text:
El Vato
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El Vato
Genre
Biographical
Created by
Jorge Dorantes
Screenplay by
José Ramón Menéndez
Ana Sofía Clerici
José Miguel Núñez
Augusto Mendoza
Directed by
Javier Solar
Starring
El Dasa
Cristina Rodlo
Gustavo Egelhaaf
Ricardo Polanco
Music by
El Dasa
Country of origin
United States
Original language(s)
Spanish
No. of seasons
2
No. of episodes
23 (list of episodes)
Production
Executive producer(s)
Patricia Morales Galindo
Alejandro Rincón
Bilai Joa Silar
Sergio Lazarov
Marcel Ferrer
Margie Moreno
Producer(s)
Sergio Guerrero
Cinematography
Andrés León Becker
Editor(s)
Mauricio Sariñana
Camera setup
Multi-camera
Running time
43 minutes[1]
Production company(s)
Boomdog Films
Endemol Shine International
Distributor
NBC Universal Television Distribution International
Release
Original network
NBC Universo
Picture format
HDTV 1080i
Audio format
Stereophonic sound
Original release
April 17, 2016 (2016-04-17) – present
El Vato is an American biographical television series based on the life of Mexican singer El Dasa and created by Endemol Shine International and Boomdog Films for NBC Universo.[2] The plot focuses of the story of Mexican singer El Vato and his friends in their attempt to triumph in the treacherous and seductive musical world of Los Angeles, California.[2] The series is starred El Dasa, Cristina Rodlo, Gustavo Egelhaaf and Ricardo Polanco.[3] The first season of the series was broadcast simultaneously by Telemundo and by NBC Universo.[4]
On May 19, 2016 NBC Universo renewed the series for a second season and premiered on August 27, 2017.[5][6]
Contents
[hide]
1 Synopsis
1.1 Season 1 (2016)
1.2 Season 2 (2017)
2 Cast
3 Episodes
3.1 Series overview
3.2 Season 1 (2016)
3.3 Season 2 (2017)
4 References
5 External links
Synopsis[edit]
Season 1 (2016)[edit]
El Vato offers you a unique opportunity in your life to record the next great album that will give you the leap to fame, but in return you have to leave your simple life in Sonora to live under the brightness of the lights of Los Angeles and try to stay focused in the midst of all the temptations of the big city. For El Vato, it's time to jump to stardom or go home.
Season 2 (2017)[edit]
The scripted-drama inspired by Regional Mexican singer El Dasa’s incredible real life story follows El Vato and his friends as they continue fighting for their dreams in Los Angeles in pursuit of a coveted spot in the Regional Mexican music world. After signing a contract, El Vato realizes he is trapped. Lolo Lozada (Horacio Castelo) the owner of his contract, only signed him to stop him from competing with other ‘norteño’ singers in his record label company. His friends, Mariana, (Cristina Rodlo), Brandon (Ricardo Polanco), and ‘El Pollo’ (Gustavo Egelhaaf) as usual will accompany him on his adventures but the journey to stardom will not be easy. El Vato will have to face people who want take him down, deal with new love affairs and do the impossible to continue moving forward with his friends.[7]
Cast[edit]
El Dasa as Miguel Cisneros / El Vato
Cristina Rodlo as Mariana Gaxiola
Gustavo Egelhaaf as El Pollo
Ricardo Polanco as Brandon
Itatí Cantoral as Wendy Lozada
Mauricio Martínez as Marcos Gutiérrez
Arcelia Ramírez as Doña Eli
Mónica Dionne as Jackie
Patricio Sebastián as El Vato child
Leonardo Daniel as Emiliano Galeana
Alejandro Calva as Don Jesús "Chucho" Durán
José María de Tavira as Rogelio Galeana
Luz Ramos as Roxana Sotomayor
Ana Bárbara as Herself
Paty Cantú as Herself
Antonio de la Vega as Leandro León
Sebastián Ferrat as Filiberto Cisneros
Mauricio Isaac as Germán Lozada
Giancarlo Vidrio as Joey
Episodes[edit]
Series overview[edit]
Season
Episodes
Originally aired
First aired
Last aired
1 10 April 17, 2016 (2016-04-17) June 19, 2016 (2016-06-19)
2 13[8] August 27, 2017 (2017-08-27)[6] November 26, 2017 (2017-11-26)
Season 1 (2016)[edit]
No.
overall
No. in
season
Title
Original air date
1
1 "El Wolf de Hollywood Hills" April 17, 2016 (2016-04-17)
At a party at his mansion in Hollywood Hills, El Vato is officially presented and faces the famous singer Marcos Gutierrez.
2
2 "Happy birthday Mr. Lobo" April 24, 2016 (2016-04-24)
El Vato and his compas learn that the recorder who signed them washes money; Decide to sneak into Lolo's birthday party to impress him.
3
3 "Movimiento Alternado" May 1, 2016 (2016-05-01)
Wendy does not answer El Vato's call, reason why he and his band look for to obtain a contract. The opportunity comes with the offer to compose a narcocorrido.
4
4 "¿Tienes talento?" May 8, 2016 (2016-05-08)
El Vato competes in a talent show where La Sultana del Norte is a judge, Lolo appears and makes the Vato tremble.
5
5 "Cougars, yeguas y video" May 15, 2016 (2016-05-15)
El Pollo gets a job for El Vato in the luxury ranch in which he works; El Vato proposes to sneak a music video to upload it to social networks.
6
6 "Secretos" May 22, 2016 (2016-05-22)
Vato ends up driving for Rogelio, the son of the legendary band singer Emiliano Galena, who has to endure his whims.
7
7 "El corrido de Chino Prison" May 29, 2016 (2016-05-29)
El Vato receives an offer from Wendy Lozada, who is already launching her own label. At the same time, El Vato is contacted by an acquaintance of his father from jail.
8
8 "El Vato vuelve a la cima" June 5, 2016 (2016-06-05)
El Vato finally signs with Lolo. And the American dream returns. El Vato and his band celebrate. Vato's dad asks for money he needs to pay bail and get out of jail.
9
9 "El Vato One on One" June 12, 2016 (2016-06-12)
A few months have passed and El Vato has gone from scandal to scandal and from party to party. He has his 15 minutes of fame by a shooting, but they say that the bad press does not exist.
10
10 "Nuestros premios, nuestra gente" June 19, 2016 (2016-06-19)
Awards are given to the best of the RMM and Vato discovers that there are no good shortcuts to success.
Season 2 (2017)[edit]
No.
overall
No. in
season
Title
Original air date
11
1 "El corrido de la fuga" August 27, 2017 (2017-08-27)
El Vato goes ahead after an accident in which he almost lost his life. Lolo continues to sabotage his career while his friends accompany him on a very peculiar film project.
12
2 "Baraja de oro" September 3, 2017 (2017-09-03)
El Vato participates in a game of clandestine poker next to his father. If they win, they can settle the debt with Lolo. When the "enturanch" gets involved, the mission gets complicated.
13
3 "Viral" September 10, 2017 (2017-09-10)
When El Vato discovers that his videos are achieving a large number of views on the internet and that will also generate profits, he decides to risk everything.
14
4 "Power of the people" September 17, 2017 (2017-09-17)
El Vato joins the tour in homage to Wendy and Lolo makes his life impossible. Marcos manages to earn points with Mariana and her friends.
15
5 "El contrato" October 1, 2017 (2017-10-01)
El Vato seeks legal help to get out of his ominous contract with Lolo. Filiberto convinces the Vato to sing a new song that he has composed for a very powerful narco.
16
6 "La jaula de oro" October 8, 2017 (2017-10-08)
Although the entourage manages El Vato to annul his contract with Lolo, happiness lasts little. They find that their work visas are no longer valid and must make a decision urgently.
17
7 "El hijo pródigo" October 15, 2017 (2017-10-15)
After losing their visas and the right to their artistic name, Vato, Pollo and Brandon return to Hermosillo. There, new professional opportunities arise and El Vato meets with an old love.
18
8 "El paraíso perdido" October 22, 2017 (2017-10-22)
Things in Hermosillo begin to work for El Vato. All the entourage, except Brandon, adapt to their life in Mexico but the shadow of Lolo chases after them and they must return to Los Angeles.
19
9 "Y volver, volver" October 29, 2017 (2017-10-29)
Vato, Pollo and Brandon try to return to the US to reach his dreams and confront Lolo, but his journey takes an unexpected turn. Lolo confesses to Estela his hidden past.
20
10 "Vato vs Vato" November 5, 2017 (2017-11-05)
Lolo finally plans to destroy Vato by throwing another singer with his stage name. The entourage decides to offer a free concert, but producing it will not be easy.
21
11 "Sonaron cuatro balazos" November 12, 2017 (2017-11-12)
Vato and his friends do everything possible to raise the funds they need for the concert. With this strategy they want to expose Lolo and his fake Vato.
22
12 "El que hierro mata..." November 19, 2017 (2017-11-19)
El Vato must respond to the press after the violent incidents that occurred during his concert and decides to reveal Lolo's secret about the murder of Wendy.
23
13 "El corrido de Miguel Cisneros" November 26, 2017 (2017-11-26)
El Vato finally wins the battle against Lolo and decides to open an independent label with his friends and his father, but an action by Filiberto complicates happiness.
References[edit]
Jump up ^ "El Vato (Serie de TV)". filmaffinity.com (in Spanish). Retrieved 28 May 2017.
^ Jump up to: a b "La serie "El Vato" protagonizada por el cantante mexicano "El Dasa" estrena en abril". semananews.com (in Spanish). Retrieved 28 May 2017.
Jump up ^ "'El Vato' inicia producción para su segunda temporada (FOTOS)". mundohispanico.com (in Spanish). Retrieved 28 May 2017.
Jump up ^ "NBC Universo y Telemundo transmitirán en simultáneo estreno de "El Vato"". tvboricuausa.com (in Spanish). Retrieved 28 May 2017.
Jump up ^ "El Dasa's 'El Vato' Gets Second Season on NBC Universo". billboard.com. Retrieved 28 May 2017.
^ Jump up to: a b "Segunda temporada serie El Vato". mastelenovelas.com (in Spanish). Retrieved 11 July 2017.
Jump up ^ Newswire, MultiVu - PR. "Universo's Original Scripted Series "El Vato" Returns With Second Season Premiere Set For Sunday, August 27 At 10pm/9c". Multivu. Retrieved 2017-07-19.
Jump up ^ "Así será la segunda temporada de El Vato". peopleenespanol.com (in Spanish). People en Español. Retrieved 11 July 2017.
External links[edit]
El Vato on IMDb
Retrieved from "https://en.wikipedia.org/w/index.php?title=El_Vato&oldid=833128876"
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Chewbacca Mask Lady
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Chewbacca Mask Lady
A still from the video
Starring
Candace Payne
Release date
May 19, 2016 (2016-05-19)
Running time
4 minutes
Chewbacca Mask Lady (also known as Chewbacca Mom) is an internet viral video[1][2][3][4] featuring 37-year-old Texas mother Candace Payne filming herself heartily laughing while wearing a Star Wars Chewbacca mask. The video was posted to Facebook with the description "It's the simple joys in life...." on May 19, 2016.[5]
Contents
[hide]
1 Reaction
2 Other videos
3 References
4 External links
Reaction[edit]
The video became so popular that Forbes reported that the mask sold out from every online retailer.[6] In response to the video, Kohl's, where the mask was purchased, rewarded Payne with about $2,500 in gift cards, Star Wars toys and 10,000 reward points.[7][8] On May 23, 2016, Holly Willoughby and Phillip Schofield wore the masks on This Morning.[9] On the same day, Payne was featured on Good Morning America. On the show, Hasbro rewarded her with more Star Wars toys.[10] Later that day, The Gregory Brothers uploaded an autotuned remix of the video.[11] Payne was later featured on The Late Late Show with James Corden with J. J. Abrams.[12] She was also featured on "The Star Wars Show" on the Star Wars official YouTube channel on May 25, 2016.[13] Additionally, Payne received $7,500 for a Memorial Day weekend visit at Disney's Hollywood Studios, $2,000 to attend the Fan Dallas Expo with Chewbacca actor Peter Mayhew, and $400,000 in scholarship money from Southeastern University, bringing the total value of her gift to more than $420,000 as of June 7, 2016.[14][15]
On May 24, 2016, she was invited by Mark Zuckerberg to visit the Facebook headquarters in California.[16] As of that date, the video had gathered over 140 million views on Facebook and was the most viewed Facebook Live video of all time.[11] The video also has over three million Facebook "reshares".[16]
Payne visited Hasbro headquarters with her family on June 19 and was presented with a "Chewbacca Mom" action figure. The body looks like Chewbacca but the head is a representation of Payne, including a removable Chewbacca mask; it also has 13 prerecorded phrases such as "That's not me making that noise, it's the mask," and "I am such a happy Chewbacca."[17]
Other videos[edit]
On July 9, 2016, Payne posted a video on Facebook of her cover of Michael Jackson's song "Heal the World" and dedicated it to the victims of the 2016 shooting of Dallas police officers, which happened days earlier in Dallas near her home.[18]
References[edit]
Jump up ^ Mack, David (May 21, 2016). "The Chewbacca Mask Lady Is Laughing All The Way To Internet Super Stardom". BuzzFeed. Retrieved May 22, 2016.
Jump up ^ Trending, BBC (May 20, 2016). "Mum in Chewbacca mask shatters Facebook Live record". BBC News. Retrieved May 22, 2016.
Jump up ^ Rogers, Christopher (May 21, 2016). "Chewbacca: Lady Wears Hilarious 'Star Wars' Mask & The World Laughs With Her -- Watch". Hollywood Life. Retrieved May 22, 2016.
Jump up ^ "Watch A Chewbacca Mask Turn This Woman Into The Happiest Star Wars Fan On The Planet". CINEMABLEND. May 20, 2016. Retrieved May 22, 2016.
Jump up ^ "Candace Payne". Facebook. May 20, 2016. Retrieved May 22, 2016.
Jump up ^ "Video Of Woman Laughing In Chewbacca Mask Sells Out Mask, Kohl's Says". Forbes. May 20, 2016. Retrieved May 22, 2016.
Jump up ^ Hall, Gerrad (May 21, 2016). "Chewbacca Mask Lady ‘overwhelmed’ by support as video hits 114 million views". Entertainment Weekly's EW.com. Retrieved May 22, 2016.
Jump up ^ McCrum, Kirstie (May 23, 2016). "Chewbacca lady gets Star Wars haul for kids - including their own wookie masks". Mirror. Retrieved May 23, 2016.
Jump up ^ Miller, Adam (May 23, 2016). "WATCH: Holly and Phillip in hysterics as they host This Morning in Chewbacca masks". Express.co.uk. Retrieved May 23, 2016.
Jump up ^ "'Chewbacca Mom' Candace Payne, Live on 'GMA'". Retrieved May 23, 2016.
^ Jump up to: a b Martinelli, Marissa (May 24, 2016). "How Could That Chewbacca Mask Video Get Any More Joyful? Add Autotune.". Slate. Retrieved May 24, 2016.
Jump up ^ Shepherd, Jack (May 24, 2016). "The 'Chewbacca' mum who conquered Facebook had the time of her life on James Corden's show". The Independent. Retrieved May 25, 2016.
Jump up ^ Hicks, Tony (May 26, 2016). "Watch: Chewbacca mom visits Lucasfilm HQ in San Francisco on 'The Star Wars Show'". www.mercurynews.com. Retrieved June 9, 2016.
Jump up ^ Mauney, Matt (June 2, 2016). "'Chewbacca mom' visits Disney's Hollywood Studios". OrlandoSentinel.com. Retrieved June 9, 2016.
Jump up ^ "‘Chewbacca mask lady' gets more than $420,000 in gifts". WJXT. June 7, 2016. Retrieved June 9, 2016.
^ Jump up to: a b Lawler, Richard (May 25, 2016). "Mom behind most-watched Facebook Live video visits its HQ". Engadget. Retrieved May 25, 2016.
Jump up ^ Nick Romano (June 19, 2016). "Chewbacca Mom gets her own action figure from Hasbro". Entertainment Weekly. Retrieved June 19, 2016.
Jump up ^ Mahjouri, Shakiel (July 9, 2016). "‘Chewbacca Mom’ Roars Beautiful Rendition Of ‘Heal The World’". ET Canada. Retrieved July 9, 2016.
External links[edit]
Original video
Retrieved from "https://en.wikipedia.org/w/index.php?title=Chewbacca_Mask_Lady&oldid=807117187"
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Aggressive periodontitis
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis:[1]
Localized aggressive periodontitis (LAP)
Generalized aggressive periodontitis (GAP)
LAP is localised to first molar or incisor interproximal attachment loss, whereas GAP is the interproximal attachment loss affecting at least three permanent teeth other than incisors and first molar.[2] The prevalence of LAP is less than 1% and that of GAP is 0.13%.[2] Approximately 0.1% of white Caucasians[3] (with 0.1% in northern and in central Europe, 0.5% in southern Europe, and 0.1-0.2% in North America[2]) and 2.6% of black Africans may suffer from LAP.[3] Estimates of the disease prevalence are 1-5% in the African population and in groups of African descent, 2.6% in African-Americans, 0.5-1.0% in Hispanics in North America, 0.3-2.0% in South America, and 0.2-1.0% in Asia.[2] On the other hand, in Asia, the prevalence rate of 1.2% for LAP and 0.6% for GAP in Baghdad and Iran population, and 0.47% in Japanese population.[2]
Therefore, the prevalence of LAP varies considerably between continents, and differences in race or ethnicity seem to be a major contributing factor.[2]
Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger patients than does the chronic form.[2][3] Around 1 in every 1000 patients suffer more rapid loss of attachment.[4] Males seem to be at higher risk of GAP than females[2]
The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis.
Contents
[hide]
1 Aetiology
1.1 Microbiology
1.2 Pathophysiology
2 Features
2.1 Primary features
2.2 Secondary features
3 Clinical & Radiographic Features of Localised and Generalized Aggressive Periodontitis
3.1 Localised Aggressive Periodontitis
3.1.1 Clinical Features
3.1.2 Radiographic Features
3.2 Generalized Aggressive Periodontitis
3.2.1 Clinical Features
3.2.2 Radiographic Features
4 Screening
4.1 Clinical examination
4.2 Radiographs
4.3 Strong family association
5 Treatment
5.1 Cause Related Therapy
5.2 Re-examination/Response to Therapy
5.3 Definitive Therapy
5.4 Maintenance
6 References
Aetiology[edit]
Microbiology[edit]
Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present.[5] Aggressive periodontitis is often characterised by a rapid loss of periodontal attachment associated with highly pathogenic bacteria and an impaired immune response. Various studies have associated Aggregatibacter actinomycetemcomitans, formerly known as Actinobacillus actinomycetemcomitans, with aggressive periodontitis. An early study dating back to 1983 explains its prevalence and documents its role in localised aggressive periodontitis.[6]
Virulence factors are the attributes of microorganisms that enable it to colonise a particular niche in its host, overcome the host defences and initiate a disease process.[7] Fives Taylor et al. (2000) have categorised the virulence factors of Aggregatibacter actinomycetemcomitans as follows.[7]
Promote colonization and persistence in the oral cavity:
Interfere with host defences:
Destroy host tissues:
Inhibit host repair of tissues:
Adhesins Leukotoxin Cytotoxins Inhibitors of fibroblast proliferation
Invasins Chemotactic inhibitors Collagenase
Bacteriocins Immunosuppressive proteins Bone resorption agents Inhibitors of bone formation
Antibiotic resistance Fc-binding proteins Stimulators of inflammatory mediators
Samaranayake notes the evidence for the specific involvement of Aggregatibacter actinomycetemcomitans includes: an increased incidence of it found in subgingival plaque obtained from lesional sites, high level of its antibody which tends to fall following successful treatment, its possession of a wide range of potentially pathogenic products and its elimination with concordant disease regression, following treatment with successful periodontal therapy and adjunctive tetracycline.[5]
Porphyromonas gingivalis is a Gram-negative anaerobe associated with the pathogenicity of periodontal disease,[8] and aggressive periodontitis is no exception. Greater numbers of both Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were found in active, destructive periodontal lesions in comparison to non-active sites.[8]
Capnocytophaga spp are implicated as prime periodontal pathogens, especially in localised aggressive periodontitis.[5] Both Capnocytophaga spp and Prevotella intermedia were the most frequently detected microorganisms in a study,[9] which also noted that Capnocytophaga spp was the most prominent bacteria in subgingival samples of aggressive periodontitis sufferers.[9][10]
An impaired ability of peripheral blood lymphocytes to react to chemotactic stimuli is found in the majority of patients suffering from aggressive periodontitis. As well as Aggregatibacter actinomycetemcomitans being associated with this, the synergism of the disease also accounts for both Capnocytophaga spp and Porphyromonas gingivalis.[5]
Pathophysiology[edit]
Aggressive periodontitis is a multifactorial disease with many complex interactions including host factors, microbiology and genetics.
Host defences involve multiple factors; saliva, epithelium, inflammatory response, immune response and chemical mediators. The inflammatory exudate in the gingival tissues and gingival crevicular fluid is mostly polymorph neutrophils but also includes B cells and plasma cells. The neutrophils may show an intrinsic functional defect and respond abnormally when challenged by certain pathogens.[11] The plasma cells produce specific antibodies in response to the periodontal pathogens, which diffuse into the gingival crevicular fluid. They produce mainly IgG, with some IgA.[11] It has been suggested that these gingival crevicular fluid antibody levels could be potentially useful in the development of a vaccine.[12] Patients with localised aggressive periodontitis have large amount of Aggregatibacter actinomycetemcomitans specific IgG2. This is suggested to be protective against wider spread periodontal breakdown. However, patients with generalized aggressive periodontitis have decreased ability to mount high titres of IgG to Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans.
It has also been found that a low T-helper to T-suppressor ratio is found in aggressive periodontitis which may alter local immune regulation. Monocytes respond to bacterial and inflammatory stimuli with very high levels of local release inflammatory mediators and induce hyper-inflammatory reaction with activation of tissue degrading matrix-metalloproteinases. These is also evidence they produce increased amounts IL-1α and IL-1β which cause osteoclastic bone resorption. These amounts are greatly reduced following treatment.[11]
Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis.[13] A person’s genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait. However, for the disease process to initiate the person must be exposed to the presence of periodontal pathogens and potentially also various environmental factors.
Smoking is a generalized risk factor for generalized forms of aggressive periodontitis. Studies found that smokers have more affected teeth than non-smokers and high levels of attachment loss. This is due to the suppression of serum IgG2 and antibody against Aggregatibacter actinomycetemcomitans found in smokers.[14]
Features[edit]
According to the 1999 International Workshop for the Classification of Periodontal Diseases, aggressive periodontitis was defined according to 3 primary features, in contrast to chronic periodontitis. These features are common for both localized and generalized form of disease.[15][16]
Primary features[edit]
Patients are clinically healthy.[15]
Patients do not have any underlying systemic disease that would contribute to aggressive periodontitis.[17] For instance, diabetes is proved to be associated with periodontitis- it is a major risk factor when glycaemic control is poor.[18]
The rate of loss of attachment and bone loss is rapid.[15]
Loss of attachment refers to the destruction of periodontium whereas the bone refers to the alveolar bone supporting the teeth.[19] The loss can be determined by using a calibrated periodontal probe and taking radiographs of the dentition.[20] Usually the loss of attachment is greater than 2mm per year.
Aggressive periodontitis runs in the patient’s family.[15]
Familial aggregation of aggressive periodontitis is often discovered by taking a thorough medical history of the patient. The patient is said to have a high genetic susceptibility to aggressive periodontitis. Many studies have shown that genetic factors contribute to the pathogenesis of this disease.[21] In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.[21]
Secondary features[edit]
Secondary features are characteristics which are frequently seen but not always present in every patient diagnosed with aggressive periodontitis.
The amount of bacteria is out of proportion to the severity of periodontal tissue destruction.[15]
The amount of bacteria is often indicated by the level of dental plaque.[22] This feature implies that when aggressive periodontitis is present, loss of attachment and bone loss tend to occur even if the plaque level is low.
High levels of Aggregatibacter (or Actinobacillus) actinomycetemcomitans and, in some populations, Porphyromonas gingivalis.[15]
These gram-negative microbes are considered the chief aetiological agent of aggressive periodontitis. They are implicated in the development of aggressive periodontitis by triggering inflammatory response in periodontal tissue.
There are abnormalities associated with phagocytes.[15]
Phagocytes are essential in resolving inflammation. The impairment of the their phagocytic activity results in persistent inflammation in periodontal tissues.[23]
Hyper-responsive macrophage phenotype.[15]
Due to the increased responsiveness, the macrophages produce excessive levels of inflammatory mediator and cytokine, such as prostaglandin E2 (PGE2) and interleukin-1β (IL-1B).[15] Their hyperactivity is associated with periodontal tissue destruction and bone loss.[24]
Progression of attachment loss and bone loss may be self-arresting.[15]
In some patients, the disease may burnout without any cause-related therapy.[25]
Clinical & Radiographic Features of Localised and Generalized Aggressive Periodontitis[edit]
Localised Aggressive Periodontitis[edit]
Clinical Features[edit]
LAP begins around the age of puberty where there is interproximal loss of attachment of the first molar, and or incisors[26] on at least two permanent teeth (one which is a first molar) and no involvement of more than two teeth other than the first molars and incisors,[26][27] lack of inflammation and evidence of deep periodontal pocket with advanced bone loss.[26] There is also a relatively fast progression of periodontal tissue loss.[27]

With an increase in the age of the patient, there may be progression of the disease involving the adjacent teeth and lead to the patient developing GAP.[28][29] The periodontal tissue also exhibits minimal signs of inflammation clinically[30] and show a robust response with serum antibodies to pathogens.[27]
The amount of plaque present is inconsistent with the amount and severity of tissue destruction [26][27] but with a high plaque pathogenicity due to the presence of increased levels of bacteria like Aggregatibacter actinomycetemcomitans (A.a) and Porphyromonas Gingivalis (P.g).[26]
Secondary features of LAP may also be present including;[26]
diastema formation with disto-labial migration of the incisors
increased mobility of the affected teeth, sensitivity due to exposed root,
deep dull pain that radiates to the jaw
periodontal abscess with lymph node enlargement
Radiographic Features[edit]
Radiographically, the periodontal lesion often presents with alveolar bone loss in a vertical pattern at the interproximal surface of the permanent first molars [26][27][28] and usually horizontal bone pattern of bone loss at the interproximal surface of the incisors as the bone is thinner than at the interproximal surface of the molars.[27]
The alveolar bone loss patterns are usually bilateral and similar on both sides and has been referred to as being a ‘mirror-image’ pattern.[28][27]
In advanced cases the alveolar bone loss may be depicted as a horizontal bone loss pattern radiographically.[27][28]
Generalized Aggressive Periodontitis[edit]
Clinical Features[edit]
Mostly in individuals under 30 years old[31]
In GAP, the clinical appearance of the disease resembles chronic periodontitis. The difference is that individuals affected by GAP are much younger and the progression of disease appears more rapid.[30]
There is a poor serum response against infecting agents[31]:
Destruction is present that is not in balance with the amount of local irritants present[30]
Generalized inter-proximal attachment loss on 3 or more permanent teeth, excluding the first molars or incisors[31]:
The main distinction between the localized and generalized form of AgP lies in the number of teeth affected. GAP brings about attachment loss involving more than 30% of sites on teeth;[1] effectively being at least three permanent teeth other than the first molars or incisors.[16]
Episodic nature of attachment loss: Two main tissue responses have been found in GAP cases:[31]
Tissue may have severe acute inflammation and often presents with an angry red appearance and ulceration. There may be spontaneous bleeding or suppuration. This response is known to be present in the destructive phase, where there is presence of bone and attachment loss.
The other response is known as a period of quiescence, where gingival tissue may appear with no inflammation, pink appearance with some possible stippling. In addition to this mild appearance there may be deep pockets upon probing.
Radiographic Features[edit]
The key diagnostic feature of AgP is vertical bone loss around teeth including the first molars and incisors. This tends to begin around puberty in otherwise healthy individuals.[31] There may be an appearance of “arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar”.[32]
In GAP, generalized bone destruction is present that ranges from mild crestal bone resorption to severe alveolar bone destruction, depending on the severity of the disease.[32] There may be a combination of vertical and horizontal bone loss defects.[32]
Screening[edit]
Early diagnosis of aggressive periodontitis is important as it can cause rapid permanent destruction of the periodontal tissues. It is essential that all patients undergo a routine periodontal examination to screen for any form of periodontal disease during a dental checkup.
Clinical examination[edit]
At the start of the clinical examination of the gingival and periodontal tissues, the dental practitioner would look at the appearance of the gingiva first. A healthy periodontium in a Caucasian would appear stippled and pink with a knife edge margin where it abuts the tooth (pigmentation may differ in other races).[33] After that, gingival probing depths would be checked. This would normally be carried out using a basic periodontal probe (WHO CPI).[34] On probing, patients with AgP should have evidence of significant periodontal pocket depths and loss of attachment (LOA). Dental practitioners should also be aware of false pocketing around erupting/newly erupted teeth in the mixed dentition phase and also in the presence of gingival inflammation.[34][35] The presence of bleeding on probing (BOP) should be noted which is an indicator of active disease.
Radiographs[edit]
Radiographic assessment should be carried out for patients with evidence of periodontitis to observe alveolar bone levels which can help to identify signs of AgP.[34] In healthy periodontal tissues, the distance from the amelocemental junction (ACJ) to the alveolar bone crest is typically in the order of 1mm in young people.[36] If the distance between the ACJ and alveolar bone crest is more than 2-3mm then there is a possible suggestion of AgP. In addition to that, presence of angular or vertical bone loss (especially at 6’s) and arrowhead or furcation lesions are also a strong suggestion of AgP.
Strong family association[edit]
It is also important for a dental practitioner to check for family history of periodontal disease for each patient. This is because AgP may have an autosomal dominant inheritance pattern which suggests that up to 50% of siblings could be affected if one parent has the disease.[37] Careful interpretation of the history is required but it may provide vital evidence in diagnosing AgP. If a case of Agp is diagnosed, it is important to screen the patient’s family members as well for AgP.[38][39] Early detection of AgP allows intervention to be carried out before extensive periodontal destruction has taken place which further simplifies treatment.
Treatment[edit]
Following the initial assessment and diagnosis of AgP, a treatment plan is usually developed for each individual undergoing therapy. As the overall treatment concepts and goals for AgP are not significantly different from that of chronic periodontitis, the different treatment phases (cause related therapy; re-examination for response to therapy; definitive therapy; and maintenance) are similar for both types of periodontitis.
Nevertheless, the considerable amount of bone loss relative to the young age of the individual in AgP necessitates an often more aggressive treatment approach, to halt further periodontal destruction and regain as much periodontal attachment as possible. The objective of treatment is to create a conducive clinical condition for retaining as many teeth, for as long as possible.[40]
Cause Related Therapy[edit]
This stage involves discussion of the disease with the patient.
Oral Hygiene Instructions: The clinician should advise the patient of his intrinsic susceptibility to plaque, which his body induces a strong, pro-inflammatory response to.[41] It is thus essential to keep his oral hygiene immaculate. This involve going over both smooth surfaces (tooth brushing instructions) and the use of interproximal aids (e.g. floss).
Smoking cessation (if applicable): Smoking is a significant risk factor for AgP, with patients who smoke having more affected teeth with loss of clinical attachment and more bone loss than non-smoking patients with AgP.[42] Non-smokers also tend to have a better response to periodontal therapy as compared to smokers. As such, individuals must be advised of the benefits of smoking cessation and the otherwise potential risks of a worsening periodontal condition.[43]
Removal of plaque retentive factors: Local plaque retentive factors such as mal-positioned teeth, overhanging restorations, crown and bridgework, partial dentures and fixed/removable orthodontic appliances can increase the risk of periodontal disease and prevent successful treatment and resolution of associated pockets. Prior to starting periodontal treatment, any overhanging or poorly contoured restorations should be modified or replaced. Instructions should also be given on how to clean adequately around fixed restorations and appliances, and how to clean removable prostheses. These intra-oral appliances should also be well-designed and fitting.[44]
The periodontal therapy carried out at this stage is of a non-surgical approach, which is aimed at the removal of supra- and sub-gingival plaque and calculus deposits, to decrease the microbial load, bacteria biofilm, and calculus from the periodontally involved sites.[45]
Scale and Polish
Root Surface Debridement (RSD)
Antibiotics: There is evidence that the additional use of systemic antibiotics in conjunction with non-surgical periodontal treatment results in a more favourable clinical response, as compared to just periodontal treatment alone, as it helps to suppress pathogenic bacteria and create a health-associated biofilm.[46] There have been many antibiotic regimes proposed for the treatment of AgP. However, the combination of choice according to current research is a combination of amoxicillin (500 mg, thrice/day) and metronidazole (200 mg, thrice/day), for 7 days, starting on the day of the final debridement. Doxycycline (100 mg, once/day, with a starting first dose of 200 mg) is the choice of antibiotics for patients allergic to penicillin.[47]
Light Amplification by Stimulated Emission of Radiation (LASER) Therapy
Photodynamic Therapy (PDT): This potentially has all the advantages of low-level LASER therapy, which allows the disinfection of periodontal pocket and the eradication of bacteria in areas of difficult access, without the thermal damage to tissues associated with the high-powered LASER. A significant reduction in the aggregatibacter actinomycetemcomitans count following PDT suggests that the use of PDT in conjunction with conventional non-surgical periodontal treatment can potentially result in a more effective treatment.[48] Considering the global issue of antibiotic resistance, further development and research in PDT successes may prove to present it an ideal adjunct to conventional non-surgical periodontal therapy, as compared to the use of systemic antibiotics.
Re-examination/Response to Therapy[edit]
This stage of treatment involves the reassessment of the individual’s compliance (i.e. level of oral hygiene) and the tissue response to the treatment. This is carried out 10–12 weeks following RSD. If the disease is stabilised, the treatment progresses on to the maintenance stage. In the case where the disease is not stabilised, the cause of failure should be considered, and the treatment progresses on to the stage of definitive therapy, if the cause is correctable.
Definitive Therapy[edit]
Further RSD at sites which require treatment
Use of Locally Delivered Antimicrobials (LDA) as an adjunct to non-surgical periodontal treatment: For use in deep pockets which fail to respond to repeated non-surgical treatment in patients with adequate oral hygiene. Currently, the available LDA include tetracycline, minocycline, chlorhexidine gluconate and doxycycline, with the mode of delivery being in the form of fibers, chips, polymers and trays.[49] There has yet to be much research into the effects of LDA in AgP, but current studies report an insignificant difference to the adjunctive effect of systemic antibiotics.[40]
Periodontal surgery: If it is a localised problem and if the case is non-response to non-surgical treatment despite the oral hygiene being consistently excellent. This could involve an open flap debridement with or without regenerative procedures, with the aim of gaining access and visibility to root and furcation areas so that a thorough instrumentation and debridement can be carried out.
Regenerative surgical therapy currently available include the use of bone replacement grafts, barrier membranes or guided tissue regeneration (GTR), biologic modifiers like growth and differentiation factors (GDF), and extracellular matrix proteins like enamel matrix proteins (EMD).[43] There is however, a great variation in periodontal gains reported in the literature available, signifying that results are not entirely predictable.
Maintenance[edit]
Periodontal treatment may help to stabilise the disease, but it does not change one’s susceptibility to the disease. Given the high susceptibility for disease progression of the individual with AgP, there is a higher risk of disease recurrence.[50] It is thus necessary to attend frequent review appointments at the dentist to ensure there is no relapse of the disease, and that the periodontal health is maintained after active periodontal therapy.[40]
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^ Jump up to: a b c Teughels, Wim; Dhondt, Rutger; Dekeyser, Christel; Quirynen, Marc (2014-06-01). "Treatment of aggressive periodontitis". Periodontology 2000. 65 (1): 107–133. doi:10.1111/prd.12020. ISSN 1600-0757.
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Jump up ^ Mullally, Brian H.; Breen, Blanaid; Linden, Gerard J. (1999-04-01). "Smoking and Patterns of Bone Loss in Early-Onset Periodontitis". Journal of Periodontology. 70 (4): 394–401. doi:10.1902/jop.1999.70.4.394. ISSN 0022-3492.
^ Jump up to: a b Roshna, T.; Nandakumar, K. (2012). "Generalized Aggressive Periodontitis and Its Treatment Options: Case Reports and Review of the Literature". Case Reports in Medicine. 2012: 1–17. doi:10.1155/2012/535321. ISSN 1687-9627.
Jump up ^ (SDCEP), Scottish Dental Clinical Effectiveness Programme (June 2014). "Prevention and Treatment of Periodontal Diseases in Primary Care, Dental Clinical Guidance" (PDF). Retrieved 7 Dec 2017.
Jump up ^ Aimetti, Mario (2014). "Nonsurgical periodontal treatment". The International Journal of Esthetic Dentistry. 9 (2): 251–267. ISSN 2198-591X. PMID 24765632.
Jump up ^ Keestra, J. a. J.; Grosjean, I.; Coucke, W.; Quirynen, M.; Teughels, W. (2015-12-01). "Non-surgical periodontal therapy with systemic antibiotics in patients with untreated aggressive periodontitis: a systematic review and meta-analysis". Journal of Periodontal Research. 50 (6): 689–706. doi:10.1111/jre.12252. ISSN 1600-0765.
Jump up ^ (BSP), British Society of Periodontology (Mar 2016). "The Good Practitioner's Guide to Periodontology" (PDF). Retrieved 7 Dec 2017.
Jump up ^ Vohra, Fahim; Akram, Zohaib; Safii, Syarida Hasnur; Vaithilingam, Rathna Devi; Ghanem, Alexis; Sergis, Konstantinos; Javed, Fawad. "Role of antimicrobial photodynamic therapy in the treatment of aggressive periodontitis: A systematic review". Photodiagnosis and Photodynamic Therapy. 13: 139–147. doi:10.1016/j.pdpdt.2015.06.010.
Jump up ^ Collins, Fiona. "Periodontal Treatment: The Delivery and Role of Locally Applied Therapeutics" (PDF). Retrieved 7 Dec 2017.
Jump up ^ Kamma, Joanna J.; Baehni, Pierre C. (2003-06-01). "Five-year maintenance follow-up of early-onset periodontitis patients". Journal of Clinical Periodontology. 30 (6): 562–572. doi:10.1034/j.1600-051x.2003.00289.x. ISSN 1600-051X.
[show]
v
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Dentistry involving supporting structures of teeth (Periodontology)
Anatomy
Periodontium
Alveolar bone
Biologic width
Bundle bone
Cementum
Free gingival margin
Gingiva
Gingival fibers
Gingival sulcus
Junctional epithelium
Mucogingival junction
Periodontal ligament
Sulcular epithelium
Stippling
Disease
Diagnoses
Chronic periodontitis
Localized aggressive periodontitis
Generalized aggressive periodontitis
Periodontitis as a manifestation of systemic disease
Periodontosis
Necrotizing periodontal diseases
Abscesses of the periodontium
Combined periodontic-endodontic lesions
Infection
A. actinomycetemcomitans
Capnocytophaga sp.
F. nucleatum
P. gingivalis
P. intermedia
T. forsythia
T. denticola
Red complex
Entamoeba gingivalis
Trichomonas tenax
Other
Calculus
Clinical attachment loss
Edentulism
Fremitus
Furcation defect
Gingival enlargement
Gingival pocket
Gingival recession
Gingivitis
Horizontal bony defect
Linear gingival erythema
Occlusal trauma
Periodontal pocket
Periodontal disease
Periodontitis
Plaque
Vertical bony defect
Treatment and prevention
Periodontal examination
Ante's law
Brushing
Bleeding on probing
Chlorhexidine gluconate
Flossing
Hydrogen peroxide
Mouthwash
Oral hygiene
Tetracycline
Triclosan
Host modulatory therapy
Treatment
Conventional therapy
Debridement
Scaling and root planing
Full mouth disinfection
Full mouth ultrasonic debridement
Surgery
Apically positioned flap
Bone graft
Coronally positioned flap
Crown lengthening
Open flap debridement
Gingival graft
Gingivectomy
Guided bone regeneration
Guided tissue regeneration
Enamel matrix derivative
Implant placement
Lateral pedicle graft
Pocket reduction surgery
Socket preservation
Sinus lift
Subepithelial connective tissue graft
Tools
Curette
Membrane
Probe
Scaler
Important personalities
Tomas Albrektsson
Frank Beube
Per-Ingvar Brånemark
Robert Gottsegen
Gary Greenstein
Jan Lindhe
Brian Mealey
Preston D. Miller
Willoughby D. Miller
Carl E. Misch
John Mankey Riggs
Jay Seibert
Jørgen Slots
Paul Roscoe Stillman
Dennis P. Tarnow
Hom-Lay Wang
James Leon Williams
W. J. Younger
Other specialties
Endodontology
Orthodontology
Prosthodontology
[show]
v
t
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Dentistry
Specialties
Endodontics
Oral and maxillofacial pathology
Oral and maxillofacial radiology
Oral and maxillofacial surgery
Orthodontics and dentofacial orthopedics
Pediatric dentistry
Periodontics
Prosthodontics
Dental public health
Cosmetic dentistry
Dental implantology
Geriatric dentistry
Restorative dentistry
Forensic odontology
Dental traumatology
Holistic dentistry
Dental surgery
Dental extraction
Tooth filling
Root canal therapy
Root end surgery
Scaling and root planing
Teeth cleaning
Dental bonding
Tooth polishing
Tooth bleaching
Socket preservation
Dental implant
Organisations
American Association of Orthodontists
British Dental Association
British Dental Health Foundation
British Orthodontic Society
Canadian Association of Orthodontists
Dental Technologists Association
Indian Dental Association
National Health Service
Orthodontic National Group
Orthodontic Technicians Association
General Dental Council
See also
Index of oral health and dental articles
Outline of dentistry and oral health
Oral hygiene
Dental fear
Dental instruments
Dental material
Infant oral mutilation
Mouth assessment
Retrieved from "https://en.wikipedia.org/w/index.php?title=Aggressive_periodontitis&oldid=832663374"
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