Dental Fluorosis

Dental fluorosis is a common disorder, characterized by hypomineralization of tooth enamel caused by ingestion of excessive fluoride during enamel formation.

It appears as a range of visual changes in enamel causing degrees of intrinsic tooth discoloration, and, in some cases, physical damage to the teeth. The severity of the condition is dependent on the dose, duration, and age of the individual during the exposure. The "very mild" (and most common) form of fluorosis, is characterized by small, opaque, "paper white” areas scattered irregularly over the tooth, covering less than 25% of the tooth surface. In the "mild" form of the disease, these mottled patches can involve up to half of the surface area of the teeth. When fluorosis is moderate, all of the surfaces of the teeth are mottled and teeth may be ground down and brown stains frequently "disfigure" the teeth. Severe fluorosis is characterized by brown discoloration and discrete or confluent pitting; brown stains are widespread and teeth often present a corroded-looking appearance.

People with fluorosis are relatively resistant to dental caries (tooth decay caused by bacteria), although there may be cosmetic concern. In moderate to severe fluorosis, teeth are weakened and suffer permanent physical damage.

DIAGNOSIS
The adequate diagnosis of fluorosis can be diagnosed by visual clinical examination. This requires inspection of dry and clean tooth surfaces under a good lighting. There are individual variations in clinical fluorosis manifestation which are highly dependent on the duration, timing, and dosage of fluoride exposure.There are different classifications to diagnose the severity based on the appearances. The clinical manifestation of mild dental fluorosis is mostly characterised a snow flaking appearance that lack a clear border, opaque, white spots, narrow white lines following the perikymata or patches as the opacities may coalesce with an intact, hard and smooth enamel surface on most of the teeth. With increasing severity, the subsurface enamel, all along the tooth becomes more porous. Enamel may appear yellow/ brown discolouration and/ or many and pitted white-brown lesions that look like cavities. They are often described as “mottled teeth”. Fluorosis does not cause discolouration to the enamel directly, as upon eruption into the mouth, affected permanent teeth are not discoloured yet. In dental enamel, fluorosis causes subsurface porosity or hypomineralizations, which extend toward the dentinal-enamel junction as severity increases. Hence, affected teeth are more susceptible to staining. Due to diffusion of exogenous ions (ex, iron and copper), the stains would develop into the abnormally porous enamel.

The differential diagnosis for this condition includes:

1. Turner's hypoplasia (although this is usually more localized)
2. Enamel defects caused by an undiagnosed and untreated celiac disease.
3. Some mild forms of amelogenesis imperfecta and enamel hypoplasia
4. Enamel defects caused by infection of a primary tooth predecessor
5. Dental caries: Fluorosis-resembling enamel defects are often misdiagnosed as dental caries.
6. Dental Trauma: Mechanical trauma to the primary tooth may cause disturbance to the maturation phase of enamel formation, which may result in enamel opacities on the permanent successors.

Classification

Severe fluorosis: brown discolored and mottled enamel of an individual from a region with high levels of naturally occurring fluoride.

Severe fluorosis: the enamel is pitted and discolored

The two main classification systems are described below. Others include the tooth surface fluorosis index (Horowitz et al. 1984), which combines Deans index and the TF index; and the fluorosis risk index (Pendrys 1990), which is intended to define the time at which fluoride exposure occurs, and relates fluorosis risk with tooth development stage.

Dean's index

Dean's fluorosis index was first published in 1934 by H. Trendley Dean. The index underwent two changes, appearing in its final form in 1942. An individual's fluorosis score is based on the most severe form of fluorosis found on two or more teeth.

Classification	Code	Criteria – description of enamel
Normal	0	The enamel represents the usual translucent semivitriform (glass-like) type of structure. The surface is smooth, glossy and usually of pale creamy white color
Questionable	1	The enamel discloses slight aberrations from the translucency of normal enamel, ranging from a few white flecks to occasional white spots. This classification is utilised in those instances where a definite diagnosis is not warranted and a classification of ‘normal’ not justified
Very Mild	2	Small, opaque, paper white areas scattered irregularly over the tooth but not involving as much as approximately 25% of the tooth surface. Frequently included in this classification are teeth showing no more than about 1 – 2mm of white opacity at the tip of the summit of the cusps, of the bicuspids or second molars.
Mild	3	The white opaque areas in the enamel of the teeth are more extensive but do involve as much as 50% of the tooth.
Moderate	4	All enamel surfaces of the teeth are affected and surfaces subject to attrition show wear. Brown stain is frequently a disfiguring feature
Severe	5	All enamel surfaces are affected and hypoplasia is so marked that the general form of the tooth may be affected. The major diagnostic sign of this classification is discrete or confluent pitting. Brown stains are widespread and teeth often present a corroded-like appearance.

TF index

Proposed by Thylstrup and Fejerskov in 1978, the TF index represents a logical extension of Dean's index, incorporating modern understanding of the underlying pathology of fluorosis. It scores the spectrum of fluorotic changes in enamel from 0 to 9, allowing more precise definition of mild and severe cases.

Causes

Dental fluorosis is caused by a higher than normal amount of fluoride ingestion whilst teeth are forming. Primary dentine fluorosis and enamel fluorosis can only happen during tooth formation, so fluoride exposure occurs in childhood. Enamel fluorosis has a white opaque appearance which is due to the surface of the enamel being hypomineralised.

The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition (the adult teeth). The period when these teeth are at highest risk of developing fluorosis is between when the child is born up to 6 years old, though there has been some research which proposes that the most crucial course is during the first 2 years of the child's life. From roughly 7 years old thereafter, most children's permanent teeth would have undergone complete development (except their wisdom teeth), and therefore their susceptibility to fluorosis is greatly reduced, or even insignificant, despite the amount of intake of fluoride. The severity of dental fluorosis depends on the amount of fluoride exposure, the age of the child, individual response, weight, degree of physical activity, nutrition, and bone growth. Individual susceptibility to fluorosis is also influenced by genetic factors.

Many well-known sources of fluoride may contribute to overexposure including dentifrice/fluoridated mouthrinse (which young children may swallow), excessive ingestion of fluoride toothpaste, bottled waters which are not tested for their fluoride content, inappropriate use of fluoride supplements, ingestion of foods especially imported from other countries, and public water fluoridation. The last of these sources is directly or indirectly responsible for 40% of all fluorosis, but the resulting effect due to water fluoridation is largely and typically aesthetic. Severe cases can be caused by exposure to water that is naturally fluoridated to levels above the recommended levels, or by exposure to other fluoride sources such as brick tea or pollution from high fluoride coal.

Dental fluorosis has been growing in the United States concurrent with fluoridation of municipal water supplies, although disproportionately by race. A 2010 CDC report acknowledges an overall incidence of dental fluorosis of 22% from 1986-87 increased to 41% in the early 21st century, with an increase in moderate to severe dental fluorosis from 1% to 4%. The 2011-12 NHANES figures documented another 31% overall increase among American teens since the previous decade, with a total adolescent population impact of 61% afflicted. More than one in five American teens (23%) have moderate to severe dental fluorosis on at least two teeth.

Mechanism

Teeth are the most studied body tissues to examine the impact of fluoride to human health. There are a few possible mechanisms that have been proposed. It is generally believed that the hypomineralization of affected enamel is mainly due to in-situ toxic effects of the fluoride on the ameloblasts in the enamel formation, and not caused by the general effects of fluoride on the calcium metabolism, or by the poisoning effects that suppress the fluoride metabolism. However, despite decades of research and studies, there have yet to be any studies that substantiates the believed mechanism whereby dental fluorosis is a result of alteration in the mineralisation that takes place when fluroide interacts with mineralising tissues.

In the extra-cellular environment of maturing enamel, an excess of fluoride ions alters the rate at which enamel matrix proteins (amelogenin) are enzymatically broken down and the rate at which the subsequent breakdown products are removed. Fluoride may also indirectly alter the action of protease via a decrease in the availability of free calcium ions in the mineralization environment. This results in the formation of enamel with less mineralization. This hypomineralized enamel has altered optical properties and appears opaque and lusterless relative to normal enamel.

Traditionally severe fluorosis has been described as enamel hypoplasia, however, hypoplasia does not occur as a result of fluorosis. The pits, bands, and loss of areas of enamel seen in severe fluorosis are the result of damage to the severely hypomineralized, brittle and fragile enamel which occurs after they erupt into the mouth.

Hydroxyapatite is converted to fluorohydroxyapatite as follows:

Dental fluorosis can be prevented at a population level through defluoridation. It is the downward adjustment of the level of fluoride in drinking water.

Management

Dental fluorosis may or may not be of cosmetic concern. In some cases, there may be varying degrees of negative psychosocial effects. The treatment options are:

• Mild cases: Tooth bleaching
• Moderate cases: Micro-abrasion (outer affected layer of enamel is abraded in an acidic environment)
• Severe cases: Composite fillings, Micro-abrasion, Veneers, Crowns

Epidemiology

Fluorosis is extremely common, with 41% of adolescents having definite fluorosis, and another 20% "questionably" having fluorosis according to the Centers for Disease Control. As of 2005 surveys conducted by the National Institute of Dental and Craniofacial Research in the USA between 1986 and 1987 and by the Center of Disease Control between 1999 and 2004 are the only national sources of data concerning the prevalence of dental fluorosis. Before the 1999-2004 study was published, CDC published an interim report covering data from 1999 to 2002.

CDC findings on children and adolescents

Deans Index	2002
Questionable fluorosis	11.5%
Very mild fluorosis	21.68%
Mild fluorosis	6.59%
Moderate to severe fluorosis	3.26%
Total confirmed fluorosis prevalence	31.65%
Total confirmed and questionable fluorosis prevalence	43.15%

The U.S. Centers for Disease Control found a 9 percentage point increase in the prevalence of confirmed dental fluorosis in a 1999-2002 study of American children and adolescents than was found in a similar survey from 1986-1987 (from 22.8% in 1986-1987 to 32% in 1999-2002). In addition, the survey provides further evidence that African Americans suffer from higher rates of fluorosis than Caucasian Americans.

The condition is more prevalent in rural areas where drinking water is derived from shallow wells or hand pumps.[citation needed] It is also more likely to occur in areas where the drinking water has a fluoride content greater than 1 ppm (part per million).

Age group	Reference weight kg (lb)	Adequate intake (mg/day)	Tolerable upper intake (mg/day)
Infants 0–6 months	7 (16)	0.01	0.7
Infants 7–12 months	9 (20)	0.5	0.9
Children 1–3 years	13 (29)	0.7	1.3
Children 4–8 years	22 (48)	1.0	2.2
Children 9–13 years	40 (88)	2.0	10
Boys 14–18 years	64 (142)	3.0	10
Girls 14–18 years	57 (125)	3.0	10
Males 19 years and over	76 (166)	4.0	10
Females 19 years and over	61 (133)	3.0	10

If the water supply is fluoridated at the level of 1 ppm, one must consume one litre of water in order to take in 1 mg of fluoride. It is thus improbable a person will receive more than the tolerable upper limit from consuming optimally fluoridated water alone.

Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste, consuming food with a high fluoride content, or consuming fluoride supplements. The use of fluoride supplements as a prevention for tooth decay is rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early 1990s.

In November 2006 the American Dental Association published information stating that water fluoridation is safe, effective and healthy; that enamel fluorosis, usually mild and difficult for anyone except a dental health care professional to see, can result from ingesting more than optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix infant formula; and that the probability of babies developing fluorosis can be reduced by using ready-to-feed infant formula or using water that is either free of fluoride or low in fluoride to prepare powdered or liquid concentrate formula. They go on to say that the way to get the benefits of fluoride but minimize the risk of fluorosis for a child is to get the right amount of fluoride, not too much and not too little. "Your dentist, pediatrician or family physician can help you determine how to optimize your child’s fluoride intake."

PREVENTION

Dental fluorosis can be prevented by lowering the amount of fluoride intake to below the tolerable upper limit. The number of cases of dental fluorosis occurring in a population could be reduced by defluoridation drinking water. However, there are other sources of fluoride such as fluoride containing toothpastes. Also, defluoridation of water will not reverse the condiiton in an individual once exposure to excessive levels of fluoride during the years of tooth enamel formation has already occurred.

History

In ancient times, Galen describes what is thought to be dental fluorosis. However, it was not until the early 20th century that dental fluorosis became increasingly recognized and scientifically studied.

In 1901 Eager published the first description of the "mottled enamel" of immigrants from a small village near Naples, Italy. He writes that the condition is called "Denti di Chiaie" (Chiaie teeth), named after Stefano Chiaie, an Italian professor. In the United States of America, a dentist, Frederick McKay, set up practice in Colorado Springs in 1901 and discovered a high proportion of the residents had stained teeth, locally termed the "Colorado brown stain". He took this information to Greene Vardiman Black, a prominent American dentist of the time. After examining specimens of affected enamel, in 1916 Black described the condition as "[a]n endemic imperfection of the enamel of the teeth, heretofore unknown in the literature of dentistry." They made the interesting observation that although the mottled enamel was hypomineralized, and therefore should be more susceptible to decay, this was not the case.Gradually, they became aware of existing and further reports of a similar condition worldwide.

In 1931, 3 different groups of scientists around the world published their discoveries that this condition was caused by fluoride in drinking water during childhood. The condition then started to become termed "dental fluorosis". Through epidemiological studies in the US, Henry Trendley Dean helped to identify a causal link between high concentrations of fluoride in the drinking water and mottled enamel. He also produced a classification system for dental fluorosis that is still used in modern times, Dean's Index. As research continued, the protective effect of fluoride against dental decay was demonstrated.

References:

1.  Dean JA (10 August 2015). McDonald and Avery's Dentistry for the Child and Adolescent (10th ed.). Elsevier Health Sciences. p. 132. ISBN 978-0-323-28746-3.
2.  Neville BW, Chi AC, Damm DD, Allen CM (13 May 2015). Oral and Maxillofacial Pathology (4th ed.). Elsevier Health Sciences. pp. 52–54. ISBN 978-1-4557-7052-6.
3.  Wong MC, Glenny AM, Tsang BW, Lo EC, Worthington HV, Marinho VC (January 2010). "Topical fluoride as a cause of dental fluorosis in children". The Cochrane Database of Systematic Reviews (1): CD007693. doi:10.1002/14651858.CD007693.pub2. PMID 20091645.
4.  Bergc JH, Slayton RL (26 October 2015). Early Childhood Oral Health. John Wiley & Sons. p. 113. ISBN 978-1-118-79210-0.
5.  Meiers P. "HT Dean´s epidemiology of Mottled Teeth". The History of Fluorine, Fluoride and Fluoridation. Retrieved 12 November 2015.
6.  Whelton H, Browne D, Felicia P, Whelton J. "E-training for Dean's Index Version 2". Oral Health Services Research Centre, University College Cork, Ireland. Retrieved 12 November 2015.
7.  Abanto Alvarez J, Rezende KM, Marocho SM, Alves FB, Celiberti P, Ciamponi AL (February 2009). "Dental fluorosis: exposure, prevention and management" (PDF). Medicina Oral, Patologia Oral Y Cirugia Bucal. 14 (2): E103–7. PMID 19179949.
8.  Ritter AV (2005). "Dental fluorosis". Journal of Esthetic and Restorative Dentistry. 17 (5): 326–7. doi:10.1111/j.1708-8240.2005.tb00139.x. PMID 16225799.
9.  Dental Enamel Defects and Celiac Disease Archived March 5, 2016, at the Wayback Machine National Institute of Health (NIH)
10.  Sabokseir A, Golkari A, Sheiham A (2016-02-25). "Distinguishing between enamel fluorosis and other enamel defects in permanent teeth of children". PeerJ. 4: e1745. doi:10.7717/peerj.1745. PMC 4782718. PMID 26966672.
11.  Skaare AB, Maseng Aas AL, Wang NJ (April 2013). "Enamel defects in permanent incisors after trauma to primary predecessors: inter-observer agreement based on photographs". Dental Traumatology. 29 (2): 79–83. doi:10.1111/j.1600-9657.2012.01153.x. PMID 22676308.
12.  Fejerskov O, Kidd E (16 March 2009). Dental Caries: The Disease and Its Clinical Management. John Wiley & Sons. pp. 299–327. ISBN 978-1-4443-0928-7.
13.  Wagner BM (1993). Health effects of ingested fluoride. Washington, D.C. : National Academy Press. p. 171. ISBN 9786610211333.
14.  Denbesten P, Li W (2011). "Chronic fluoride toxicity: dental fluorosis". Monographs in Oral Science. Monographs in Oral Science. 22: 81–96. doi:10.1159/000327028. ISBN 978-3-8055-9659-6. PMC 3433161. PMID 21701193.
15.  Hong L, Levy SM, Broffitt B, Warren JJ, Kanellis MJ, Wefel JS, Dawson CV (2006). "Timing of fluoride intake in relation to development of fluorosis on maxillary central incisors". Community Dentistry and Oral Epidemiology. 34 (4): 299–309. doi:10.1111/j.1600-0528.2006.00281.x. PMID 16856950.
16.  Buzalaf MAR, Levy SM (2011): Fluoride intake of children: considerations for dental caries and dental fluorosis in Fluoride and the Environment. Editor: MAR Buzalaf, Karger, Basel. Pages 1-19
17.  "Dental Fluorosis" (PDF).
18.  Abanto Alvarez J, Rezende KM, Marocho SM, Alves FB, Celiberti P, Ciamponi AL (February 2009). "Dental fluorosis: exposure, prevention and management" (PDF). Medicina Oral, Patologia Oral Y Cirugia Bucal. 14 (2): E103–7. PMID 19179949.
19.  Clark MB, Slayton RL (September 2014). "Fluoride use in caries prevention in the primary care setting". Pediatrics. 134 (3): 626–33. doi:10.1542/peds.2014-1699. PMID 25157014.
20.  United States Environmental Protection Agency (2010). "Comment-Response Summary Report for the Peer Review of the Fluoride: Dose-Response Analysis for Non-Cancer Effects Document". Lay summary (PDF) – EPA (2010).
21.  Yeung CA (2008). "A systematic review of the efficacy and safety of fluoridation". Evidence-Based Dentistry. 9 (2): 39–43. doi:10.1038/sj.ebd.6400578. PMID 18584000. Lay summary (PDF) – NHMRC (2007).
22.  Fawell J, Bailey K, Chilton J, Dahi E, Fewtrell L, Magara Y (2006). "Environmental occurrence, geochemistry and exposure". Fluoride in Drinking-water (PDF). World Health Organization. pp. 5–27. ISBN 92-4-156319-2. Retrieved 2009-01-24.
23.  Beltrán-Aguilar ED et al. Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis --- United States, 1988--1994 and 1999–2002. CDC MMWR. August 26, 2005 / 54(03);1-44. https://www.cdc.gov/mmwr/preview/mmwrhtml/ss5403a1.htm
24.  Beltrán-Aguilar, E. D; Barker, L; Dye, B. A (2010). "Prevalence and severity of dental fluorosis in the United States, 1999-2004" (PDF). NCHS data brief (53): 1–8. PMID 21211168.
25.  Wiener, R. C; Shen, C; Findley, P; Tan, X; Sambamoorthi, U (2018). "Dental Fluorosis over Time: A comparison of National Health and Nutrition Examination Survey data from 2001-2002 and 2011-2012". Journal of dental hygiene : JDH. 92 (1): 23–29. PMC 5929463. PMID 29500282.
26.  Aoba, T; Fejerskov, O (2016). "Dental Fluorosis: Chemistry and Biology". Critical Reviews in Oral Biology & Medicine. 13 (2): 155–70. doi:10.1177/154411130201300206. PMID 12097358.
27.  "Archived copy" (PDF). Archived (PDF) from the original on 2016-06-16. Retrieved 2011-04-26.
28.  Fluoridation Facts (PDF). American Dental Association. 2005. p. 29.
29.  "Table 23, Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis --- United States, 1988--1994 and 1999--2002". Centers for Disease Control and Prevention. 2005. Retrieved 2006-10-29.
30.  Frequently Asked Questions (FAQ), American Dental Association Website accessed February 4, 2012 Archived January 12, 2016, at the Wayback Machine
31.  Eager JM (November 1, 1901). "Denti di Chiaie (Chiaie teeth)". Public Health Reports. 16 (44): 2576–2577. Reprinted in "Public Health Reports, November 1, 1901: Denti di Chiaie (Chiaie teeth), by J.M. Eager". Public Health Reports. 91 (3): 284–5. 1976. PMC 1438998. PMID 818673.
32.  Velu H, Balozet L (1931). "Reproduction experimentale chez Ie mouton de la dystrophie dentaire des animaux des zones phosphates". Bull Acad Vet France. 4: 373.
33.  Churchill HV (1931). "Occurrence of fluorides in some water of the United States". Ind Eng Chem. 23 (9): 996–998. doi:10.1021/ie50261a007.
34.  Smith MC, Lantz EM, Smith HV (September 1931). "THE CAUSE OF MOTTLED ENAMEL". Science. 74 (1914): 244. Bibcode:1931Sci....74..244C. doi:10.1126/science.74.1914.244. PMID 17755565.
35.  Teotia SP (1999). "Dental fluorosis" (PDF). The National Medical Journal of India. 12 (3): 96–8. PMID 10492579. Archived from the original (PDF) on 2016-03-04.

Source: https://en.wikipedia.org/wiki/Dental_fluorosis

What is Root Canal Treatment (RCT)? Why do I need to Do RCT?

Root canal Treatment, a sophisticated term as it may seem to the general public, is the treatment done to a tooth with severe decay to such an extent that it has already involved the innermost pulpal layer of the tooth. It is not to be feared as many people do and have negative emotions attached to the term as well as the procedure.


The tooth is a mineralized tissue of the body, which once formed completely, doesn't regenerate if it is lost due to caries or is broken. The tooth tissue once lost due to demineralization and cavitation will not be restored unless some inert and biocompatible material is filled into the cavity after removing the decayed portion and the causative bacteria from the lesion.

The tooth decay which begins as a pit and fissure caries at first is reversible and can be arrested if a favorable environment for remineralization is provided. The initial carious lesion involving enamel only or superficial layer of dentin can be restored with Glass Ionomer Cements or Dental Composite Restorative resins by simply preparing a cavity of adequate shape and size for the restorative material to remain there and function properly for a long time. If the decay is to that extent that it involves the pulp, simply filling the cavity  will not eliminate the pain and halt the carious process. So, the pulpal tissue within the crown portion of tooth (the part of tooth that is seen clinically) as well as from the root canal. The canal should be cleaned up to clear all the bacteria and the root canal should be shaped and enlarged such that it can receive an inert filler into it (gutta percha) and then it can be restored to function as a normal tooth.

Root canal treatment is the best option to treat irreversible pulpitis and conserves natural tooth structure because:
- Artificial prostheses are not as good as natural dentition however close they may resemble it
- The patient doesn't have to undergo extraction (invasive procedure much feared  by patients) and the need for prosthesis
- Cost of treatment is cheaper and the tooth becomes functional very early.

Hence, Root canal treatment is the best treatment plan for your severely painful tooth in which the caries has already reached upto pulp but that can be saved via endodontic treatment.

# Gingiva is attached to tooth by:

# Gingiva is attached to tooth by:

A. Epithelial attachment

B. Periodontal Ligament

C. Connective tissue fibers

D. Lamina Propria

Answer: A, Epithelial Attachment

- Gingiva is attached to tooth by Junctional Epithelium which forms a collar around the tooth. It is wider (15-30 cells thick) at the floor of the gingival sulcus and tapers apically to a final thickness of some 3-4 cells. 

- Surface cells of the junctional epithelium provide the actual attachment of gingiva to tooth tissue (the epithelium being sometimes referred to as attachment epithelium)

- The internal basal lamina of Junctional epithelium unites the epithelium to tooth whereas the external basal lamina of junctional epithelium unites the epithelium to the connective tissue of the gingiva. 

- Basal lamina of junctional epithelium is devoid of type IV collagen and type VIII is present.

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Types of Cementum / Classification of Cementum

Schroeder has classified Cementum as follows:

A. Acellular Afibrillar Cementum (AAC)
- Contains neither cells nor extrinsic or intrinsic collagen fibers apart from a mineralized ground substance
- It is a product of cementoblasts
- In humans, it is found in the coronal cementum

B. Acellular Extrinsic Fiber Cementum (AEFC)
- It is composed entirely of densely packed bundles of Sharpey's fibers and lacks cells.
- It is a product of fibroblasts and cementoblasts
- In humans, it is found in the cervical 1/3rd of roots but may extend further apically


C. Cellular Mixed Stratified Cementum (CMSC)
- It is composed of extrinsic (Sharpey's) and predominantly intrinsic fibers and contains cells
- It is coproduct of fibroblasts and cementoblasts
- In humans, it appears primarily in the apical third of the roots and the apices and in the furcation areas

D. Cellular Intrinsic Fiber Cementum (CIFC)
- Contains cells but no collagen fibers
- It is formed by cementoblasts.
- In humans, it fills resorption lacunae.

# Width of attached gingiva:

# Width of attached gingiva:
A. Decreases with age
B. Increases with age
C. Remains the same
D. Is not age-related

Answer:
B. Increases with age


Because the mucogingival junction remains stationary throughout adult life, changes in the width of attached gingiva are caused by the modification in the position of the coronal end.

The width of attached gingiva increases with age and in supraerupted teeth, with the wear of the incisal edge and continued tooth eruption. The gingival margin of the tooth, therefore the entire dentogingival complex, moves coronally with a resulting increase in width of the attached gingiva.

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How Long Do Dental Restorations Last?

This is one of the most frequently faced questions by a dentist, "Doctor, How long will my dental restoration last?" In the competitive world of today, people are taken away by the fake promises and guarantees the corporations and manufacturer companies make and expect everything to have a guarantee. But, this question, in particular, is ridiculous because we cannot predict the health or disease of any person or how long will he last!

But, answering the  question, the life of any dental restoration depends principally upon four factors:
- remaining tooth structure
- material with which the tooth is being restored
- clinical technique & expertise of the dentist i.e. how well the restoration is done
- post-restoration environmental challenges the tooth is subjected to

Let's see all these one by one.

i) Remaining tooth structure

"A stitch in time saves nine." This age-old proverb can be well realized in dentistry. We can expect the dental restorations' cost to be cheaper, less time consuming and successful for a long time too if the treatment is done as early as possible. We cannot expect a tooth with cavity extending up to the cervical third of crown involving pulp with almost two-thirds of the crown lost already to have the same prognosis as that of the tooth with cavity extending only up to the enamel layer or superficial dentinal layer.

A restoration may fail due to several reasons:
No 1. - Restoration may fracture if its bulk is too small or its mechanical strength is too low.
No 2. - The tooth may fracture if most of the tooth structure is already lost or excessive occlusal force is applied on the restored tooth.
No. 3 - Failure at the tooth restoration junction: If there is no proper seal at the tooth restoration junction, the food materials, and bacteria can percolate through the breach into the tooth and can cause secondary caries.


Let's see the second factor determining the life of dental restoration.

ii) Material with which the tooth is being restored :

Three major dental restorative materials currently used in dentistry are: 

- Glass ionomer cement

- Dental composite resins

- Amalgams (not used in many countries but still used in some due to the environmental hazard of mercury)

Different types of glass ionomer cement according to their use are available. Glass ionomers are used mostly in the deciduous teeth of children but they can be used adults too and latest GICs with improved properties have been reported to last about 3-5 years too.

Regarding dental composite resins and amalgams, they have similar strength and longevity provided that, the restoration is done meticulously in ideal conditions.

A rule of thumb for clinical service of restoration is that occlusal restorations are stressed an average of one million times per year. And, typically material fails in the range of 10-100 million cycle range during laboratory testing. 

Also, different products from different manufacturers have different mechanical properties. You cannot expect a composite resin from some unknown manufacturer in China to work equally well as that from an internationally renowned brand. 

The third factor determining the longevity of restoration is the clinical technique and expertise. 

iii) How well the dentist has restored the tooth?

Just because the dentist is old and experienced doesn't mean that he will do the restoration well. A dentist who can do well, may not do his best at all times if he is inattentive or is in a hurry. Improper isolation of tooth and contamination by saliva during the procedure also might have compromised the strength. 

And the last and most important factor for the longevity of dental restorations is:

iv) Post-restoration environmental challenges the tooth is subject to

How long would your house last if it were subjected to hot sweet coffee and immediately to freezing cold ice cream? How long would it last if it were struck for about 5000 times daily? What if it is subjected to acidic pH as low as 3 and to alkaline pH as high as 11 within a few minutes? That is what our dental restoration has to sustain. We eat and drink acidic and alkaline foods, hard and soft foods, cold and hot foods, every sort of food without any consideration. How long will it be before the material fatigue occurs in the restoration and breaks down?

By now, you might have understood what I mean to say. But it is a safe bet to say that dental restorations will last about an average of 6-8 years if all the above factors are considered. However, there are cases of restoration failures the very next day as well as some amalgam restorations about 30 years old.

How long has your restoration lasted? What was the material? Please Comment Below for record purpose. Feedback and Suggestions for the article are heartily welcome.

What is Halal Food? - FAO Guidelines for Halal Food

GENERAL GUIDELINES FOR USE OF THE TERM “HALAL”

CAC/GL 24-1997[27]

The Codex Alimentarius Commission accepts that there may be minor differences in opinion in the interpretation of lawful and unlawful animals and in the slaughter act, according to the different Islamic Schools of Thought. As such, these general guidelines are subjected to the interpretation of the appropriate authorities of the importing countries. However, the certificates granted by the religious authorities of the exporting country should be accepted in principle by the importing country, except when the latter provides justification for other specific requirements.


1 SCOPE

1.1 These guidelines recommend measures to be taken on the use of Halal claims in food labeling.

1.2 These guidelines apply to the use of the term halal and equivalent terms in claims as defined in General Standard for the Labelling of Prepackaged Foods and include its use in trademarks, brand names and business names.

1.3 These guidelines are intended to supplement the Codex General Guidelines on Claims and do not supersede any prohibition contained therein.

2 DEFINITION

2.1 Halal Food means food permitted under Islamic Law and should fulfill the following conditions:

2.1.1 does not consist of or contain anything which is considered to be unlawful according to Islamic Law;