Wikipedia

Karies gigi

kerusakan gigi akibat bakteri
Revisi sejak 8 Desember 2007 11.13 oleh Andreas Erick (bicara | kontrib) (→Etiologi)

Karies gigi adalah sebuah penyakit infeksi yang merusak struktur gigi.[1] Penyakit ini menyebabkan gigi berlubang. Jika tidak ditangani, penyakit ini dapat menyebabkan nyeri, penanggalan gigi, infeksi, berbagai kasus berbahaya, dan bahkan kematian. Penyakit ini telah dikenal sejak masa lalu, berbagai bukti telah menunjukkan bahwa penyakit ini telah dikenal sejak zaman Perunggu, zaman Besi, dan masa pertengahan.[2] Peningkatan prevalensi karies banyak dipengaruhi perubahan dari pola makan.[2][3] Kini, karies gigi telah menjadi penyakit yang tersebar di seluruh dunia.

Karies gigi
Kerusakan gigi berupa lubang yang disebabkan karies
Informasi umum
SpesialisasiKedokteran gigi Sunting ini di Wikidata

Ada beberapa cara untuk mengelompokkan karies gigi.[4] Walaupun apa yang terlihat dapat berbedam faktor-faktor risiko dan perkembangan karies hampir serupa. Mula-mula, lokasi terjadinya karies dapat tampak seperti daerah berkapur namun berkembang menjad lubang coklat. Walaupun karies mungkin dapat saja dilihat dengan mata telanjang, terkadang diperlukan bantuan radiografi untuk mengamati daerah-daerah pada gigi dan menetapkan seberapa jauh penyakit itu merusak gigi.

Lubang gigi disebabkan oleh beberapa tipe dari bakteri penghasil asam yang dapat merusak karena reaksi fermentasi karbohidrat termasuk sukrosa, fruktosa, dan glukosa.[5][6][7] Asam yang diproduksi tersebut mempengaruhi mineral gigi sehingga menjadi sensitif pada pH rendah. Sebuah gigi akan mengalami demineralisasi dan remineralisasi. Ketika pH turun menjadi di bawah 5,5, proses demineralisasi menjadi lebih cepat dari remineralisasi. Hal ini menyebabkan lebih banyak mineral gigi yang luluh dan membuat lubang pada gigi.

Bergantung pada seberapa besarnya tingkat kerusakan gigi, sebuah perawatan dapat dilakukan. Perawatan dapat berupa penyembuahan gigi untuk mengembalukan bentuk, fungsi, dan estetika. Namun belum diketahui cara bagaimana untuk meregenerasi secara besar-besaran pada struktur gigi. Maka, organisasi kesehatan gigi terus menjalankan penyuluhan untuk mencegah kerusakan gigi, misalnya dengan menjaga kesehatan gigi dan makanan.[8]

Sejarah

 
Sebuah gambar dari tahun 1300 Masehi. Seorang dokter mencabut gigi pasiennya.

Bukti arkeologis menunjukkan bahwa karies gigi sudah ada sejak masa prasejarah. Sebuah tengkorak yang diperkirakan berasal dari satu juta tahun yang lalu dari masa neolitikum memberi petunjuk adanya karies.[2] Adanya peningkatan prevalensi karies sejak masa neolitikum mungkin disebabkan banyaknya konsumsi makanan dari tumbuhan yang banyak mengandung karbohidrat.[9] Sebuah gurdi atau bor dari kayu ditemukan pada masa neolitikum. gurdi tersebut diperkirakan digunakan sebagai pelubang gigi untuk mengeluarkan abses dari gigi.[10] Perubahan kebudayaan berupa penemuan teknik pertanian di Asia Selatan dipercayai juga sebagai salah satu peningkat prevalensi karies.

Sebuah teks dari Sumeria (5000 SM) menggambarkan sebuah "cacing gigi" sebagai penyebab karies.[11] Bukti pada kepercayaan ini juga ditemukan pada India, Mesir, Jepang, dan Tiongkok.[3]

Banyak fosil tengkorak yang dapat menunjukkan adanya perawatan gigi yang primitif. Di Pakistan, sebuah gigi yang diperkirakan berasal dari 5500 SM hingga 7000 SM menunjukkan sebuah lubang yang mungkin disebabkan gurdi gigi. [12] Karies juga dituliskan oleh Homer dan Guy de Chauliac dalam tulisan mereka.[3] Papirus Ebers, sebuah tulisan Mesir kuno (1550 SM) menyebutkan sebuah penyakit gigi.[11] Selama pemerintahan dinasti Sargonid Assyria pada 668 SM hingga 626 SM, dituliskan bahwa dokter kerajaan memerlukan tindakan pencabutan gigi untuk mencegah penyebaran radang.[3] Selama masa pendudukan bangsa Romawi di Eropa, proses pemasakan makanan menurunkan tingkat terjadinya karies.[13] Pada masa peradaban Yunani dan Romawi dan Mesir, memiliki perawatan untuk meredakan rasa nyeri karena karies.[3]

Tingkat kejadian karies menurun pada masa Perungggu dan Besi, namun meningkat tajam pada masa pertengahan.[2] Peningkatan prevalensi karies secara periodik ini serupa dengan kejadi pada masa tahun 1000, ketika gula menjadi lebih mudah didapatkan di dunia Barat. Perawatan yang diberikan berupa obat-obatan herbal dan jampi-jampi, serta pencabutan gigi.[14][3]Umat Katolik menyampaikan doa dengan penyertaan Santo Appolonia, santo pelindung untuk dokter gigi.[15]

Ada pula bukti yang menunjukkan adanya peningkatan tingkat karies di suku Indian, Amerika Utara setelah memulai kontak dengan kolonial Eropa. Sebelum kolonisasi, Indian Amerika Utara menggantungkan hidupnya pada berburu, kemudian berubah menjadi bertani jagung. Pergantian diet makan ini menyebabkan peningkatan karies.[2]

Pada masa pencerahan, kepercayaan bahwa "cacing gigi" sebagai penyebab karies ditepis oleh kelompok ilmuwan kedokteran.[16] Pierre Fauchard, yang dikenal sebagai bapak kedokteran gigi masa kini, adalah salah satu pihak pertama yang menolak ide cacing gigi tersebut. Ia menyebutkan bahwa konsumsi gula-lah yang menjadi penyebab karies gigi.[17] Pada 1850, prevalensi karies meningkat lagi dan disebabkan oleh pergeseran pola makan.[3]

Pada 1890-an, W.D. Miller memulai rangkaian penelitian untuk menyelediki perihal penyakit karies gigi. Ia menemukan bahwa ada bakteri yang hidup di rongga mulut dan mengeluarkan asam sehingga melarutkan struktur gigi ketika terdapat sisi karbohidrat.[18] Penjelasan ini dikenal sebagai teori karies kemoparasitik.[19] Penemuan Miller, bersamaan penelitian terhadap plak gigi oleh G.V. Black dan J.L. Williams, membuat sebuah dasar sebagai penjelasan patofisiologi karies yang diterima hingga kini.[3]

Epidemiologi

Diperkirakan bahwa 90% dari anak-anak usia sekolah di seluruh dunia dan sebagian besar orang dewasa pernah menderita karies. Prevalensi karies tertinggi terdapat di Asia dan Amerika Latin. Prevalensi terendah terdapat di Afrika.[20] Di Amerika Serikat, karies gigi merupakan penyakit kronis anak-anak yang sering terjadi dan tingkatnya 5 kali lebih tinggi dari asma.[21] Karies merupakan penyebab patologi primer atas penanggalan gigi pada anak-anak.[22] Antara 29% hingga 59% orang dewasa dengan usia lebih dari limapuluh tahun mengalami karies.[23]

Jumlah kasus karies menurun di berbagai negara berkembang, karena adanya peningkatan kesadaran atas kesehatan gigi dan tindakan pencegahan dengan terapi florida.[24]

Klasifikasi

Karies gigi dapat dikelompokan berdasarkan lokasi, tingkat laju perkembangan, dan jaringan keras yang terkena.[4]

Lokasi

Secara umum, ada dua tipe karies gigi bila dibedakan lokasinya, yaitu karies yang ditemukan di permukaan halus dan karies di celah atau fisura gigi.[25]

 
Celah atau fisura gigi dapat menjadi lokasi karies.

Karies celah dan fisura

Celah dan fisura adalah tanda anatomis gigi. Fisura terbentuk saat perkembangan alur, dan tidak sepenuhnya menyatu, dan membuat suatu turunan atau depresio yang khas pada strutkur permukaan email. Tempat ini mudah sekali menjadi lokasi karies gigi.[26] Celah yang ada daerah pipi atau bukal ditemukan di gigi geraham.

Karies celah dan fisura terkadang sulit dideteksi. Semakin berkembangnya proses perlubangan akrena karies, email atau enamel terdekat berlubang semakin dalam. Ketika karies telah mencapai dentin pada pertemuan enamel-dental, lubang akan menyebar secara lateral. Di dentin, proses perlubangan akan mengikuti pola segitiga ke arah pulpa gigi.

Karies permukaan halus

Ada tiga macam karies permukaan halus. Karies proksimal, atau dikenal juga sebagai karies interproksimal, terbentuk pada permukaan halus antara batas gigi. Karies akar terbentuk pada permukaan akar gigi. Tipe ketiga karies ini terbentuk pada permukaan lainnya.

 
Pada radiograf ini, titik hitam pada batas gigi menunjukkan sebuah karies proksimal.

Karies proksimal adalah tipe yang paling sulit dideteksi.[27] Tipe ini kadang tidak dapat dideteksi secara visual atau manual dengan sebuah explorer gigi. Karies proksimal ini memerlukan pemeriksaan radiografi.[28]

Karies akar adalah tipe karies yang sering terjadi dan biasanya terbentuk ketika permukaan akar telah terbuka karena resesi gusi. Bila gusi sehat, karies ini tidak akan berkembang karena tidak dapat terpapar oleh plak bakteri. Permukaan akar lebih rentan terkena proses demineralisasi daripada enamel atau email karena sementumnya demineraliasi pada pH 6,7, di mana lebih tinggi dari enamel.[29] Karies akar lebih sering ditemukan di permukaan fasial, permukaan interproksimal, dan permukaan lingual. Gigi geraham atas merupakan lokasi tersering dari karies akar.

Deskripsi umum lainnya

Di samping pengelompokan diatas, lesi karies dapat dikelompokkan sesuai lokasinya di permukaan tertentu pada gigi. Karies pada permukaan gigi yang dekat dengan permukaan pipi atau bibir disebut "karies fasial", dan karies yang lebih dekat ke arah lidah disebut "karies lingual". Karies fasial dapat dibagi lagi menjadi bukal (dekat pipi) dan labial (dekat bibir). Karies lingual juga dapat disebut palatal bila ditemukan di permukaan lingual dari gigi pada rahang atas (maksila) dan dekat dengan pallatum durum atau bagian langit-langit mulut yang keras.

Karies di dekat leher gigi disebut karies servikal.

Etiologi

 
Karies yang merajalela karena penggunaan metamfetamin.

Karies botol susu atau karies kanak-kanak adalah pola lubang yang ditemukan di anak-anak pada gigi susu. Gigi yang sering terkena adalah gigi depan di rahang atas, namun kesemua giginya dapat terkena juga.[30] Sebutan "karies botol susu" karena karies ini sering muncul pada anak-anak yang tidur dengan cairan yang manis (misalnya susu) dengan botolnya. Sering pula disebabkan oleh seringnya pemberian makan pada anak-anak dengan cairan manis.

Ada juga karies yang merajalela atau akries yang menjalar ke semua gigi.Radiographic Classification of Caries. Hosted on the Ohio State University website. Page accessed August 14, 2006.</ref> Tipe karies ini sering ditemukan pada pasien dengan xerostomia, kebersihan mulut yang buruk, pengonsumsi gula yang tinggi, dan pengguna metamfetamin karena obat ini membuat mulut kering. [31] Bila karoies yang parah ini merupakan hasil karena radiasi kepala dan leher, ini mungkin sebuah karies yang dipengaruhi radiasi.

Laju penyakit

Laju karies dapat membagi akries menjadi karies akut atau kronis. Karies rekuren berarti karies yang terjadi pada bekas karies terdahulu.

Jaringan keras yang terpengaruh

Bergantung pda jaringan keras mana yang terpengaruh, maka dapat dibedakan karies yang mempengaruhi enamel, dentin, atau sementum. Pada awal perkembangannya, karies mungkin hanya mempengaruhi enamel. Namun ketika karies semakin luas, dapat berpengaruhi dentin. Sementum adalah jaringan keras yang melapisi akar gigi, maka sementum dapat terkena bila akar gigi terbuka.

Signs and symptoms

 
Dental explorer used for caries diagnosis.

Until caries progresses, a person may not be aware of it.[32] The earliest sign of a new carious lesion, referred as incipient decay, is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation, a "cavity". The process before this point is reversible, but once a cavitation forms, the lost tooth structure cannot be regenerated. A lesion which appears brown and shiny suggests dental caries was once present but the demineralization process has stopped, leaving a stain. A brown spot which is dull in appearance is probably a sign of active caries.

As the enamel and dentin are destroyed further, the cavitation becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed and cause the tooth to hurt. The pain can be worsened by heat, cold, or sweet foods and drinks.[1] Dental caries can also cause bad breath and foul tastes.[33] In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues which may become life-threatening, as in the case with Ludwig's angina.[34]

Diagnosis

 
This preoperative photo of tooth #3, (A), reveals no clinically apparent decay other than a small spot within the central fossa. In fact, decay could not be detected with an explorer. Radiographic evaluation, (B), however, reveals an extensive region of demineralization within the dentin (arrows) of the mesial half of the tooth. When a bur was used to remove the occlusal enamel overlying the decay, (C), a large hollow was found within the crown and it was discovered that a hole in the side of the tooth large enough to allow the tip of the explorer to pass was contiguous with this hollow. After all of the decay had been removed, (D), the pulp chamber had been exposed and most of the mesial half of the crown was either missing or poorly supported.

Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer. Dental radiographs, produced when X-rays are passed through the jaw and picked up on film or digital sensor, may show dental caries before it is otherwise visible, particularly in the case of caries on interproximal (between the teeth) surfaces. Large dental caries are often apparent to the naked eye, but smaller lesions can be difficult to identify. Unextensive dental caries was formerly found by searching for soft areas of tooth structure with a dental explorer. Visual and tactile inspection along with radiographs are still employed frequently among dentists, particularly for pit and fissure caries.[35]

Some dental researchers have cautioned against the use of dental explorers to find caries.[27] In cases where a small area of tooth has begun demineralizing but has not yet cavitated, the pressure from the dental explorer could cause a cavitation. Since the carious process is reversible before a cavitation is present, it may be possible to arrest the caries with fluoride to remineralize the tooth surface. When a cavitation is present, a restoration will be needed to replace the lost tooth structure. A common technique used for the diagnosis of early (uncavitated) caries is the use of air blown across the suspect surface, which removes moisture, changing the optical properties of the unmineralized enamel. This produces a white 'halo' effect detectable to the naked eye. Fiberoptic transillumination, lasers and disclosing dyes have been recommended for use as an adjunct when diagnosing smaller carious lesions in pits and fissures of teeth.

Causes

There are four main criteria required for caries formation: a tooth surface (enamel or dentin); cariogenic (or potentially caries-causing) bacteria; fermentable carbohydrates (such as sucrose); and time.[36] The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures which are retained within the bone.[37]

Teeth

There are certain diseases and disorders affecting teeth which may leave an individual at a greater risk for caries. Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not form fully or in insufficient amounts and can fall off a tooth.[38] Dentinogenesis imperfecta is a similar disease. In both cases, teeth may be left more vulnerable to decay because the enamel is not as able to protect the tooth as it would in health.[39]

In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent of tooth enamel is composed of minerals.[40] These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5.[41] Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content.[42] Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, the tooth is susceptible to dental caries.

The anatomy of teeth may affect the likelihood of caries formation. In cases where the deep grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop. Also, caries are more likely to develop when food is trapped between teeth.

 
A gram stain image of Streptococcus mutans.

Bacteria

The mouth contains a wide variety of bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans and Lactobacilli among them.[5][7] Particularly for root caries, the most closely associated bacteria frequently identified are Lactobacillus acidophilus, Actinomyces viscosus, Nocardia spp., and Streptococcus mutans. Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called plaque, which serves as a biofilm. Some sites collect plaque more commonly than others. The grooves on the biting surfaces of molar and premolar teeth provide microscopic retention, as does the point of contact between teeth. Plaque may also collect along the gingiva. In addition, the edges of fillings or crowns can provide protection for bacteria, as can intraoral appliances such as orthodontic braces or removable partial dentures.

Fermentable carbohydrates

Bacteria in a person's mouth convert sugars (glucose and fructose, and most commonly sucrose - or table sugar) into acids such as lactic acid through a glycolytic process called fermentation.[6] If left in contact with the tooth, these acids may cause demineralization, which is the dissolution of its mineral content. The process is dynamic, however, as remineralization can also occur if the acid is neutralized; suitable minerals are available in the mouth from saliva and also from preventative aids such as fluoride toothpaste, dental varnish or mouthwash.[43] Caries advance may be arrested at this stage. If sufficient acid is produced over a period of time to the favor of demineralization, caries will progress and may then result in so much mineral content being lost that the soft organic material left behind would disintegrate, forming a cavity or hole.

Time

The frequency of which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development.[44] After meals or snacks containing sugars, the bacteria in the mouth metabolize them resulting in acids as by-products which decreases pH. As time progresses, the pH returns to normal due to the buffering capacity of saliva and the dissolved mineral content from tooth surfaces. During every exposure to the acidic environment, portions of the inorganic mineral content at the surface of teeth dissolves and can remain dissolved for 2 hours.[45] Since teeth are vulnerable during these periods of acidic environments, the development of dental caries relies greatly on the frequency of these occurrences. For example, when sugars are eaten continuously throughout the day, the tooth is more vulnerable to caries for a longer period of time, and caries are more likely to develop than if teeth are exposed less frequently to these environments and proper oral hygiene is maintained. This is because the pH never returns to normal levels, thus the tooth surfaces cannot remineralize, or regain lost mineral content.

The carious process can begin within days of a tooth erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates, but may begin at any other time thereafter. The speed of the process is dependent on the interplay of the various factors described above but is believed to be slower since the introduction of fluoride.[46] Compared to coronal smooth surface caries, proximal caries progress quicker and take an average of 4 years to pass through enamel in permanent teeth. Because the cementum enveloping the root surface is not nearly as durable as the enamel encasing the crown, root caries tends to progress much more rapidly than decay on other surfaces. The progression and loss of mineralization on the root surface is 2.5 times faster than caries in enamel. In very severe cases where oral hygiene is very poor and where the diet is very rich in fermentable carbohydrates, caries may cause cavitation within months of tooth eruption. This can occur, for example, when children continuously drink sugary drinks from baby bottles. On the other hand, it may take years before the process results in a cavity being formed, if at all.

Other risk factors

In addition to the four main requirements for caries formation, reduced saliva is also associated with increased caries rate since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, particularly the parotid gland, are likely to cause widespread tooth decay. Some examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis.[47] Medications, such as antihistamines and antidepressants, can also impair salivary flow.[48] Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side effect.[47] Radiation therapy to the head and neck may also damage the cells in salivary glands, increasing the likelihood for caries formation.[49]

The use of tobacco may also increase the risk for caries formation. Smokeless tobacco frequently contains high sugar content in some brands, possibly increasing the susceptibility to caries.[50] Tobacco use is a significant risk factor for periodontal disease, which can allow the gingiva to recede.[51] As the gingiva loses attachment to the teeth, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids in comparison to enamel.[29] Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but there is suggestive evidence of a causal relationship between smoking and root-surface caries.[52]

Pathophysiology

 
The progression of pit and fissure caries resembles two triangles with their bases meeting along the junction of enamel and dentin.

Enamel

Enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. The effects of this process include the demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically penetrate the dentin. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by caries generally follows the direction of the enamel rods, the different triangular patterns between pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel rods are different in the two areas of the tooth .[53]

As the enamel loses minerals , and dental caries progress, they develop several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone.[54] The translucent zone is the first visible sign of caries and coincides with a 1-2% loss of minerals.[55] A slight remineralization of enamel occurs in the dark zone, which serves as an example of how the development of dental caries is an active process with alternating changes.[56] The area of greatest demineralization and destruction is in the body of the lesion itself. The surface zone remains relatively mineralized and is present until the loss of tooth structure results in a cavitation.

Dentin

Unlike enamel, the dentin reacts to the progression of dental caries. After tooth formation, the ameloblasts, which produce enamel, are destroyed once enamel formation is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is produced continuously throughout life by odontoblasts, which reside at the border between the pulp and dentin. Since odontoblasts are present, a stimulus, such as caries, can trigger a biologic response. These defense mechanisms include the formation of sclerotic and tertiary dentin.[57]

In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the translucent zone, the zone of bacterial penetration, and the zone of destruction.[53] The translucent zone represents the advancing front of the carious process and is where the initial demineralization begins. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin.

 
The faster spread of caries through dentin creates this triangular appearance in smooth surface caries.

Sclerotic dentin

The structure of dentin is an arrangement of microscopic channels, called dentinal tubules, which radiate outward from the pulp chamber to the exterior cementum or enamel border.[58] The diameter of the dentinal tubules is largest near the pulp (about 2.5 μm) and smallest (about 900 nm) at the junction of dentin and enamel.[59] The carious process continues through the dentinal tubules, which are responsible for the triangular patterns resulting from the progression of caries deep into the tooth. The tubules also allow caries to progress faster.

In response, the fluid inside the tubules bring immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules.[60] This results in a constriction of the tubules, which is an attempt to slow the bacterial progression. In addition, as the acid from the bacteria demineralizes the hydroxyapatite crystals, calcium and phosphorus are released, allowing for the precipitation of more crystals which fall deeper into the dentinal tubule. These crystals form a barrier and slow the advancement of caries. After these protective responses, the dentin is considered sclerotic.

Fluids within dentinal tubules are believed to be the mechanism by which pain receptors are triggered within the pulp of the tooth.[61] Since sclerotic dentin prevents the passage of such fluids, pain that would otherwise serve as a warning of the invading bacteria may not develop at first. Consequently, dental caries may progress for a long period of time without any sensitivity of the tooth, allowing for greater loss of tooth structure.

Tertiary dentin

In response to dental caries, there may the production of more dentin toward the direction of the pulp. This new dentin is referred to as tertiary dentin.[59] Tertiary dentin is produced to protect the pulp for as long as possible from the advancing bacteria. As more tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been subdivided according to the presence or absence of the original odontoblasts.[62] If the odontoblasts survive long enough to react to the dental caries, then the dentin produced is called "reactionary" dentin. If the odontoblasts are killed, the dentin produced is called "reparative" dentin.

In the case of reparative dentin, other cells are needed to assume the role of the destroyed odontoblasts. Growth factors, especially TGF-β,[62] are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp.[63] Reparative dentin is produced at an average of 1.5 μm/day, but can be increased to 3.5 μm/day. The resulting dentin contains irregularly-shaped dentinal tubules which may not line up with existing dentinal tubules. This dimishes the ability for dental caries to progress within the dentinal tubules.

Treatment

 
An amalgam used as a restorative material in a tooth.

Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level.[1] For the small lesions, topical fluoride is sometimes used to encourage remineralization. For larger lesions, the progression of dental caries can be stopped by treatment. The goal of treatment is to preserve tooth structures and prevent further destruction of the tooth.

Generally, early treatment is less painful and less expensive than treatment of extensive decay. Anesthetics — local, nitrous oxide ("laughing gas"), or other prescription medications — may be required in some cases to relieve pain during or following treatment or to relieve anxiety during treatment.[64] A dental handpiece ("drill") is used to remove large portions of decayed material from a tooth. A spoon is a dental instrument used to remove decay carefully and is sometimes employed when the decay in dentin reaches near the pulp.[65] Once the decay is removed, the missing tooth structure requires a dental restoration of some sort to return the tooth to functionality and aesthetic condition.

Restorative materials include dental amalgam, composite resin, porcelain, and gold.[66] Composite resin and porcelain can be made to match the color of a patient's natural teeth and are thus used more frequently when aesthetics are a concern. Composite restorations are not as strong as dental amalgam and gold; some dentists consider the latter as the only advisable restoration for posterior areas where chewing forces are great.[67] When the decay is too extensive, there may not be enough tooth structure remaining to allow a restorative material to be placed within the tooth. Thus, a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.

 
A tooth with extensive caries eventually requiring extraction.

In certain cases, root canal therapy may be necessary for the restoration of a tooth.[68] Root canal therapy, also called "endodontic therapy", is recommended if the pulp in a tooth dies from infection by decay-causing bacteria or from trauma. During a root canal, the pulp of the tooth, including the nerve and vascular tissues, is removed along with decayed portions of the tooth. The canals are instrumented with endodontic files to clean and shape them, and they are then usually filled with a rubber-like material called gutta percha.[69] The tooth is filled and a crown can be placed. Upon completion of a root canal, the tooth is now non-vital, as it is devoid of any living tissue.

An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is performed if the tooth is too far destroyed from the decay process to effectively restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause further problems in the future, as may be the case for wisdom teeth.[70] Extractions may also be preferred by patients unable or unwilling to undergo the expense or difficulties in restoring the tooth.

Prevention

 
Toothbrushes are commonly used to clean teeth.

Oral hygiene

Personal hygiene care consists of proper brushing and flossing daily.[8] The purpose of oral hygiene is to minimize any etiologic agents of disease in the mouth. The primary focus of brushing and flossing is to remove and prevent the formation of plaque. Plaque consists mostly of bacteria.[71] As the amount of bacterial plaque increases, the tooth is more vulnerable to dental caries. A toothbrush can be used to remove plaque on most surfaces of the teeth except for areas between teeth. When used correctly, dental floss removes plaque from areas which could otherwise develop proximal caries. Other adjunct hygiene aids include interdental brushes, water picks, and mouthwashes.

Professional hygiene care consists of regular dental examinations and cleanings. Sometimes, complete plaque removal is difficult, and a dentist or dental hygienist may be needed. Along with oral hygiene, radiographs may be taken at dental visits to detect possible dental caries development in high risk areas of the mouth.

Dietary modification

For dental health, the frequency of sugar intake is more important than the amount of sugar consumed.[44] In the presence of sugar and other carbohydrates, bacteria in the mouth produce acids which can demineralize enamel, dentin, and cementum. The more frequently teeth are exposed to this environment, the more likely dental caries are to occur. Therefore, minimizing snacking is recommended, since snacking creates a continual supply of nutrition for acid-creating bacteria in the mouth. Also, chewy and sticky foods (such as dried fruit or candy) tend to adhere to teeth longer, and consequently are best eaten as part of a meal. Brushing the teeth after meals is recommended. For children, the American Dental Association and the European Academy of Paediatric Dentistry recommend limiting the frequency of consumption of drinks with sugar, and not giving baby bottles to infants during sleep.[72][73] Mothers are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the mother's mouth.[74]

It has been found that milk and certain kinds of cheese like cheddar can help counter tooth decay if eaten soon after the consumption of foods potentially harmful to teeth.[44] Also, chewing gum containing xylitol (wood sugar) is widely used to protect teeth in some countries, being especially popular in the Finnish candy industry.[75] Xylitol's effect on reducing plaque is probably due to bacteria's inability to utilize it like other sugars.[76] Chewing and stimulation of flavour receptors on the tongue are also known to increase the production and release of saliva, which contains natural buffers to prevent the lowering of pH in the mouth to the point where enamel may become demineralised.[77]

 
Common dentistry trays used to deliver fluoride.

Other preventive measures

The use of dental sealants is a good means of prevention. Sealants are thin plastic-like coating applied to the chewing surfaces of the molars. This coating prevents the accumulation of plaque in the deep grooves and thus prevents the formation of pit and fissure caries, the most common form of dental caries. Sealants are usually applied on the teeth of children, shortly after the molars erupt. Older people may also benefit from the use of tooth sealants, but their dental history and likelihood of caries formation are usually taken into consideration.

Fluoride therapy is often recommended to protect against dental caries. It has been demonstrated that water fluoridation and fluoride supplements decrease the incidence of dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite crystals in enamel.[78] The incorporated fluoride makes enamel more resistant to demineralization and, thus, resistant to decay.[79] Topical fluoride is also recommended to protect the surface of the teeth. This may include a fluoride toothpaste or mouthwash. Many dentists include application of topical fluoride solutions as part of routine visits.

Furthermore, recent research shows that low intensity laser radiation of argon ion lasers may prevent the susceptibility for enamel caries and white spot lesions.[80] Also, as bacteria are a major factor contributing to poor oral health, there is currently research to find a vaccine for dental caries. As of 2004, such a vaccine has been successfully tested on non-human animals,[81] and is in clinical trials for humans as of May 2006.[82]


Catatan kaki dan sumber

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