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Menampilkan terjemahan untuk Dental caries begins beneath a biofilm dental plaque when
environmental factors favor the growth and metabolism of acidogenic bacteria. The population of
bacteria that are present in carious lesions is mixed and variable. A variety of products are
released or formed on the death of the bacteria. These include acids and proteinases that dissolve
and digest the enamel and dentin, and toxins including lipopolysaccharide (LPS) and
lipoteichoic acid (LTA). Although bacteria can readily travel within dentinal tubules (Figure 1),
toxins pass through dentin and enamel well ahead of the bacteria themselves. Thus, the pulps
inflammatory response is to the toxins rather than the bacteria themselves. Bacteria only invade
the pulp at a late stage of the caries process that clinically would present as a carious exposure.
All connective tissues are capable of mounting an immune response that will follow the same
basic pattern but is affected by local factors.The pulps response differs from that in some other
tissues. Because bacteria enter the tissue only at a very late stage, the pulps blood supply is
limited and the tissue is within a low-compliance chamber. If the tissue is presented with a new
antigen, the innate immune response is initiated and is followed a few days later by the specific
response. If the tissue is presented with an antigen it has met before, the specific response will be
initiated immediately. All three antigen-presenting cell types expressing the type II major
histocompatibility complex (MHC) surface proteins, macrophages, dendritic cells, and B
lymphocytes, are present and active in the pulps response to bacteria and toxins. In addition, it is
now becoming clear that odontoblasts, being in the ideal position to detect antigens via Toll-like
receptors (TLRs), produce a variety of cytokines and chemokines. In a normal healthy pulp,
macrophages (Figure 3) are present in a resting form, as monocytes. Macrophages require
stimulation by bacteria or cytokines before they express type II MHC molecules. At rest they are
found predominantly around blood vessels though a few are distributed throughout the tissue.
Dendritic cells (Figure 4) are characterized by the shape that provides their name. They form a
network throughout the pulp concentrating around blood vessels (Figure 5) and the odontoblast
layer. Some of the dendritic cells in the odontoblast layer extend their processes into the dentinal
tubules. Recent studies indicate that there are two populations of dendritic cell in the dental pulp,
one beneath the odontoblast layer and the other around the blood vessels (Figure 7). The number
of dendritic cells increases in the pulp when it becomes inflamed and they accumulate beneath
the carious lesion (see Figure 6). B cells are specialized lymphocytes that will become plasma
cells. They secrete antibodies during the specific immune response and express the MHC
molecules. They have also been reported in the normal pulp but are rather rare. Their role in the
initial stages of antigen recognition and presentation in the pulp is unclear. Occasional T cells are
found in normal pulp (Figure 8) and may be activated by antigenpresenting cells locally.
Odontoblasts are the first cells to encounter an antigen diffusing along the dentinal tubules.
Odontoblasts respond differentially to the toxins produced by gram-positive and gramnegative
bacteria. A gram-negative toxin activating TLR-4 up-regulates mRNAs for interleukin-1b,
interleukin- 8, tumor necrosis factor-a, and chemokines and TLRs. A synthetic peptide
mimicking a toxin from gram-positive bacteria activating TLR-2 downregulates these mRNAs.

The Process of Antigen Recognition Dendritic cells and macrophages bind to and phagocytize
antigen that is then processed intracellularly, bound to MHC molecules, and moved to the cell
membrane for recognition by T cells. B cells bind antigen to specific cell surface receptors. All
the antigen-presenting cell types enter the blood stream and carry the surface molecules to the
lymph nodes where T cell activation takes place, though some may occur locally (see Figure
8).16 Each type of antigenpresenting cell carries different types of antigen. The T cells respond
not to the antigen itself but to the modified complex in the cell membrane of the antigenpresenting cells. Being stationary, the odontoblast does not participate directly in the activation
of T cells but, presumably, activates dendritic cells. With hematoxylin and eosin stained sections,
dendritic cells cannot be distinguished, but macrophages and neutrophils can be distinguished.
The macrophages (and dendritic cells) will recognize a foreign antigen and carry its details to the
lymph nodes, though this is a histologically invisible process. Resting macrophages (monocytes)
enlarge and become active. Neutrophils leave the blood stream by diapedesis and migrate to the
scene of action (Figure 14). This accumulation of phagocytic cells is dominated numerically by
neutrophils, recognizable by their lobed nuclei, and is the key morphologic feature in the early
response to caries. Mast cells may also be present, but they are difficult to detect in routine
preparations due to their extreme fragility. They are most common in surface tissues in response
to inhaled or ingested antigens. At the same time, vascular and then neural changes (described
elsewhere in this chapter) occur. Nerves are not well visualized in hematoxylin and eosin stained
sections, and observations of changes in them during inflammation require other techniques.
Sometimes an apparent dilation of local blood vessels may be seen.
Terjemahkan selain dari Dental caries begins beneath a biofilm ofdental plaque when
environmental factors favor the growth and metabolism of acidogenic bacteria. The population of
bacteria that are present in carious lesions is mixed and variable. A variety of products are
released or formed on the death of the bacteria. These include acids and proteinases that dissolve
and digest the enamel and dentin, and toxins including lipopolysaccharide (LPS) and lipotechoic
acid (LTA). Although bacteria can readily travel within dentinal tubules (Figure 1), toxins pass
through dentin and enamel well ahead of the bacteria themselves. Thus, the pulps inflammatory
response is to the toxins rather than the bacteria themselves. Bacteria only invade the pulp at a
late stage of the caries process that clinically would present as a carious exposure. All connective
tissues are capable of mounting an immune response that will follow the same basic pattern but
is affected by local factors.The pulps response differs from that in some other tissues. Because
bacteria enter the tissue only at a very late stage, the pulps blood supply is limited and the tissue
is within a low-compliance chamber. If the tissue is presented with a new antigen, the innate
immune response is initiated and is followed a few days later by the specific response. If the
tissue is presented with an antigen it has met before, the specific response will be initiated
immediately. All three antigen-presenting cell types expressing the type II major
histocompatibility complex (MHC) surface proteins, macrophages, dendritic cells, and B
lymphocytes, are present and active in the pulps response to bacteria and toxins. In addition, it is
now becoming clear that odontoblasts, being in the ideal position to detect antigens via Toll-like
receptors (TLRs), produce a variety of cytokines and chemokines. In a normal healthy pulp,
macrophages (Figure 3) are present in a resting form, as monocytes. Macrophages require
stimulation by bacteria or cytokines before they express type II MHC molecules. At rest they are
found predominantly around blood vessels though a few are distributed throughout the tissue.
Dendritic cells (Figure 4) are characterized by the shape that provides their name. They form a
network throughout the pulp concentrating around blood vessels (Figure 5) and the odontoblast

layer. Some of the dendritic cells in the odontoblast layer extend their processes into the dentinal
tubules. Recent studies indicate that there are two populations of dendritic cell in the dental pulp,
one beneath the odontoblast layer and the other around the blood vessels (Figure 7). The number
of dendritic cells increases in the pulp when it becomes inflamed and they accumulate beneath
the carious lesion (see Figure 6). B cells are specialized lymphocytes that will become plasma
cells. They secrete antibodies during the specific immune response and express the MHC
molecules. They have also been reported in the normal pulp but are rather rare. Their role in the
initial stages of antigen recognition and presentation in the pulp is unclear. Occasional T cells are
found in normal pulp (Figure 8) and may be activated by antigenpresenting cells locally.
Odontoblasts are the first cells to encounter an antigen diffusing along the dentinal tubules.
Odontoblasts respond differentially to the toxins produced by gram-positive and gramnegative
bacteria. A gram-negative toxin activating TLR-4 up-regulates mRNAs for interleukin-1b,
interleukin- 8, tumor necrosis factor-a, and chemokines and TLRs. A synthetic peptide
mimicking a toxin from gram-positive bacteria activating TLR-2 downregulates these mRNAs.
The Process of Antigen Recognition Dendritic cells and macrophages bind to and phagocytize
antigen that is then processed intracellularly, bound to MHC molecules, and moved to the cell
membrane for recognition by T cells. B cells bind antigen to specific cell surface receptors. All
the antigen-presenting cell types enter the blood stream and carry the surface molecules to the
lymph nodes where T cell activation takes place, though some may occur locally (see Figure
8).16 Each type of antigenpresenting cell carries different types of antigen. The T cells respond
not to the antigen itself but to the modified complex in the cell membrane of the antigenpresenting cells. Being stationary, the odontoblast does not participate directly in the activation
of T cells but, presumably, activates dendritic cells. With hematoxylin and eosin stained sections,
dendritic cells cannot be distinguished, but macrophages and neutrophils can be distinguished.
The macrophages (and dendritic cells) will recognize a foreign antigen and carry its details to the
lymph nodes, though this is a histologically invisible process. Resting macrophages (monocytes)
enlarge and become active. Neutrophils leave the blood stream by diapedesis and migrate to the
scene of action (Figure 14). This accumulation of phagocytic cells is dominated numerically by
neutrophils, recognizable by their lobed nuclei, and is the key morphologic feature in the early
response to caries. Mast cells may also be present, but they are difficult to detect in routine
preparations due to their extreme fragility. They are most common in surface tissues in response
to inhaled or ingested antigens. At the same time, vascular and then neural changes (described
elsewhere in this chapter) occur. Nerves are not well visualized in hematoxylin and eosin stained
sections, and observations of changes in them during inflammation require other techniques.
Sometimes an apparent dilation of local blood vessels may be seen.
karies gigi dimulai di bawah plak gigi biofilm ketika faktor lingkungan mendukung pertumbuhan
dan metabolisme bakteri Acidogenic. Populasi bakteri yang hadir dalam lesi karies adalah
campuran dan variabel.
Berbagai produk yang dikeluarkan atau dibentuk pada kematian bakteri. Ini termasuk asam dan
proteinase yang larut dan mencerna enamel dan dentin, dan racun termasuk lipopolisakarida
(LPS) dan asam lipoteikoat (LTA). Meskipun bakteri mudah dapat melakukan perjalanan dalam
tubulus dentin (Gambar 1), racun melewati dentin dan enamel baik di depan bakteri sendiri.
Dengan demikian, respon inflamasi pulpa adalah untuk racun daripada bakteri sendiri. Bakteri
hanya menyerang pulp pada tahap akhir dari proses karies yang secara klinis akan hadir sebagai
paparan karies.
Semua jaringan ikat mampu pemasangan respon imun yang akan mengikuti pola dasar yang

sama tetapi dipengaruhi oleh respon factors.The pulpa lokal berbeda dari yang di beberapa
jaringan lain. Karena bakteri masuk jaringan hanya pada tahap yang sangat terlambat, suplai
darah pulpa adalah terbatas dan jaringan adalah dalam ruang rendah-kepatuhan. Jika jaringan
disajikan dengan antigen baru, respon imun bawaan dimulai dan diikuti beberapa hari kemudian
oleh respon tertentu. Jika jaringan disajikan dengan antigen itu telah bertemu sebelumnya, respon
tertentu akan dimulai segera.
Ketiga jenis sel antigen-presenting mengungkapkan tipe II histocompatibility kompleks utama
(MHC) protein permukaan, makrofag, sel dendritik, dan B limfosit, yang hadir dan aktif dalam
menanggapi pulp untuk bakteri dan racun. Selain itu, sekarang menjadi jelas bahwa odontoblasts,
berada di posisi yang ideal untuk mendeteksi antigen melalui reseptor Toll-like (TLR),
menghasilkan berbagai sitokin dan kemokin.
Dalam bubur yang sehat normal, makrofag (Gambar 3) yang hadir dalam bentuk istirahat,
sebagai monosit. Makrofag membutuhkan stimulasi oleh bakteri atau sitokin sebelum mereka
mengungkapkan tipe II molekul MHC. Pada saat istirahat mereka ditemukan terutama di sekitar
pembuluh darah meskipun beberapa didistribusikan di seluruh jaringan.
sel dendritik (Gambar 4) yang ditandai dengan bentuk yang menyediakan nama mereka. Mereka
membentuk jaringan di seluruh pulp berkonsentrasi di sekitar pembuluh darah (Gambar 5) dan
lapisan odontoblast. Beberapa sel dendritik dalam lapisan odontoblast memperpanjang proses
mereka ke dalam tubulus dentin. Studi terbaru menunjukkan bahwa ada dua populasi sel
dendritik dalam pulpa gigi, salah satu di bawah lapisan odontoblast dan lain di sekitar pembuluh
darah (Gambar 7). Jumlah sel dendritik kenaikan pulp ketika menjadi meradang dan mereka
menumpuk di bawah lesi karies (lihat Gambar 6).
Sel-sel B adalah limfosit khusus yang akan menjadi sel plasma. Mereka mengeluarkan antibodi
selama respon imun spesifik dan mengekspresikan molekul MHC. Mereka juga telah dilaporkan
dalam pulpa normal, tetapi agak jarang. peran mereka dalam tahap awal pengenalan antigen dan
presentasi di pulp jelas. Sel T sesekali ditemukan dalam pulp normal (Gambar 8) dan dapat
diaktifkan dengan antigenpresenting sel lokal.
Odontoblasts adalah sel pertama yang menemukan sebuah antigen menyebar di sepanjang
tubulus dentin. Odontoblasts merespon berbeda-beda terhadap racun yang dihasilkan oleh bakteri
gram positif dan gramnegative. Sebuah toksin gram-negatif mengaktifkan TLR-4 up-mengatur
mRNA untuk interleukin-1b, interleukin- 8, tumor necrosis factor-a, dan kemokin dan TLRs.
Sebuah peptida sintetik meniru toksin dari bakteri gram positif mengaktifkan TLR-2
downregulates mRNA ini.
Proses Antigen Pengakuan
sel dendritik dan makrofag mengikat dan antigen memfagositosis yang kemudian diolah
intraseluler, terikat pada molekul MHC, dan pindah ke membran sel untuk pengakuan oleh sel T.
sel B mengikat antigen dengan reseptor permukaan sel tertentu. Semua jenis sel antigenpresenting memasuki aliran darah dan membawa molekul permukaan ke kelenjar getah bening di
mana aktivasi sel T berlangsung, meskipun beberapa mungkin terjadi secara lokal (lihat Gambar
8) .16 Setiap jenis antigenpresenting sel membawa berbagai jenis antigen. Sel T merespon untuk
tidak antigen itu sendiri tetapi untuk kompleks dimodifikasi dalam membran sel dari sel-sel
menyajikan antigen. Menjadi stasioner, odontoblast tidak berpartisipasi secara langsung dalam
aktivasi sel T tetapi, mungkin, mengaktifkan sel-sel dendritik.
Dengan hematoxylin dan eosin bagian bernoda, sel dendritik tidak dapat dibedakan, tetapi
makrofag dan neutrofil dapat dibedakan. Makrofag (dan sel dendritik) akan mengenali antigen
asing dan membawa rinciannya ke kelenjar getah bening, meskipun ini adalah proses histologis

terlihat. Beristirahat makrofag (monosit) membesar dan menjadi aktif. Neutrofil meninggalkan
aliran darah oleh diapedesis dan bermigrasi ke tempat kejadian (Gambar 14). Akumulasi dari sel
fagosit didominasi numerik oleh neutrofil, dikenali oleh inti mereka lobed, dan fitur morfologis
kunci dalam respon awal untuk karies. sel mast juga dapat hadir, tetapi mereka sulit untuk
dideteksi dalam persiapan rutin karena kerapuhan ekstrim mereka. Mereka yang paling umum
pada jaringan permukaan dalam menanggapi antigen inhalasi atau tertelan. Pada saat yang sama,
perubahan pembuluh darah dan kemudian saraf (dijelaskan di bagian lain dalam bab ini) terjadi.
Saraf tidak baik divisualisasikan dalam hematoxylin dan eosin bernoda bagian, dan pengamatan
perubahan mereka selama peradangan memerlukan teknik lainnya. Kadang-kadang pelebaran
jelas pembuluh darah lokal dapat dilihat.
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