością autonomiczną i mózgową związaną z pobudzeniem. Badania wykazały, że przed pierwszym kontaktem zębów występuje sekwencja zdarzeń fizjologicznych, obejmująca aktywację autonomicznego układu sercowego (na około 4 minuty przed epizodem), aktywność mózgową (około 4 sekundy wcześniej), wzrost napięcia mięśni otwierających szczękę z 2 głębokimi oddechami oraz przyspieszenie tętna na sekundę przed wystąpieniem zgrzytania. Ta sekwencja występuje w prawie 80% rytmicznych ruchów szczęki związanych ze zgrzytaniem zębami podczas snu.12

Bruksizm nocny pojawia się jako przesadzona odpowiedź oromotoryczna na naturalne mikrowybudzenia związane ze snem, charakteryzujące się wzrostem autonomicznej aktywności sercowej i oddechowej, występujące 8-14 razy na godzinę podczas snu. Rytmiczna aktywność mięśniowa osiąga szczyt tuż przed fazą REM, co sugeruje obecność mechanizmu związanego z przejściami między fazami snu, który wpływa na neurony motoryczne odpowiedzialne za bruksizm.12

Rola układu dopaminergicznego

Istnieją dowody sugerujące, że zaburzenia w układzie dopaminergicznym ośrodkowego układu nerwowego odgrywają istotną rolę w etiologii bruksizmu. Badania na modelach zwierzęcych z wykorzystaniem agonistów i antagonistów receptorów dopaminowych potwierdzają tę hipotezę. Niezrównoważenie transmisji neuronalnej zależnej od dopaminy może występować w niektórych typach bruksizmu, co pokazuje fakt, że krótkotrwałe stosowanie prekursorów dopaminy, takich jak L-dopa, hamuje bruksizm, podczas gdy długotrwałe stosowanie L-dopy nasila go.123

Odnotowano również korelację między podwyższonym poziomem katecholamin a nasileniem bruksizmu, co sugeruje, że zwiększone napięcie sympatyczne może być czynnikiem wyzwalającym rytmiczną aktywność mięśni żuchwy (RMMA). Centralne struktury, w tym miejsca sinawoczarne, twór siatkowaty i jądra szwu brzusznego, wykazano jako wpływające na ten rodzaj przetwarzania sensomotorycznego.12

Mechanizm stresowy

Stres jest najczęściej akceptowanym czynnikiem zaangażowanym w patogenezę bruksizmu. Mówiąc precyzyjniej, musimy odnosić się do pojęć dystresu i obciążenia alostatycznego. Gdy ludzie znajdują się w warunkach stresu, aktywowana jest oś podwzgórze-przysadka-nadnercza (HPA), będąca główną neuroendokrynną odpowiedzią na stres.12

Aktywacja ścieżki brzuszna część podprogu (vSub) – brzuszna część gałki bladej (VP) – jądro półleżące (N.Acc) zazwyczaj występuje w warunkach ostrego, łagodnego i przewidywalnego stresu, prowadząc do stanów hiperdopaminergicznych. Odwrotnie, w przypadku przewlekłego, łagodnego stresu, ścieżka ta jest osłabiona, a aktywowana jest ścieżka jądro boczne ciała migdałowatego (BLA) – brzuszna część gałki bladej (VP). Aktywacja N.Acc. występuje albo poprzez ścieżkę vSub-VP, albo poprzez ścieżkę BLA-VP.12

Przewlekła ekspozycja na stres i podwyższony poziom kortykosteronu mogą powodować zaburzenia w proliferacji komórek progenitorowych, hamować różnicowanie neuronów i tłumić przeżywalność komórek w zakręcie zębatym hipokampa, co wpływa na neurogenezę hipokampa. Badania wykazały podobne zmiany degeneracyjne u pacjentów z bruksizmem.123

Zaburzenia równowagi między neuroprzekaźnikami pobudzającymi (glutaminian) a hamującymi (GABA) jest kluczowe w patofizjologii bruksizmu. Podwyższony poziom glutaminianu, neuroprzekaźnika pobudzającego, może nasilać bruksizm nocny i dzienny. Wysoki poziom glutaminianu prowadzi do ekscytotoksyczności neuronalnej, przyczyniając się do nadpobudliwości w ośrodkowym układzie nerwowym (OUN). Ta nadpobudliwość, szczególnie w układzie nerwowym trójdzielnym, może powodować mimowolne skurcze mięśni, w tym te obserwowane w bruksizmie.12

Czynniki genetyczne

Badania wykazują istotny związek między bruksizmem a czynnikami genetycznymi. Stwierdzono pozytywne powiązanie z genami kodującymi receptory serotoniny i dopaminy, odpowiednio 5-HTR2A i DRD1. Zaburzenia w funkcjonowaniu receptorów 5-HT2 mogą odgrywać główną rolę w patogenezie bruksizmu. Rola receptorów 5-HT2 w pośredniczeniu w funkcjonowaniu mięśni orofacjalnych jest dobrze udokumentowana. Stres może wpływać na receptory 5-HT, ale efekt ten różni się w zależności od obszaru mózgu.12

Istnieją umiarkowane dowody na znaczenie genetyki jako czynnika ryzyka w powstawaniu bruksizmu nocnego. Badania kliniczne wykazały, że bruksizm może mieć podłoże genetyczne i może być dzielony między różnymi członkami tej samej rodziny. System Online Mendelian Inheritance in Man (OMIM) klasyfikuje bruksizm nocny wraz z parasomnią i używa alternatywnego określenia „mioklonia twarzowo-żuchwowa”.12

Kluczowe struktury neurologiczne

Dwa ważne obszary neuronalne są zaangażowane w powstawanie bruksizmu i są silnie dotknięte przez stres: jądro mezencefaliczne nerwu trójdzielnego (Me5) i mezokortykalna droga dopaminergiczna. Me5 kontroluje odruch hamujący mięśnia żwacza, który po aktywacji hamuje jądro ruchowe nerwu trójdzielnego i inhibicję skurczu mięśni żwaczy i skroniowych.1

Dowody sugerują centralną dysregulację dróg bezpośrednich i pośrednich jąder podstawy jako główną patologię w bruksizmie. Bruksizm, jako towarzyszący objaw, jest znacznie zwiększony w niektórych zaburzeniach jąder podstawy, takich jak dystonia kranio-szeryjna i choroba Huntingtona. W tym kontekście można argumentować, że bruksizm jest formą dystonii ustno-żuchwowej.12

Związek z zaburzeniami snu

Bruksizm nocny jest często powiązany z zaburzeniami oddychania podczas snu, takimi jak obturacyjny bezdech senny (OSA). Około 50% dorosłych z obturacyjnym bezdechem sennym ma współistniejący bruksizm nocny. Badania sugerują, że bruksizm nocny może pełnić rolę ochronną w przywracaniu normalnej drożności dróg oddechowych i oddychania po zdarzeniu oddechowym. Zgrzytanie zębami podczas snu może być mechanizmem obronnym pacjenta śpiącego z OSA – jest to próba ustabilizowania i udrożnienia dróg oddechowych przez poprawę pozycji żuchwy.123

Osoby cierpiące na bezdechy senne mogą nieświadomie reagować na epizody zatrzymania oddychania podczas snu poprzez zgrzytanie zębami. Ruch szczęki podczas zgrzytania może potencjalnie pomóc w przywróceniu przepływu powietrza, przeciwdziałając skutkom bezdechu sennego. Co ciekawe, niemal jedna czwarta osób z OSA doświadcza również bruksizmu nocnego.12

Czynniki farmakologiczne

Stosowanie amfetamin, leków przeciwpsychotycznych, selektywnych inhibitorów wychwytu zwrotnego serotoniny (SSRI), inhibitorów wychwytu zwrotnego serotoniny i noradrenaliny, inhibitorów wychwytu zwrotnego noradrenaliny i dopaminy oraz leków uzależniających o działaniu katecholaminergicznym, takich jak kokaina i 3,4-metylenodioksymetamfetamina, może być związane z bruksizmem nocnym. Zaburzenia neurologiczne i psychiatryczne związane z bruksizmem nocnym obejmują lęk, chorobę Alzheimera, chorobę Huntingtona, zanik wieloukładowy, uraz mózgu, zespół Downa, zespół Retta, mózgowe porażenie dziecięce i zespół nadpobudliwości psychoruchowej z deficytem uwagi.12

Niektóre leki, zwłaszcza przeciwdepresyjne (takie jak SSRI), przeciwpsychotyczne oraz stymulujące, mogą wywoływać lub nasilać bruksizm. Kofeina, znana jako stymulant ośrodkowego układu nerwowego, zwiększa ryzyko bruksizmu nocnego 1,5-krotnie. Również nielegalne substancje, takie jak 3,4-metylenodioksymetamfetamina i kokaina, mogą wpływać na występowanie bruksizmu.12

Zaproponowano, że mechanizm bruksizmu wywołanego przez SSRI może obejmować nadmierne działanie serotoninergiczne na neurony mezokortykalne pochodzące z pola brzusznego nakrywki. To działanie prowadzi do deficytu dopaminergicznego, który powoduje specyficzną formę akatyzji i ruchów podobnych do akatyzji w mięśniach szczęki, prowadząc do bruksizmu. Buspiron, jako agonista receptora 5-HT1A, zwiększa wydzielanie dopaminy w korze przedczołowej, co może łagodzić bruksizm wywołany lekami.1

Inne czynniki etiologiczne

Oprócz głównych mechanizmów neurologicznych i stresu, bruksizm może być związany z innymi czynnikami, takimi jak:123

  • Zgryz: Nieprawidłowy zgryz lub problemy z mięśniami jamy ustnej i twarzy mogą powodować niezamierzone zgrzytanie zębami.
  • Schorzenia neurologiczne: Bruksizm został powiązany z takimi stanami jak choroba Parkinsona, Huntingtona i padaczka.
  • Stany zapalne: Alergie i infekcje ucha mogą przyczyniać się do zgrzytania zębami u dzieci.
  • Substancje stymulujące: Tytoń, alkohol, kofeina lub pewne rodzaje narkotyków mogą sprzyjać rozwojowi tego zaburzenia.
  • Niedobory żywieniowe: W rzadkich przypadkach niedobór witamin (szczególnie witaminy B5) lub minerałów (jak magnez i wapń) może skutkować bruksizmem.

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Mechanizm bruksizmu

Mechanizm bruksizmu jest złożony i wieloczynnikowy, angażujący różne układy neurologiczne i fizjologiczne. Poniżej szczegółowo omówione zostały kluczowe aspekty mechanizmu tego zaburzenia.

Mechanizm motoryczny

Drogi motoryczne dla ruchów dowolnych powszechnie uznaje się za rozpoczynające się od komórek piramidowych kory ruchowej. Rola jąder podstawy, związanych z nimi struktur oraz powiązanych szlaków dopaminergicznych, glutaminergicznych i GABA-ergicznych w ruchach dowolnych jest dobrze znana. W przypadku bruksizmu dochodzi do nieprawidłowej aktywacji mięśni żucia (skroniowego, żwacza, skrzydłowego przyśrodkowego i skrzydłowego bocznego), które działają wspólnie, aby poruszać żuchwą.12

Bruksizm obejmuje aktywację mięśni żucia, co prowadzi do zaciskania zębów i zgrzytania podczas snu. Mięśnie żucia są sparowane po obu stronach i współpracują, aby poruszać żuchwą, która zawiasa się i przesuwa wokół swojego podwójnego połączenia z czaszką w stawach skroniowo-żuchwowych. Bruksizm można również postrzegać jako zaburzenie powtarzalnego, nieświadomego skurczu mięśni. Zazwyczaj obejmuje to mięsień żwacz i przednią część mięśnia skroniowego (duże mięśnie zewnętrzne, które zaciskają), oraz mięśnie skrzydłowe boczne, stosunkowo małe mięśnie obustronne, które działają razem, aby wykonywać zgrzytanie boczne.12

Rola neuroprzekaźników

Główna teza dotycząca mechanizmu bruksizmu zakłada, że zaburzenie równowagi między neuroprzekaźnikami pobudzającymi (glutaminian) a hamującymi (GABA) jest kluczowe dla patofizjologii tego zaburzenia. Bruksizm, zarówno nocny, jak i dzienny, może być nasilany przez podwyższone poziomy glutaminianu, neuroprzekaźnika pobudzającego. Wysokie poziomy glutaminianu prowadzą do ekscytotoksyczności neuronalnej, przyczyniając się do nadpobudliwości w ośrodkowym układzie nerwowym (OUN). Ta nadpobudliwość, szczególnie w układzie nerwowym trójdzielnym, może powodować mimowolne skurcze mięśni, w tym te obserwowane w bruksizmie.12

Jądro boczne ciała migdałowatego (BLA) jest głęboko zaangażowane w przetwarzanie stresu i lęku. Jego aktywacja może prowadzić do zwiększonej pobudliwości neuronalnej i mimowolnych ruchów mięśni, takich jak te obserwowane w bruksizmie. Skuteczne zarządzanie aktywacją BLA poprzez techniki redukcji stresu i modulację neuroprzekaźników może być kluczowe w przerwaniu cyklu bruksizmu.1

Sekwencja zdarzeń podczas bruksizmu nocnego

Badania wykazały, że bruksizm nocny występuje w związku ze zdarzeniami fizjologicznymi, które poprzedzają, występują jednocześnie lub następują po rytmicznej aktywności mięśni żuchwy (RMMA). Zdarzenia te obejmują tymczasowy wzrost aktywności układu współczulnego około czterech do ośmiu minut przed epizodem, co prowadzi do wybudzenia ze snu oraz tachykardii.1

Przed pierwszym kontaktem zębów występuje sekwencja zdarzeń fizjologicznych, która obejmuje aktywację autonomicznego układu sercowego (na około 4 minuty przed epizodem), aktywność mózgową (około 4 sekundy wcześniej), wzrost napięcia mięśni otwierających szczękę z 2 głębokimi oddechami oraz przyspieszenie tętna na sekundę przed wystąpieniem zgrzytania. Ta sekwencja występuje w prawie 80% rytmicznych ruchów szczęki związanych ze zgrzytaniem zębami podczas snu.1

Wpływ stresu na mechanizm bruksizmu

Patofizjologiczny mechanizm, w którym stres wpływa na występowanie bruksizmu, został wyjaśniony dowodami, że osoby o zwiększonym poziomie neurotyczności i zaburzeniami lękowymi mają tendencję do uwalniania napięcia emocjonalnego poprzez angażowanie się w czynności związane z bruksizmem. Stres aktywuje współczulny układ nerwowy, przygotowując organizm do walki lub ucieczki. Ta aktywacja może zwiększyć napięcie mięśniowe, w tym mięśni szczęki, co może prowadzić do zgrzytania zębami i zaciskania szczęk.12

Badania wykazały, że przewlekły stres może degenerować hipokamp i destabilizować mezokortykalny szlak dopaminergiczny, który odpowiada za kontrolę mimowolnych ruchów mięśni. Stres oksydacyjny, poprzez uwalnianie tlenku azotu i aktywację mikrogleju, prowadzi do neurodegeneracji hipokampa i destabilizacji mezokortykalnego szlaku dopaminergicznego.12

Teorie etiologiczne

Obecnie nie istnieje jedna jasna patofizjologiczna przyczyna odpowiedzialna za epizody bruksizmu. Większość danych sugeruje, że prawdopodobnie są zaangażowane wielorakie mechanizmy, w tym czynniki genetyczne i środowiskowe. Najbardziej przekonująca teoria opisuje bruksizm jako zaburzenie dysregulacji neuromotorycznej. Teoria ta zakłada, że bruksizm występuje z powodu niezdolności do zahamowania aktywności motorycznej szczęki podczas pobudzenia w stanie snu.12

Obecnie akceptowane jest wieloczynnikowe wyjaśnienie etiologiczne, które uwzględnia, że genetyka, czynniki środowiskowe i psychospołeczne, zaburzenia oddychania podczas snu oraz mechanizmy neurochemiczne mogą odgrywać rolę. Długo utrzymujące się w stomatologii przekonanie, że bruksizm nocny jest znacząco związany z czynnikami anatomicznymi lub obwodowymi, obecnie nie znajduje potwierdzenia w dowodach naukowych.12

Aktualna wiedza klasyfikuje bruksizm jako powszechne zachowanie, które może być rozpatrywane w trzech różnych kierunkach: 1) Nie jest czynnikiem ryzyka ani ochronnym, ale nieszkodliwym zachowaniem; 2) jest czynnikiem ryzyka, gdy bruksizm jest związany z jedną lub więcej negatywnymi konsekwencjami zdrowotnymi; 3) jest czynnikiem ochronnym, gdy bruksizm jest związany z jednym lub więcej pozytywnymi lub ochronnymi wynikami.1

Podsumowanie mechanizmów bruksizmu

Patogeneza bruksizmu jest złożona i wieloczynnikowa, obejmująca wzajemne oddziaływanie czynników neurologicznych, psychologicznych, genetycznych i środowiskowych. Kluczowe mechanizmy patofizjologiczne obejmują:123

  • Dysregulację ośrodkowego układu nerwowego, szczególnie w obrębie jąder podstawy i pnia mózgu
  • Zaburzenia równowagi neuroprzekaźników (dopamina, serotonina, glutaminian, GABA)
  • Wpływ stresu na oś podwzgórze-przysadka-nadnercza i związaną z tym aktywację układu współczulnego
  • Mikrowybudzenia podczas snu i związane z nimi zmiany autonomicznej aktywności sercowo-oddechowej
  • Potencjalny mechanizm obronny w przypadku zaburzeń oddychania podczas snu
  • Predyspozycje genetyczne wpływające na funkcjonowanie receptorów dopaminergicznych i serotoninergicznych
  • Wpływ leków i substancji psychoaktywnych na szlaki neuronalne

123

Zrozumienie tych złożonych mechanizmów ma kluczowe znaczenie dla opracowania skutecznych strategii diagnostycznych i terapeutycznych dla pacjentów cierpiących na bruksizm. Ważne jest, aby pamiętać, że w aktualnej definicji bruksizm traktowany jest jako zachowanie, a nie zaburzenie u osób skądinąd zdrowych. Ta istotna zmiana w definicji pomaga wyjaśnić fakt, że u niektórych pacjentów ten stan występuje bez konsekwencji, a u innych ma poważne implikacje dla różnych obszarów zdrowia.1

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  1. 09.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Neurobiology of bruxism: The impact of stress (Review)
    https://pmc.ncbi.nlm.nih.gov/articles/PMC10895390/
    Bruxism is a non-functional involuntary muscle activity that affects more than one-third of the population at some point in their lives. A number of factors have been found to be related to the etiopathogenesis of bruxism; therefore, the condition is considered multifactorial. The most commonly accepted factor is stress. Current evidence indicates that exposure to chronic stress, distress and allostatic load ignite neurological degeneration and the attenuation of critical neuronal pathways that are highly implicated in the orofacial involuntary muscle activity. The present review discusses the negative effects that chronic stress exerts on certain parts of the central nervous system and the mechanisms through which these changes are involved in the etiopathogenesis of bruxism. The most widely accepted factor in the etiopathogenesis of bruxism is stress, with recent evidence highlighting that exposure to chronic stress may affect the attenuation of neuronal pathways involved in the orofacial involuntary muscle activity. Stress is the most commonly accepted factor involved in the pathogenesis of bruxism. To be more precise, we must refer to Distress and Allostatic load. When humans are under conditions of stress, the HPA axis, the main neuroendocrine response to stress, is activated. The activation of the vSub-ventral pallidum (VP)-nucleus accumbens (N.Acc) normally occurs under acute, mild and predictable stressors and leads to hyperdopaminergic states. Conversely, in chronic mild stressors, this pathway is attenuated, and the BLA-VP pathway is activated. The activation of the N.Acc. occurs either via the vSub-VP pathway or via the BLA-VP pathway. However, acute and chronic stress exposure, and subsequently an increase in circulating corticosterone levels, are also known to diminish progenitor cell proliferation, inhibit neuronal differentiation and suppress cell survival in the hippocampus dentate gyrus; all of these actions affect hippocampal neurogenesis. Overall, the current review has highlighted the role of stress both as a precipitating and an initiating factor in the genesis of bruxism. Based on clinical evidence, it has been demonstrated that chronic stress can degenerate the hippocampus and destabilize the mesocortical dopaminergic pathway, which is responsible for the control of involuntary muscle movements.
  • #1 Bruxism Management – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482466/
    Bruxism, characterized by involuntary rhythmic contractions of the masseter muscles and excessive teeth grinding, is a commonly overlooked yet significant condition. […] Through this evidence-based review, healthcare professionals explore the latest advancements in understanding the causes of bruxism, including its multifactorial nature, pathophysiology, and clinical manifestations. […] The pathophysiology of bruxism is related to the circadian phase. Sleep bruxism, a sleep-related movement disorder, is believed to be regulated by the central nervous system, involving autonomic and brain activity related to arousal or alertness. […] Sleep bruxism appears to be an exaggerated oromotor response to natural sleep-related microarousals distinguished by a rise in autonomic cardiac and respiratory activity occurring 8 to 14 times per hour during sleep.
  • #1 Bruxism – Wikipedia
    https://en.wikipedia.org/wiki/Bruxism
    Bruxism is excessive teeth grinding or jaw clenching. It is an oral parafunctional activity; i.e., it is unrelated to normal function such as eating or talking. The causes of bruxism are not completely understood, but probably involve multiple factors. Awake bruxism is thought to have different causes from sleep bruxism. There is evidence that sleep bruxism is caused by mechanisms related to the central nervous system, involving sleep arousal and neurotransmitter abnormalities. Disturbance of the dopaminergic system in the central nervous system has also been suggested to be involved in the etiology of bruxism. The relationship of bruxism with temporomandibular joint dysfunction (TMD, or temporomandibular pain dysfunction syndrome) is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD. The muscles of mastication (the temporalis muscle, masseter muscle, medial pterygoid muscle and lateral pterygoid muscle) are paired on either side and work together to move the mandible, which hinges and slides around its dual articulation with the skull at the temporomandibular joints. Bruxism can also be regarded as a disorder of repetitive, unconscious contraction of muscles. This typically involves the masseter muscle and the anterior portion of the temporalis (the large outer muscles that clench), and the lateral pterygoids, relatively small bilateral muscles that act together to perform sideways grinding. The exact location and pattern of attrition depends on how the bruxism occurs.
  • #1 Bruxism an issue between the myths and fact
    http://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S2215-34112022000300015
    Current knowledge classifies bruxism as a common behavior, a situation that can take in to account three different directions: 1) Not a risk or protective factor, but a harmless behavior; 2) a risk factor when bruxism is associated with 1 or more negative health consequences; 3) a protective factor when bruxism is associated with 1 or more positive or protective results. […] Literature has reported the relationship of elevated catecholamines with the severity of bruxism, suggesting than an increased sympathetic tone that can be a triggering factor for RMMA. […] It is hypothesized that anxiety and emotional stress increase the general arousal system, thus facilitating the presence of involuntary muscle activity on susceptible subjects. […] More recent studies on bruxism have pointed out an association between sleep arousal and cardiac/motor activity while sleeping.
  • #1 Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review)
    https://www.spandidos-publications.com/10.3892/etm.2023.12262
    Stress has been welldocumented to have a significant role in the etiopathogenesis of bruxism. Activation of the hypothalamicpituitaryadrenal axis (HPA) and subsequent release of corticosteroids lead to increased muscle activity. Neurological studies have demonstrated that chronic stress exposure induces neurodegeneration of important neuronal structures and destabilization of the mesocortical dopaminergic pathway. These disruptions impair the abilities to counteract the overactivity of the HPA axis and disinhibit involuntary muscle activity, while at the same time, there is activation of the amygdala. Recent evidence shows that overactivation of the amygdala under stressful stimuli causes rhythmic jaw muscle activity by over activating the mesencephalic and motor trigeminal nuclei. […] Although numerous factors have been implied to contribute to the etiopathogenesis of bruxism, stress and emotional disturbances are the most commonly accepted. Emotional stress is associated with an increase in head and muscle tonicity, as well as an increase in non-functional muscle activity. In addition, the activation of the sympathetic system in response to stressful stimuli leads to increased muscle tone and reduced pain thresholds.
  • #1 Reddit – The heart of the internet
    https://www.reddit.com/r/bruxism/comments/1em7hw3/comprehensive_approach_to_managing_bruxism/
    Chronic stress can degenerate the hippocampus and destabilize the mesocortical dopaminergic pathway, which is responsible for controlling involuntary muscle movements. […] The principle thesis here is that an imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters is central to the pathophysiology of bruxism. […] Bruxism, both nocturnal and diurnal, can be exacerbated by elevated levels of glutamate, an excitatory neurotransmitter. High glutamate levels lead to neural excitotoxicity, contributing to hyperexcitability in the central nervous system (CNS). This excitability, particularly in the trigeminal nervous system, can cause involuntary muscle contractions, including those seen in bruxism. […] Chronic stress is a significant factor in the genesis of bruxism. It increases muscle tone, lowers pain thresholds, and can lead to neurological degeneration, particularly affecting the hippocampus and mesocortical dopaminergic pathways. These changes can promote the activation of the basolateral amygdala (BLA), causing rhythmic jaw movements and perpetuating a cycle of stress and bruxism.
  • #1 Sleep related bruxism—comprehensive review of the literature based on a rare case presentation – Thomas – Frontiers of Oral and Maxillofacial Medicine
    https://fomm.amegroups.org/article/view/67995/html
    Recent studies demonstrate a robust relationship between SRB and genetics. A positive association with genes that code for the serotonin and dopamine receptors, 5-HTR2A and DRD1 respectively, were found. […] The Online Mendelian Inheritance in Man (OMIM) website classifies sleep bruxism along with parasomnias, and uses the alternative title facio-mandibular myoclonus. There is moderate evidence for the role of genetics as a risk factor in the causation of SRB.
  • #1 Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review)
    https://www.spandidos-publications.com/10.3892/etm.2023.12262
    Based on findings in neurological diseases and pharmacological interactions, it appears that a malfunction of 5-hydroxytryptamine (HT)2 receptors may have a major role in the pathogenesis of bruxism. The role of 5-HT2 receptors in the mediation of orofacial musculature is well documented. Stress can affect 5-HT receptors, but this effect varies from area to area. […] Two important neuronal areas are implicated in the genesis of bruxism and are highly affected by stress: The mesencephalic trigeminal nucleus (Me5) and the mesocortical dopaminergic pathway. Me5 controls the masseter inhibitory reflex, which, when activated, suppresses the trigeminal motor nucleus and inhibits masseter and temporalis contraction. […] Chronic stress exposure and increased circulating levels of corticosterone impair progenitor cell proliferation, inhibit neuronal differentiation and suppress cell survival in the hippocampal dentate gyrus, events that affect hippocampal neurogenesis.
  • #1 Bruxism in the Neurology Clinic
    https://practicalneurology.com/articles/2015-sept/bruxism-in-the-neurology-clinic
    Bruxism can occur during wake and/or sleep and can involve multiple muscles of mastication including the temporalis, masseter, and ptyergoids. […] More importantly for neurologists, evidence suggests a central dysregulation of the direct and indirect pathways of the basal ganglion as a main pathology in bruxism. […] Bruxism, as an associated symptom, is significantly increased in some disorders of the basal ganglia such as cranio-cervical dystonia and Huntingtons disease. […] Within this context, an argument can be made that bruxism is a form of oromandibular dystonia. […] Psychosocial factors including anxiety, depression, and stress sensitivity also appear to be associated with clenching. […] The use of botulinum toxin therapy may be the most important advancement in the treatment of bruxism, and neurologists are well-equipped to provide this service. […] These small and limited trials do not allow for a meaningful conclusion regarding the use of botulinum toxins.
  • #1 Bruxism Management – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482466/
    Awake bruxism is often associated with stress and heightened alertness, which can lead to increased autonomic cardiac activity. […] Sleep apnea and anxiety are the most common risk factors associated with sleep bruxism. […] Studies reveal that hereditary factors can contribute to bruxism. […] Approximately 50% of adults with obstructive sleep apnea have comorbid sleep bruxism. […] The use of amphetamines, antipsychotics, selective serotonin reuptake inhibitors, serotonin-noradrenaline reuptake inhibitors, noradrenaline-dopamine reuptake inhibitors, and drugs of abuse with catecholaminergic effects such as cocaine and 3,4-methylenedioxymethamphetamine can be associated with sleep bruxism. […] Additional linked neurologic and psychiatric disorders associated with sleep bruxism include anxiety, Alzheimer’s disease, Huntington’s disease, multiple system atrophy, traumatic brain injury, Down syndrome, Rett syndrome, cerebral palsy, and attention deficit hyperactivity disorder.
  • #1 Teeth Grinding and its Connection to Sleep Apnea
    https://www.pittsburghdentalsleepmedicine.com/teeth-grinding-its-connection-to-sleep-apnea
    Teeth grinding, also known as bruxism, is a common condition that can lead to significant dental issues and compromised overall oral health. […] The relationship between teeth grinding and sleep apnea remains an area of ongoing investigation, but researchers have identified various connections between these sleep disorders. Some studies suggest that teeth grinding may be a protective mechanism for individuals experiencing sleep apnea, as the movement of the jaw can aid in keeping the airway open and preventing the cessation of breathing during sleep. […] Research suggests that bruxism may be associated with sleep apnea for the following reasons: 1. Protective Mechanism: Some doctors believe that teeth grinding may serve as an unconscious response to episodes of paused breathing during sleep. The movement of the jaw during grinding can potentially aid in reestablishing airflow, offsetting the effects of sleep apnea.
  • #1 Fundamental Concepts of Sleep Bruxism – Decisions in Dentistry
    https://decisionsindentistry.com/article/sleep-bruxism/
    It is often thought that sleep bruxism is a hereditable trait, yet a specific gene has not yet been identified. […] Caffeine is known to be a central nervous system stimulant and has been shown to increase the risk of sleep bruxism by 1.5 times. […] Certain pharmacologic agents are also known to induce or enhance sleep bruxism. These are typically selective serotonin reuptake inhibitors and amphetamines, as well as illegal substances, such as 3,4-methylenedioxymethamphetamine and cocaine. […] Studies have suggested that children and adults reporting self-awareness of tooth grinding are more anxious, aggressive and hyperactive. […] Sleep bruxism has often been found to be associated with sleep disordered breathing (SDB). It has been suggested that sleep bruxism may play a protective role in restoring normal airway patency and respiration after a respiratory event.
  • #1 Paroxetine-induced severe sleep bruxism successfully treated with buspirone | Clinics
    https://www.elsevier.es/en-revista-clinics-22-articulo-paroxetine-induced-severe-sleep-bruxism-successfully-S1807593222018865
    Sleep bruxism is characterized by the involuntary clenching or grinding of the teeth during sleep and can cause severe health problems, including the destruction of tooth structure, temporo-mandibular joint dysfunction, myofascial pain, and severe sleep disturbances (1). […] The neurochemical mechanism underlying the development of bruxism remains unclear. However, recent investigations have suggested that the central dopaminergic system (especially within the meso-cortical tract), which controls muscular or motor activity, may be involved in the pathophysiology of bruxism (4). […] It has been hypothesized that the mechanism for SSRI-induced bruxism may involve excessive serotonergic action on the meso-cortical neurons arising from the ventral tegmental area. This action leads to a dopaminergic deficit, which causes a specific form of akathisia and akathisia-like movement of the jaw muscles, thereby leading to bruxism (5). […] Buspirone is an agonist of the 5-HT1A receptor that increases dopaminergic neuron firing in the ventral tegmental area and increases the synaptic release of dopamine in the prefrontal cortex. These effects ameliorate drug-induced bruxism.
  • #1 Bruxism (Teeth Grinding): Types, Causes, and Treatments – Austin Creek Dental
    https://austincreekdental.com/blog/bruxism-teeth-grinding-types-causes-and-treatments/
    Bruxism, also known as teeth grinding, is a sleep-related movement disorder that involves clenching jaw muscles together to grind upper and lower teeth together. […] Actually, researchers have discovered that sleep apnea might play a part in some cases of bruxism. […] Grinding teeth also puts a lot of pressure in the temporomandibular joint, which can lead to TMD. TMD is also sometimes called TMJ, and the disorder can cause ongoing pain in the joint muscles, clicking or popping of the jaw, as well as difficulty chewing and, sometimes, speaking. […] In bruxism, theres also a connection between some neurotransmitters and the act of grinding. In fact, one of the systems your brain uses to communicate movement to the body seems to be disrupted in bruxism. […] Its not all that surprising that sleep apnea and bruxism are connected. During an apneic episode, the airway is closed and airway pressure drops to zero. In order to alert the body to re-open the airway, the brain will initiate arousal and essentially draw one out of deeper sleep. This arousal can happen by grinding the teeth together, which will cause some movement and re-start breathing. […] Central factors for teeth grinding have to do with internal systems that may be out of balance in some way in the presence of bruxism, like the central nervous system.
  • #1 Bruxism – Causes And Treatment Of Teeth Grinding – Clínica Pardiñas
    https://clinicapardinas.com/en/bruxism-causes-treatment/
    Numerous studies have shown that bruxism can have a genetic origin and can be shared between different members of the same family. […] Having a malocclusion or problems with the muscles of the mouth and face can cause unintentional teeth grinding. […] There are other diseases that are closely related to bruxism in addition to the oral problems mentioned above. We include allergies, dementia, Parkinsons, hyperactivity, gastroesophageal reflux disorder, epilepsy, night terrors, or other sleep-related problems. […] Some psychiatric medications (such as antidepressants) and stimulant substances such as tobacco, alcohol, caffeine or the consumption of certain types of drugs can favor the development of this disorder. […] Bruxism causes dental attrition, a type of wear on tooth surfaces due to contact between them. Bruxism can end up causing dental fractures, flattening or significant reduction in the size of the teeth, dental abfractions and involvement of the dental pulp or nerve in advanced cases.
  • #1 Sleep related bruxism—comprehensive review of the literature based on a rare case presentation – Thomas – Frontiers of Oral and Maxillofacial Medicine
    https://fomm.amegroups.org/article/view/67995/html
    The motor pathways for volitional movements are widely considered to start from the pyramidal cells of the motor cortex. The role of the basal nuclei, their associated structures, and the related dopaminergic, glutamatergic and gabaergic pathways, in volitional movements, is well known. […] A role of dopaminergic system in the pathophysiology of SRB has been suggested. This concept has been shown in animal models employing dopamine receptor agonists and antagonists. […] With regards to the etiology of SRB, abnormalities in the central sensory motor processing have been proposed to be the cause of SRB. Central structures including, but not limited to, the locus coeruleus, the reticular formation, and the raphe magnum nuclei, have been shown to influence this type of sensory motor processing.
  • #1 Reddit – The heart of the internet
    https://www.reddit.com/r/bruxism/comments/1em7hw3/comprehensive_approach_to_managing_bruxism/
    An imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters is central to the pathophysiology of bruxism. Managing this imbalance is crucial for effective treatment. […] The basolateral amygdala (BLA) is deeply involved in processing stress and anxiety. Its activation can lead to increased neural excitability and involuntary muscle movements, such as those seen in bruxism. Effective management of BLA activation through stress reduction techniques and neurotransmitter modulation can be crucial in breaking the cycle of bruxism. Supplements that increase GABA levels and reduce glutamate activity can help mitigate the overactivation of the BLA.
  • #1 Fundamental Concepts of Sleep Bruxism – Decisions in Dentistry
    https://decisionsindentistry.com/article/sleep-bruxism/
    Previous research demonstrated that sleep bruxism occurs in association with physiological events that will precede, occur concurrently with, or follow RMMA. These events involve a temporary increase in the sympathetic nervous system tone approximately four to eight minutes prior to the event, resulting in sleep arousal, as well as tachycardia. […] Traditionally, dentistry has considered sleep bruxism to primarily have an anatomical etiology. Currently, there is no single clear pathophysiologic mechanism identified as responsible for these episodes. Most data would suggest they likely involve multiple mechanisms, including genetic and environmental factors. […] In a double-blind, randomized controlled trial, 11 subjects had strips of gold foil glued either on a selected occlusal contact area or on the buccal surface of the same tooth (control). The foil was left in place for eight days. The active occlusal interference caused a significant reduction in the number and amplitude of sleep bruxism events.
  • #1 Bruxism Management: Overview, Definition, Etiology
    https://emedicine.medscape.com/article/2066277-overview
    What has emerged in the last 10 years from extensive research is a broader hypothesis defining the genesis and pathogenesis of bruxism. The factors that have found traction from these studies include genetic predisposition, sleep architecture (eg, micro arousals occurring during sleep), psychological factors such as distress and anxiety, environmental factors, CNS catecholaminergic levels, brain trauma, brain disease, drug effects (stimulatory drugs: ecstasy, caffeine, or serotonin reuptake inhibitors, anxiolytic medication, or dopaminergic drugs, etc), and autonomic nervous system function (pattern generation). Bruxism is also considered a natural behavior that stimulates salivation during sleep. […] Current sleep study evidence suggests that even before first tooth contact a series of physiological events occur which include activation of the autonomic cardiac system at minus 4 minutes, brain activity at minus four seconds, a rise in jaw opener muscle tone with 2 big breaths, and an increase in heart rate at minus one second. This particular sequence has been found to occur in close to 80% of rhythmic jaw movements associated with tooth grinding during sleep.
  • #1 Common therapeutic approaches in sleep and awake bruxism — an overview | Matusz | Neurologia i Neurochirurgia Polska
    https://journals.viamedica.pl/neurologia_neurochirurgia_polska/article/view/90495
    Disturbances in the concentration of catecholamines, especially dopamine, which affect the mandibular motor dysfunctions, are thought to be of great importance in the mechanism of bruxism. […] The pathophysiological mechanism in which stress affects the occurrence of bruxism has been explained by evidence that individuals with increased levels of neuroticism and anxiety disorders tend to release their emotional tension by engaging in activities related to bruxism. […] Bruxism-related TMD can be explained by the craniofacial anatomy. […] It has been shown that mandibular neck weakness and craniofacial symptoms are more common in women with bruxism than in a control group. […] The first evidence of such a correlation came from a case report in which a patient suffering from Parkinsons syndrome was treated for grinding his teeth with L-3,4-dihydroxyphenylalanine (L-DOPA), a dopamine precursor.
  • #1 Fundamental Concepts of Sleep Bruxism – Decisions in Dentistry
    https://decisionsindentistry.com/article/sleep-bruxism/
    At present, a multifactorial etiological explanation has accepted that genetics, environmental and psychosocial factors, sleep related breathing disorders, and neurochemical mechanisms might all play a role. The long-held belief in dentistry that sleep bruxism is significantly related to anatomical or peripheral factors currently lacks evidentiary support.
  • #1 Frontiers | The neural substrates of bruxism: current knowledge and clinical implications
    https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2024.1451183/full
    Bruxism presents a multifactorial etiology. The development of bruxism likely involves genetic, psychological, physiological, and lifestyle factors. […] All of these factors converge on the excessive masticatory muscle activities, so it would be valuable to identify the neural pathways involved in bruxism. […] The use of different modern tools for the evaluation of the neural pathways involved in bruxism in both clinical and animal studies can provide a deeper understanding in this topic. […] The uncovering of the neural control involved in this behavior can provide important information for the development of future therapeutic approaches and prevent the consequences of severe bruxism.
  • #1 Bruxism an issue between the myths and fact
    http://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S2215-34112022000300015
    It is important to recall that the current definition treats bruxism as a behavior instead of a disorder, in otherwise healthy individuals. This major change in the definition helps to explain the fact that for some patients, this condition happens without consequences and for others it has severe implications on different areas of one’s health.
  • #2 Neurobiology of bruxism: The impact of stress (Review)
    https://www.spandidos-publications.com/10.3892/br.2024.1747
    Bruxism is a nonfunctional involuntary muscle activity that affects more than one-third of the population at some point in their lives. A number of factors have been found to be related to the etiopathogenesis of bruxism; therefore, the condition is considered multifactorial. The most commonly accepted factor is stress. Current evidence indicates that exposure to chronic stress, distress and allostatic load ignite neurological degeneration and the attenuation of critical neuronal pathways that are highly implicated in the orofacial involuntary muscle activity. The present review discusses the negative effects that chronic stress exerts on certain parts of the central nervous system and the mechanisms through which these changes are involved in the etiopathogenesis of bruxism. The most widely accepted factor in the etiopathogenesis of bruxism is stress, with recent evidence highlighting that exposure to chronic stress may affect the attenuation of neuronal pathways involved in the orofacial involuntary muscle activity. Stress is the most commonly accepted factor involved in the pathogenesis of bruxism. To be more precise, we must refer to Distress and Allostatic load. When humans are under conditions of stress, the HPA axis, the main neuroendocrine response to stress, is activated. The activation of the vSub-ventral pallidum (VP)-nucleus accumbens (N.Acc) normally occurs under acute, mild and predictable stressors and leads to hyperdopaminergic states. Conversely, in chronic mild stressors, this pathway is attenuated, and the BLA-VP pathway is activated. The activation of the N.Acc. occurs either via the vSub-VP pathway or via the BLA-VP pathway. Overall, the current review has highlighted the role of stress both as a precipitating and an initiating factor in the genesis of bruxism.
  • #2 Bruxism Management: Overview, Definition, Etiology
    https://emedicine.medscape.com/article/2066277-overview
    What has emerged in the last 10 years from extensive research is a broader hypothesis defining the genesis and pathogenesis of bruxism. The factors that have found traction from these studies include genetic predisposition, sleep architecture (eg, micro arousals occurring during sleep), psychological factors such as distress and anxiety, environmental factors, CNS catecholaminergic levels, brain trauma, brain disease, drug effects (stimulatory drugs: ecstasy, caffeine, or serotonin reuptake inhibitors, anxiolytic medication, or dopaminergic drugs, etc), and autonomic nervous system function (pattern generation). Bruxism is also considered a natural behavior that stimulates salivation during sleep. […] Current sleep study evidence suggests that even before first tooth contact a series of physiological events occur which include activation of the autonomic cardiac system at minus 4 minutes, brain activity at minus four seconds, a rise in jaw opener muscle tone with 2 big breaths, and an increase in heart rate at minus one second. This particular sequence has been found to occur in close to 80% of rhythmic jaw movements associated with tooth grinding during sleep.
  • #2 Causes Of Bruxism
    https://www.bruxism.org.uk/causes-of-bruxism.php
    Why bruxism occurs is not always clear. In the dental profession the belief that bruxism and dental occlusion are causally related has been widespread. However there is little evidence to support this belief. […] Recent research concluded that neither occlusal interference nor factors related to the oral facial skeleton have a role in the aetiology of bruxism. Recent studies suggest that sleep bruxism is secondary to sleep related arousals (defined by a rise in autonomic cardiac and respiratory activity that tends to be repeated 8-14 times per hour of sleep). The rhythmic muscle activity that occurs in sleep bruxism peaks in the minutes before rapid eye movement sleep. This suggests that there is some mechanism related to sleep stage transitions that influence the motor neurons of bruxism.
  • #2 Bruxism Management: Overview, Definition, Etiology
    https://emedicine.medscape.com/article/2066277-overview
    Other studies suggest that an imbalance in dopamine-mediated neural transmission may exist in some types of bruxism. For example, while short-term use of dopamine precursors such as L-dopa inhibits bruxism, long-term use of the L-dopa increases bruxism. […] The role of psychosocial factors in the etiology of bruxism has been assessed by a systematic search of peer-reviewed papers (PubMed Database) dealing with bruxism and psychological/psychosocial factors.
  • #2 Sleep related bruxism—comprehensive review of the literature based on a rare case presentation – Thomas – Frontiers of Oral and Maxillofacial Medicine
    https://fomm.amegroups.org/article/view/67995/html
    The motor pathways for volitional movements are widely considered to start from the pyramidal cells of the motor cortex. The role of the basal nuclei, their associated structures, and the related dopaminergic, glutamatergic and gabaergic pathways, in volitional movements, is well known. […] A role of dopaminergic system in the pathophysiology of SRB has been suggested. This concept has been shown in animal models employing dopamine receptor agonists and antagonists. […] With regards to the etiology of SRB, abnormalities in the central sensory motor processing have been proposed to be the cause of SRB. Central structures including, but not limited to, the locus coeruleus, the reticular formation, and the raphe magnum nuclei, have been shown to influence this type of sensory motor processing.
  • #2 Reddit – The heart of the internet
    https://www.reddit.com/r/bruxism/comments/1em7hw3/comprehensive_approach_to_managing_bruxism/
    Chronic stress can degenerate the hippocampus and destabilize the mesocortical dopaminergic pathway, which is responsible for controlling involuntary muscle movements. […] The principle thesis here is that an imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters is central to the pathophysiology of bruxism. […] Bruxism, both nocturnal and diurnal, can be exacerbated by elevated levels of glutamate, an excitatory neurotransmitter. High glutamate levels lead to neural excitotoxicity, contributing to hyperexcitability in the central nervous system (CNS). This excitability, particularly in the trigeminal nervous system, can cause involuntary muscle contractions, including those seen in bruxism. […] Chronic stress is a significant factor in the genesis of bruxism. It increases muscle tone, lowers pain thresholds, and can lead to neurological degeneration, particularly affecting the hippocampus and mesocortical dopaminergic pathways. These changes can promote the activation of the basolateral amygdala (BLA), causing rhythmic jaw movements and perpetuating a cycle of stress and bruxism.
  • #2 Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review)
    https://www.spandidos-publications.com/10.3892/etm.2023.12262
    Based on findings in neurological diseases and pharmacological interactions, it appears that a malfunction of 5-hydroxytryptamine (HT)2 receptors may have a major role in the pathogenesis of bruxism. The role of 5-HT2 receptors in the mediation of orofacial musculature is well documented. Stress can affect 5-HT receptors, but this effect varies from area to area. […] Two important neuronal areas are implicated in the genesis of bruxism and are highly affected by stress: The mesencephalic trigeminal nucleus (Me5) and the mesocortical dopaminergic pathway. Me5 controls the masseter inhibitory reflex, which, when activated, suppresses the trigeminal motor nucleus and inhibits masseter and temporalis contraction. […] Chronic stress exposure and increased circulating levels of corticosterone impair progenitor cell proliferation, inhibit neuronal differentiation and suppress cell survival in the hippocampal dentate gyrus, events that affect hippocampal neurogenesis.
  • #2 Reddit – The heart of the internet
    https://www.reddit.com/r/bruxism/comments/1em7hw3/comprehensive_approach_to_managing_bruxism/
    An imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters is central to the pathophysiology of bruxism. Managing this imbalance is crucial for effective treatment. […] The basolateral amygdala (BLA) is deeply involved in processing stress and anxiety. Its activation can lead to increased neural excitability and involuntary muscle movements, such as those seen in bruxism. Effective management of BLA activation through stress reduction techniques and neurotransmitter modulation can be crucial in breaking the cycle of bruxism. Supplements that increase GABA levels and reduce glutamate activity can help mitigate the overactivation of the BLA.
  • #2 Bruxism – Causes And Treatment Of Teeth Grinding – Clínica Pardiñas
    https://clinicapardinas.com/en/bruxism-causes-treatment/
    Numerous studies have shown that bruxism can have a genetic origin and can be shared between different members of the same family. […] Having a malocclusion or problems with the muscles of the mouth and face can cause unintentional teeth grinding. […] There are other diseases that are closely related to bruxism in addition to the oral problems mentioned above. We include allergies, dementia, Parkinsons, hyperactivity, gastroesophageal reflux disorder, epilepsy, night terrors, or other sleep-related problems. […] Some psychiatric medications (such as antidepressants) and stimulant substances such as tobacco, alcohol, caffeine or the consumption of certain types of drugs can favor the development of this disorder. […] Bruxism causes dental attrition, a type of wear on tooth surfaces due to contact between them. Bruxism can end up causing dental fractures, flattening or significant reduction in the size of the teeth, dental abfractions and involvement of the dental pulp or nerve in advanced cases.
  • #2 Bruxism in the Neurology Clinic
    https://practicalneurology.com/diseases-diagnoses/movement-disorders/bruxism-in-the-neurology-clinic/30531/
    Bruxism can occur during wake and/or sleep and can involve multiple muscles of mastication including the temporalis, masseter, and ptyergoids. […] More importantly for neurologists, evidence suggests a central dysregulation of the direct and indirect pathways of the basal ganglion as a main pathology in bruxism. […] Bruxism, as an associated symptom, is significantly increased in some disorders of the basal ganglia such as cranio-cervical dystonia and Huntingtons disease. […] Within this context, an argument can be made that bruxism is a form of oromandibular dystonia. […] Psychosocial factors including anxiety, depression, and stress sensitivity also appear to be associated with clenching. […] The use of botulinum toxin therapy may be the most important advancement in the treatment of bruxism, and neurologists are well-equipped to provide this service.
  • #2 Fundamental Concepts of Sleep Bruxism – Decisions in Dentistry
    https://decisionsindentistry.com/article/sleep-bruxism/
    It is often thought that sleep bruxism is a hereditable trait, yet a specific gene has not yet been identified. […] Caffeine is known to be a central nervous system stimulant and has been shown to increase the risk of sleep bruxism by 1.5 times. […] Certain pharmacologic agents are also known to induce or enhance sleep bruxism. These are typically selective serotonin reuptake inhibitors and amphetamines, as well as illegal substances, such as 3,4-methylenedioxymethamphetamine and cocaine. […] Studies have suggested that children and adults reporting self-awareness of tooth grinding are more anxious, aggressive and hyperactive. […] Sleep bruxism has often been found to be associated with sleep disordered breathing (SDB). It has been suggested that sleep bruxism may play a protective role in restoring normal airway patency and respiration after a respiratory event.
  • #2 Types of Teeth Grinding and How to Treat ItGroup Copypphonellocationccreditcard
    https://bogerdental.com/teeth-grinding-types-causes-and-treatments/
    The technical term for teeth grinding is bruxism. We use this term to describe any involuntary grinding or clenching of the teeth that happens outside of normal chewing, swallowing, or speaking movements. […] Many people suffer from sleep disorders and accompanying symptoms like teeth grinding due to an insufficient airway. There’s a significant relationship between bruxism, clenching of the teeth, and airway problems. In these cases, the teeth grinding is often related to a lack of oxygen during sleep. This is connected to the sleep disorders we’ve highlighted below. Treatment can relieve bruxism, correct related digestive issues, improve mental health, and lead to more restful sleep. […] Sleep disorders are a big risk factor for teeth grinding. In fact, they’re one of the most common issues associated with bruxism, especially obstructive sleep apnea (OSA). Teeth grinding often happens after an OSA episode as part of a survival mechanism to open the airway. Almost a quarter of all people with OSA also experience sleep bruxism. Other sleep-related disorders that have a connection to teeth grinding include gastroesophageal reflux disease (GERD), chronic snoring, and sleep talking.
  • #2 Bruxism – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/bruxism/
    Bruxism is involuntary and repetitive teeth grinding and/or jaw clenching due to increased masticatory muscle activity either while asleep (sleep bruxism) or awake (awake bruxism). […] The exact causes and pathophysiology of bruxism are unknown, but the following associations have been identified. […] Primary bruxism: Psychological (e.g., stress, anxiety). […] Secondary bruxism: Sleep disorders (e.g., parasomnias), Neurological disorders (e.g., cerebral palsy, Huntington disease), Medication (e.g., methylphenidate, dextroamphetamine, antidepressants, antipsychotics), Recreational drugs; (e.g., amphetamines, cocaine, alcohol, tobacco, caffeine).
  • #2 Why do people grind their teeth? 10 Causes of Bruxism | Rejuvenation Dentistry
    https://www.rejuv-health.com/sleep-apnea/why-do-people-grind-their-teeth/
    Chronic stress that can cause teeth grinding refers to daily stressors weighing down on you. Stress is known to cause people to clench their jaw muscles and grind their teeth. […] Anxiety and/or depression may be the cause of your bruxism, especially awake bruxism. […] Certain medications can cause bruxism. […] Antidepressants like SSRIs and antipsychotic medications have been linked to increased risk of teeth grinding. […] Teeth grinding seems to run in families. Bruxism involves hereditary and genetic factors. […] Crooked or misaligned teeth are considered to be a leading cause of teeth grinding, especially at night. […] In rare cases, a nutritional or vitamin deficiency may result in bruxism. The following nutritional and vitamin deficiencies may cause teeth grinding: Vitamin B5, Magnesium, Calcium.
  • #2 Bruxism – Wikipedia
    https://en.wikipedia.org/wiki/Bruxism
    Bruxism is excessive teeth grinding or jaw clenching. It is an oral parafunctional activity; i.e., it is unrelated to normal function such as eating or talking. The causes of bruxism are not completely understood, but probably involve multiple factors. Awake bruxism is thought to have different causes from sleep bruxism. There is evidence that sleep bruxism is caused by mechanisms related to the central nervous system, involving sleep arousal and neurotransmitter abnormalities. Disturbance of the dopaminergic system in the central nervous system has also been suggested to be involved in the etiology of bruxism. The relationship of bruxism with temporomandibular joint dysfunction (TMD, or temporomandibular pain dysfunction syndrome) is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD. The muscles of mastication (the temporalis muscle, masseter muscle, medial pterygoid muscle and lateral pterygoid muscle) are paired on either side and work together to move the mandible, which hinges and slides around its dual articulation with the skull at the temporomandibular joints. Bruxism can also be regarded as a disorder of repetitive, unconscious contraction of muscles. This typically involves the masseter muscle and the anterior portion of the temporalis (the large outer muscles that clench), and the lateral pterygoids, relatively small bilateral muscles that act together to perform sideways grinding. The exact location and pattern of attrition depends on how the bruxism occurs.
  • #2 Sleep-related bruxism (tooth grinding) – UpToDate
    https://www.uptodate.com/contents/sleep-related-bruxism-tooth-grinding
    Sleep-related bruxism involves activation of the masticatory muscles, resulting in tooth clenching and grinding during sleep. […] Bruxism is defined as repetitive jaw-muscle activity characterized by grinding or clenching of the teeth and/or by bracing or thrusting of the mandible. […] Bruxism is most common during sleep, when it is referred to as sleep-related bruxism.
  • #2 Bruxism – Causes And Treatment Of Teeth Grinding – Clínica Pardiñas
    https://clinicapardinas.com/en/bruxism-causes-treatment/
    Bruxism is the involuntary action of grinding or clenching the teeth without functional purposes. This disorder can occur during the day, although it usually occurs at night. It is estimated that it affects between 10 and 20% of the worlds population, without notable differences in gender issues. […] In this case, friction of the teeth is generated by contracting and relaxing the chewing muscles. This form of bruxism can cause great dental wear or attrition. […] Bruxism is usually caused by a state of anxiety, but it can also have a genetic origin or be caused by other diseases. […] Stress and anxiety activate the sympathetic nervous system, preparing the body for fight or flight. This activation can increase muscle tension, including that of the jaw muscles, which can lead to teeth grinding and clenching.
  • #2 Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review)
    https://www.spandidos-publications.com/10.3892/etm.2023.12262
    Recent evidence has revealed similar degenerative findings in bruxists. […] The fact that bruxism is a common comorbid condition or symptom in other neurodegenerative disorders such as Parkinson’s disease or Parkisonism, as well as in rapid eye movement sleep behavior disorder, constitutes enough evidence so as to not exclude neurodegeneration from this equation. […] This review has discussed the effects of chronic stress exposure in the pathogenesis of bruxism. In particular, oxidative stress, through the release of NO and the activation of microglia, has been shown to lead to neurodegeneration of the hippocampus and destabilization of the mesocortical dopaminergic pathway.
  • #2 5 Ways to Treat Bruxism
    https://ostrowonline.usc.edu/5-ways-to-treat-bruxism/
    Bruxism can be defined as nonfunctional jaw movement that includes clenching, grinding, clicking, and gnashing of teeth during sleep. […] The pathophysiology of bruxism is unknown but has been related with endogenous factors (such as neuromotor dysregulation and changes in the basal ganglia), and exogenous situations, including stress and anxiety. Psychological stress is considered a risk factor to develop bruxism and a predictor of temporomandibular pain. […] The most cogent theory describes bruxism as a neuromotor dysregulation disorder. This theory proposes that bruxism occurs due to the failure to inhibit jaw motor activity during a sleep state arousal. […] Additional to sleep fragmentation, bruxism has been related with medical comorbidities, such as obstructive sleep apnea and epilepsy. […] Many patients that exhibit headaches, jaw aches and toothache are not due to classic bruxism but due to a sustained habitual forceful clenching of the teeth (day or night).
  • #2 Bruxism an issue between the myths and fact
    http://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S2215-34112022000300015
    Current knowledge classifies bruxism as a common behavior, a situation that can take in to account three different directions: 1) Not a risk or protective factor, but a harmless behavior; 2) a risk factor when bruxism is associated with 1 or more negative health consequences; 3) a protective factor when bruxism is associated with 1 or more positive or protective results. […] Literature has reported the relationship of elevated catecholamines with the severity of bruxism, suggesting than an increased sympathetic tone that can be a triggering factor for RMMA. […] It is hypothesized that anxiety and emotional stress increase the general arousal system, thus facilitating the presence of involuntary muscle activity on susceptible subjects. […] More recent studies on bruxism have pointed out an association between sleep arousal and cardiac/motor activity while sleeping.
  • #2 Bruxism an issue between the myths and fact
    http://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S2215-34112022000300015
    It is important to recall that the current definition treats bruxism as a behavior instead of a disorder, in otherwise healthy individuals. This major change in the definition helps to explain the fact that for some patients, this condition happens without consequences and for others it has severe implications on different areas of one’s health.
  • #3 Bruxism an issue between the myths and fact
    http://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S2215-34112022000300015
    Is our goal in this paper to discuss the current concepts about bruxism, a topic that has been a matter of discussion on the dental field for many years. […] Different etiological factors are reviewed in this paper as well the influence of external and internal mechanism related to medications, emotional stress, systemic factors, and potential pharmacological pathways. […] To date, not a single view exists about the etiology for bruxism and how the increasing muscle activity can become excessive. It is, however, well established that evidence based on literature has shown no relationship of peripheral factors such as ”stable occlusion” or skeletal factors. This suggest that these involuntary movements are centrally regulated, probably in the brainstem and basal ganglia; structures in charge of controlling or inhibiting muscle movement for adequate muscle tone.
  • #3 Sleep related bruxism—comprehensive review of the literature based on a rare case presentation – Thomas – Frontiers of Oral and Maxillofacial Medicine
    https://fomm.amegroups.org/article/view/67995/html
    The motor pathways for volitional movements are widely considered to start from the pyramidal cells of the motor cortex. The role of the basal nuclei, their associated structures, and the related dopaminergic, glutamatergic and gabaergic pathways, in volitional movements, is well known. […] A role of dopaminergic system in the pathophysiology of SRB has been suggested. This concept has been shown in animal models employing dopamine receptor agonists and antagonists. […] With regards to the etiology of SRB, abnormalities in the central sensory motor processing have been proposed to be the cause of SRB. Central structures including, but not limited to, the locus coeruleus, the reticular formation, and the raphe magnum nuclei, have been shown to influence this type of sensory motor processing.
  • #3 Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review)
    https://www.spandidos-publications.com/10.3892/etm.2023.12262
    Recent evidence has revealed similar degenerative findings in bruxists. […] The fact that bruxism is a common comorbid condition or symptom in other neurodegenerative disorders such as Parkinson’s disease or Parkisonism, as well as in rapid eye movement sleep behavior disorder, constitutes enough evidence so as to not exclude neurodegeneration from this equation. […] This review has discussed the effects of chronic stress exposure in the pathogenesis of bruxism. In particular, oxidative stress, through the release of NO and the activation of microglia, has been shown to lead to neurodegeneration of the hippocampus and destabilization of the mesocortical dopaminergic pathway.
  • #3 If you grind your teeth during sleep, Houston based Sleep Centers at REST can help cure Nocturnal Bruxism
    http://www.restdiagnostics.com/HTML/Nocturnal-Bruxism.htm
    Involuntary grinding and clenching teeth at night, known as Nocturnal Bruxism, is a significant problem for millions of Americans and can lead to a painful condition known as TMJ or TMD, Temporal Mandibular Dysfunction. […] Recent research conducted by Dr. Simmons has demonstrated that 25% of patients with OSA demonstrate Nocturnal Bruxism. […] His research concludes that the Bruxism occurs during sleep in an attempt to protect a person’s airway that would otherwise collapse during sleep. […] Additionally, explanation is given on an association between temporomandibular jaw dysfunction and bruxism during sleep.
  • #3 What is Bruxism (Teeth Grinding): Causes, Signs & Treatment?
    https://houstongeneraldentistry.net/what-is-bruxism-teeth-grinding-causes-signs-and-treatment/
    Bruxism is a complex condition with numerous causes, including: […] Bruxism has been linked to neurological conditions such as Parkinson’s, Huntington’s, and epilepsy. As a side effect of their medication, people with these conditions may grind their teeth. […] According to some research, Bruxism may have a genetic component and may run in families. […] Malocclusion (bad bite): A misaligned bite can cause additional stress on the jaw, leading to grinding or clenching. […] It should be noted that many people who grind their teeth have more than one of these causes, and in some cases, the exact cause of bruxism is unknown.
  • #3 Bruxism an issue between the myths and fact
    http://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S2215-34112022000300015
    Current knowledge classifies bruxism as a common behavior, a situation that can take in to account three different directions: 1) Not a risk or protective factor, but a harmless behavior; 2) a risk factor when bruxism is associated with 1 or more negative health consequences; 3) a protective factor when bruxism is associated with 1 or more positive or protective results. […] Literature has reported the relationship of elevated catecholamines with the severity of bruxism, suggesting than an increased sympathetic tone that can be a triggering factor for RMMA. […] It is hypothesized that anxiety and emotional stress increase the general arousal system, thus facilitating the presence of involuntary muscle activity on susceptible subjects. […] More recent studies on bruxism have pointed out an association between sleep arousal and cardiac/motor activity while sleeping.
  • #3 Bruxism an issue between the myths and fact
    http://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S2215-34112022000300015
    It is important to recall that the current definition treats bruxism as a behavior instead of a disorder, in otherwise healthy individuals. This major change in the definition helps to explain the fact that for some patients, this condition happens without consequences and for others it has severe implications on different areas of one’s health.