Из Википедии, бесплатной энциклопедии
  (Перенаправлено из Periodontics )
Перейти к навигации Перейти к поиску
Пародонтолог
Занятие
Тип занятияСпециальность
Сферы деятельностиСтоматология
Описание
Требуется образованиеСтоматологическая степень
Сферы занятостиБольницы , частные практики

Пародонтология или пародонтологии (от Древнегреческого περί , пери - «вокруг» и ὀδούς , odoús - «зуб», родительный ὀδόντος , odóntos ) является специальностью в стоматологии , что исследования поддерживающей структуру зубов , а также заболевания и состояния , которые влияют на их . Опорные ткани известны как пародонт , который включает десну (десны), альвеолярную кость , цемент и периодонтальную связку.. Пародонтолог - это стоматолог, который специализируется на профилактике, диагностике и лечении заболеваний пародонта, а также на установке зубных имплантатов. [1]

Пародонт [ править ]

Схема пародонта. A. Эмаль B. Дентин C. Альвеолярная кость D. Оральный эпителий E. Прикрепленная десна F. Десневой край G. Десневая борозда H. Соединительный эпителий I. Волокна альвеолярного гребня пародонтальной связки [PDL] J. Горизонтальные волокна PDL K. Косой волокна PDL

Термин пародонт используется для описания группы структур, которые непосредственно окружают, поддерживают и защищают зубы. Пародонт состоит в основном из десневой ткани и опорной кости. [2]

Десны [ править ]

Цвет нормальной десны может варьироваться от светло-кораллово-розового до сильно пигментированного. Мягкие ткани и соединительные волокна, которые покрывают и защищают подлежащий цемент, периодонтальную связку и альвеолярную кость, известны как десны. Десны делятся на три анатомические группы; свободная, прикрепленная и межзубная десна. Каждая из десневых групп считается биологически различной; однако все они специально разработаны для защиты от механического и бактериального разрушения. [3]

Свободная десна [ править ]

Ткани, расположенные над гребнем альвеолярной кости, считаются свободной десной. В здоровом пародонте десневой край - это фиброзная ткань, которая охватывает цементно-эмалевое соединение, линию по окружности зуба, где поверхность эмали коронки встречается с наружным цементным слоем корня. Естественное пространство, называемое десневой бороздой, лежит апикально по отношению к краю десны между зубом и свободной десной. Глубина здоровой десневой борозды, не пораженной болезнью, обычно составляет 0,5–3 мм, однако это значение может увеличиваться при наличии заболевания пародонта. Десневая борозда выстлана некератинизированным слоем, который называется эпителием бороздки ротовой полости; он начинается у края десны и заканчивается у основания борозды, где начинается соединительный эпителий и прикрепленная десна. [4]

Прикрепленная десна [ править ]

Узловой эпителий является воротник , как группа , которая лежит в основе десневой борозды и объемного зуба; он разграничивает области разделения между свободной и прикрепленной десной. Соединительный эпителий обеспечивает специальный защитный барьер для микроорганизмов, обитающих вокруг десневой борозды. [4] Коллагеновые волокна плотно связывают прикрепленную десну с подлежащим пародонтом, включая цемент и альвеолярную кость, и различаются по длине и ширине, [4] в зависимости от местоположения в полости рта и от человека., [5] [6]Прикрепленная десна располагается между свободной линией десны или бороздой и слизисто-десневым соединением. Прикрепленная десна снимает функциональную и жевательную нагрузку на ткани десны во время обычных действий, таких как жевание, чистка зубов и разговор. [7] В здоровом состоянии он обычно имеет бледно-розовый или кораллово-розовый цвет и может иметь поверхностную пунктирную или расовую пигментацию. [7]

Межзубная десна [ править ]

Межзубная десна занимает пространство под точкой контакта между двумя соседними зубами. Обычно он имеет треугольную или пирамидальную форму и образован двумя межзубными сосочками (язычным и лицевым). [4] [5] Средняя или центральная часть межзубного сосочка состоит из прикрепленной десны, тогда как края и верхушка образованы свободной десной. Центральная точка между межзубными сосочками называется кол. Это долинообразное или вогнутое углубление, расположенное непосредственно под точкой соприкосновения между лицевым и язычным сосочком. [6] Однако колба может отсутствовать, если есть рецессия десны или если зубы не соприкасаются. Основное предназначение межзубной десны - предотвратить застревание пищи во время обычного жевания. [7]


Слизистая оболочка альвеол [ править ]

Этот участок ткани не ороговевший и расположен за слизисто-десневым соединением. Она прикреплена менее плотно и краснее, чем прикрепленная десна. Обеспечивает движение щеки и губ. [8]

Пародонтальная связка [ править ]

Пародонтальная связка - это соединительная ткань, которая соединяет внешний слой корня зуба, представляющий собой цемент, с окружающей альвеолярной костью. Он состоит из нескольких сложных групп волокон, идущих в разных направлениях и вставляющихся в цемент и кость через «волокна Шарпея». [4] Пародонтальная связка состоит в основном из коллагеновых волокон, однако в ней также находятся кровеносные сосуды и нервы в рыхлой соединительной ткани. [6] Механические нагрузки, оказываемые на зубы во время жевания, и другие внешние силы поглощаются периодонтальной связкой, которая, таким образом, защищает зубы в их лунках. [7]

Альвеолярная кость [ править ]

При здоровом пародонте альвеолярная кость окружает зубы и образует костную впадину, которая поддерживает каждый зуб. Щечные и язычные пластины и выстилка лунок состоят из тонкой, но плотной компактной или кортикальной кости. [3] Внутри кортикальных пластинок и зубных впадин находится губчатая кость, губчатая или губчатая кость, которая менее плотна, чем компактная кость. [6]

Цемент [ править ]

Цемент - это внешний слой корня зуба; он покрывает слой дентина зуба и обеспечивает прикрепление коллагеновых волокон периодонтальной связки. Он также защищает дентин и обеспечивает герметизацию открытых в противном случае концов дентинных канальцев. Он не такой твердый, как эмаль или дентин, и обычно имеет светло-желтый цвет. [7]

Заболевания десен [ править ]

Гингивит - это распространенное заболевание, которое поражает десны или ткани слизистой оболочки, окружающие зубы. Состояние представляет собой форму пародонтоза; однако он наименее разрушителен, поскольку не вызывает необратимого повреждения или изменений пародонта (десны, периодонтальной связки, цемента или альвеолярной кости). Это обычно обнаруживается пациентами, когда десневое кровотечение возникает самопроизвольно во время чистки зубов или приема пищи. Также для него характерно генерализованное воспаление, отек и покраснение слизистых оболочек. Гингивит обычно безболезнен и чаще всего является результатом накопления биопленки зубного налета в сочетании с пониженной или плохой гигиеной полости рта. Другие факторы могут увеличить риск гингивита, включая, помимо прочего, системные состояния, такие как неконтролируемый сахарный диабет и прием некоторых лекарств.Признаки и симптомы гингивита можно обратить вспять с помощью улучшенных мер гигиены полости рта и увеличения разрушения зубного налета. Если не лечить гингивит, он может перерасти в пародонтит и другие связанные с ним заболевания, которые более пагубны для пародонта и общего состояния здоровья.[9]

Заболевания пародонта [ править ]

Заболевания пародонта включают ряд заболеваний тканей пародонта, которые приводят к потере прикрепления и разрушению альвеолярной кости. [10]

Заболевания пародонта принимают различные формы, но обычно являются результатом слияния бактериальных бляшек, накопления красных сложных бактерий (например, P. gingivalis , T. forsythia и T. denticola ) в деснах и зубах в сочетании с хозяином. иммуно-воспалительные механизмы и другие факторы риска, которые могут привести к разрушению опорной кости вокруг естественных зубов. Без лечения эти заболевания могут привести к потере альвеолярной кости и зубов . По состоянию на 2013 год на пародонтоз приходилось 70,8% утраченных зубов у пациентов с этим заболеванием вЮжная Корея . [11] Заболевания пародонта - вторая по частоте причина потери зубов (уступающая кариесу) в Шотландии . [12] Чистка зубов щеткой и зубной нитью два раза в день помогает предотвратить заболевания пародонта. [13]

Здоровая десна у людей европеоидной расы может быть пунктирной, бледно-розовой или кораллово-розовой, а у других рас - с различной степенью пигментации. Десневой край располагается на цементно-эмалевом переходе без патологии. Десневой карман между зубом и десной не должен быть глубже 1–3 мм, чтобы считаться здоровым. Также нет кровотечения при осторожном прощупывании. [10]

Здоровая десна

Заболевания пародонта могут быть вызваны множеством факторов, наиболее заметным из которых является зубной налет. Зубной налет образует бактериальную биопленку на поверхности зуба, если ее не удалить должным образом с поверхности зуба в непосредственной близости от десны, происходит взаимодействие между хозяином и микробами. Это приводит к дисбалансу между факторами хозяина и бактериями, что, в свою очередь, может привести к переходу от здоровья к болезни. Другие местные и / или системные факторы могут привести или еще больше усилить проявление заболеваний пародонта. Другие факторы могут включать возраст, социально-экономический статус, образование в области гигиены полости рта и диету. Системные факторы могут включать неконтролируемый диабет или курение табака. [14]

Признаки и симптомы заболеваний пародонта: кровоточивость десен, рецессия десен, неприятный запах изо рта (неприятный запах изо рта), подвижные зубы, неподходящие протезы и образование зубного налета и камня [15]

К индивидуальным факторам риска относятся: пол, курение и употребление алкоголя, диабет, ожирение и метаболический синдром, остеопороз и состояния, связанные с витамином D, стресс и генетические факторы. [16]

В 1999 г. Американская академия пародонтологии (AAP) переработала существующую классификацию заболеваний пародонта с 1989 г., чтобы устранить имеющиеся недостатки. В старой классификации слишком много внимания уделялось возрасту начала заболевания и скорости прогрессирования, которые часто трудно определить. Классификация 1999 г. была опубликована в «Анналах пародонтологии». Ниже приводится сокращенная версия классификации заболеваний и состояний пародонта 1999 года. [16]

I. Заболевания десен
A. Заболевания десен, вызванные зубным налетом
B. Поражения десен, не связанные с образованием налета

Гингивит-после

II. Хронический пародонтит
(легкий: 1-2 мм CAL; средний: 3-4 мм CAL; тяжелый:> 5 мм CAL) A. Локализованный
B. Генерализованный (поражено> 30% участков)

III. Aggressive Periodontitis
(slight: 1–2 mm CAL; moderate: 3–4 mm CAL; severe: > 5 mm CAL) A. Localised
B. Generalised (> 30% of sites are involved)

Recession parodontale

IV. Periodontitis as a Manifestation of Systemic Diseases
A. Associated with haematological disorders
B. Associated with genetic disorders
C. Not otherwise specified

Bone loss in periapical xray

V. Necrotizing Periodontal Diseases
A. Necrotizing ulcerative gingivitis
B. Necrotizing ulcerative periodontitis

VI. Abscesses of the Periodontium
A. Gingival abscess
B. Periodontal abscess
C. Pericoronal abscess

VII. Periodontitis Associated With Endodontic Lesions
A. Combined periodontic-endodontic lesions

Abscessed tooth periapical radiograph

VIII. Developmental or Acquired Deformities and Conditions
A. Localised tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis
B. Mucogingival deformities and conditions around teeth
C. Mucogingival deformities and conditions on edentulous ridges
D. Occlusal trauma

In 2018 a new classification of periodontal disease was announced. It was determined that the previous AAP 1999 classification did not cater for the needs of patients with peri-implant diseases and conditions. The new classification of periodontal and peri-implant diseases and conditions is as follows.

Periodontal Health, Gingival Diseases and Conditions:
Periodontal Health and Gingival Health
Gingivitis: Dental-Biofilm Induced
Gingival Diseases: Non-Dental Biofilm-Induced
Periodontitis:
Necrotizing Periodontal Diseases
Periodontitis
Periodontitis as a Manifestation of Systemic Disease
Other Conditions Affecting The Periodontium:
Systemic Diseases or conditions affecting the periodontal supporting tissues
Periodontal Abscesses and Endodontic-Periodontal Lesions
Mucogingival Deformities and Conditions
Traumatic Occlusal Forces
Tooth and Prosthesis Related Factors
Peri-Implant Diseases and Conditions:
Peri-Implant Health
Peri-Implant Mucositis
Peri-Implantitis
Peri-Implant Soft and Hard Tissue Deficiencies
[17]

Prevention:
The most effective prevention method is what can be achieved by the patient at home, for example, using the correct tooth brushing technique, interdental cleaning aids such as interdental brushes or floss and using a fluoridated toothpaste. It is also advised that patients receive bi annual check ups from their dental health provider along with thorough cleaning.
[15]
Treatment:
Along with specialist periodontist treatment, a general dentist or oral health therapist/dental hygienist can perform routine scale and cleans using either hand instruments or an ultrasonic scaler (or a combination of both). The practitioner can also prescribe specialised plaque removal techniques (tooth brushing, interdental cleaning). The practitioner can also perform a plaque index to indicate to the patient areas of plaque they are not removing on their own. This can be removed through the procedure of a dental prophylaxis.[15]

Peri-implantitis[edit]

Periodontology also involves the placement and maintenance of dental implants, including the treatment of peri-implantitis (inflammatory bone loss around dental implants). The etiology of peri-implantitis is thought to be very similar to periodontal disease.

Aetiology[edit]

The primary etiological factor for periodontal disease is plaque biofilm of dental biofilm. A dental biofilm is a community of microorganisms attached to a hard, non shedding surfaces. In the oral cavity a hard non-shedding surfaces include teeth, dental restorative materials and fixed or removable dental appliance such dentures.[18] It is this adherence to non-shedding surface that allows bacteria in a dental biofilm to have unique characteristics of clinical significance. The stages of biofilm formation:

  1. Formation of an acquired pellicle: Involves selective absorption of salivary and GCF molecules through an electrostatic affinity with hydroxyapatite.[19]
  2. Bacterial transportation: Bacteria will readily adhere to the acquired pellicle through adhesins, proteins and enzymes within one to two hours[19]
  3. Reversible interaction: There is electrostatic attraction or hydrophobic interaction between microorganisms and the tooth surface[19]
  4. Irreversible interaction: Bacterial adhesins recognise specific host receptors such as pili and outer membrane proteins. The different species of bacteria bind together and require specific receptors to interact with the pellicle.[20]
  5. Co-adehsion: There is a natural affinity for oral microorganisms to adhere to one another which is termed "co‐adhesion". Co-adhesion involves the adherence of planktonic or single culture cells to already attached organisms on a surface. The organisms which make first contact with the surface and allow the platform for later co-adhesion of bacteria are called "early colonisers", they facilitate the formation of complex multispecies dental biofilms[19]
  6. Multiplication: Through continued growth and maturation of existing plaque micro-organisms and the further recruitment of later colonisers[19]
  7. Climax community (homeostasis): After a prolonged period of stability the bacterial community has sufficient nutrients and protection to survive. These complex biofilms are usually found in hard to cleanse areas. Nutrition is provided from dietary consumption of the host for supra-gingival biofilm organisms and from blood and GCF for the sub gingival biofilm organisms[19]
  8. Detachment: From one surface to another or within biofilm allows colonisation at remote site[21]

Bacteria contained within the biofilm are protected by an slimy extracellular polysaccharide matrix which helps to protect them from the outside environment and chemotherapeutics agents. An example of a chemotherapeutic agent is an antiseptic such as Chlorhexidine mouth-rinse or antibiotics. Thus, antibiotics are not generally used in the treatment of periodontal disease unlike other bacterial infections around the body. The most effective way to control the plaque biofilm is via mechanical removal such as toothbrushing, interdental cleaning or periodontal debridement performed by a dental professional.[21]

Pathogenesis[edit]

An individual's host response plays an important role in the pathogenesis of periodontal disease. Even in a mouth where the gingiva appear healthy there is constant low level inflammatory response facilitated by the host to manage the constant bacterial load of plaque micro-organisms. Leukocytes and Neutrophils are the main cells that phagocytose bacteria found in the gingival crevice or pocket. They migrate from the tissues in a specialised exudate called gingival crevicular fluid also known as GCF. Neutrophils are recruited to the gingival crevice area as they are signalled to by molecules released by plaque microorganisms. Damage to epithelial cells releases cytokines which attract leukocytes to assist with the inflammatory response. The balance between normal cell responses and the beginning of gingival disease is when there is too much plaque bacteria for the neutrophils to phagocytose and they degranulate releasing toxic enzymes that cause tissue damage. This appears in the mouth as red, swollen and inflamed gingiva which may be bleeding when probed clinically or during tooth brushing. These changes are due to increased capillary permeability and an influx of inflammatory cells into the gingival tissues. When gingival disease remain established and the aetiology is not removed there is further recruitment of cells such as macrophages which assist with the phagocytic digestion of bacteria and lymphocytes which begin to initiate an immune response.[22] Pro-inflammatory cytokines are produced inside the gingival tissues and further escalate inflammation which impacts the progression of chronic systemic inflammation and disease. The result is collagen breakdown, infiltrate accumulation as well as collagen breakdown in the periodontal ligament and alveolar bone resorption. At this stage, the disease has progressed from gingivitis to periodontitis and the loss of supporting periodontium structure is irreversible.[21]

Risk factors[edit]

A risk factor is a variable that in health, can be defined as "a characteristic associated with an increased rate of a subsequently occurring disease".[23]Risk factors are variables that contribute to disease, rather than being factors that induce disease. Risk factors may be seen as modifiable and non-modifiable. Modifiable risk factors are often behavioural in nature and can be changed by the individual or environmental circumstances, whereas non-modifiable are usually intrinsic to an individuals genetics and cannot be changed. To determine risk factors for a disease, evidence based research and studies are needed for evidence, with longitudinal studies giving the most statistically significant outcomes and the best reliability for determining risk factors. Risk factors often coexist with other variables, rarely acting alone to contribute to a disease. Risk factors can be genetic, environmental, behavioural, psychological, and demographic in nature.[24]

There are many risk factors that contribute to placing an individual at higher risk for developing gingival and periodontal diseases. However, the only aetiological factor for periodontal disease is bacterial plaque, or biofilm. Identifications of ones risk factors play an important role in the diagnosis, treatment and management of periodontal diseases. It was previously believed that each human being had the same risk of developing periodontal diseases, but through the identification and classification of risk factors, it has become well understood that each individual will have a differing array of risk factors that generate susceptibility and contribute to severity of periodontal disease.

Individual, modifiable risk factors include:

  • Tobacco Smoking – Tobacco smoking is firmly established as a major risk factor for periodontal disease, with the relationship between smoking exposure and periodontal tissue destruction being supported strongly by various research papers.[25] Smoking decreases the healing abilities of the oral tissues by destroying blood vessels and supply and preventing essential immune-defence organisms from penetrating the tissues. Therefore, pathogenic bacteria are able to destruct the periodontal tissues more rapidly and escalate the severity of disease.[26] Although the clinical signs of inflammation are less pronounced, smokers have a larger portion of sites with deep pocketing depths and loss of clinical attachment when compared with nonsmokers.[27] Smoking cessation and counselling is an integral part of a dental professionals work with periodontal disease patients. Smoking cessation has been proven to prevent progression of periodontal disease and to return the oral microflora to a less pathogenic microbial state.[28]
  • Alcohol consumption – More research needs to be conducted in the form of longitudinal studies on the effects of alcohol on the periodontal tissues. However, current studies do suggest that alcohol consumption moderately increases ones risk for progression of periodontal disease.[29]
  • Diabetes Mellitus – Diabetes falls under the category of modifiable risk factors as although it cannot be cured, it can be controlled, which greatly helps periodontal disease control. A clear two-way relationship has been established with blood glucose control directly effecting periodontal disease severity and progression, and vice versa. Periodontal disease patients with diabetes mellitus also have poorer healing abilities than those without diabetes, and hence are at an increase risk for more severe diseases if blood glucose control is poor and when healing abilities are affected by systemic disease.[23]
  • Obesity and Vitamin D Deficiency are both risk factors for periodontal disease that go hand in hand. Obesity is generally associated with a decreased consumption of fruits and vegetables, with an increase in foods high in fat, salt and sugar. Having a poor diet not only contributes to obesity but also results in a lack of essential nutrients, including vitamin C, D, and calcium, which all play important roles in ensuring a healthy immune system and healthy oral tissues and bone.[30]
  • Poor Oral Hygiene – As plaque is the only etiological factor for periodontal disease,[31] poor oral hygiene is the most prominent risk factor in initiating, progressing and determining severity of disease. Performing brushing and interdental cleaning is perhaps one of the most effective ways at removing dental plaque biofilm and prevention of periodontal diseases.
  • Cardiovascular disease – Not only does poor oral hygiene have a clear relationship with an increased risk of developing cardiovascular disease, High concentrations of cholesterol and the mechanisms of oral bacteria in the process of atherosclerosis may increase in individuals with chronic periodontitis.[32]
  • Stress – Various studies have demonstrated that individuals under psychological, ongoing chronic stress are more likely to have clinical attachment loss and decreased levels of alveolar bone due to periodontal destruction.[33] This is due to the increased production of certain immune cells and interleukins, which decrease the defensive mechanisms against pathogenic bacteria, therefore increasing chances of developing periodontal disease.

Non-modifiable risk factors include:

  • Genetics and the Host response have been shown to play an important role in periodontal disease development in studies on identical twins and isolated indigenous populations.[34] Periodontal disease also may result due to an abnormal or decreased immune response, rather than aggressive properties of bacterial pathogens.[35]
  • Osteoporosis – In individuals with osteoporosis, studies have shown that alveolar bone is less dense than in a healthy adult. However, this does not demonstrate a relationship with periodontal pathogens or clinical attachment loss, therefore more research is needed to investigate if osteoporosis is a true risk factor for periodontal disease.[23]
  • Drug induced disorders – Many drugs and medications can have an adverse effect on the periodontal tissues, through contributing to various oral conditions such as dry mouth and gingival hyperplasia.[36] It is crucial that dental professionals ensure that poly-pharmacy patients have medical history reviewed at each visit to correctly evaluate the patients risk and determine appropriate course of action for dental treatment.
  • Haematological disorders – Important cells and nutrients carried in the blood to the periodontal tissues are crucial for the tissues defence mechanisms and response to toxins and pathogens, gas exchange and efficient hemostasis. Therefore, red blood cells have a pivotal role in maintaining the health of the periodontium, meaning haematological disorders can have profound detriment to the periodontal tissues and the onset of disease.[37]
  • Pregnancy – Studies have shown that the oral tissues are affected and altered during pregnancy due a decreased immune response and increased vascular blood supply and volume systemically. it is important to note that pregnancy does not cause gingival and periodontal diseases but may exacerbate the inflammatory response to a pre-existing disease. It is also important to note that pregnancy does not detract minerals from the oral tissues or teeth, as previously thought and may be heard in old wives tales. Existing disease often presents during pregnancy due to an altered oral environment, and not merely due to pregnancy causing disease. These effects can be prevented by good oral hygiene through toothbrushing and interdental cleaning.[38]

Risk characteristics must be considered in conjunction with risk factors as variables that may also contribute to increasing or decreasing ones chances of developing periodontal disease. Numerous studies show that Age, Gender, Race, Socioeconomic status, Education and Genetics also have strong relationships on influencing periodontal disease.

Periodontal disease is multifactorial, requiring dental and oral health professionals to have a clear and thorough understanding of the risk factors and their mechanisms in order to implement effective disease management in clinical practice.[24]

Diagnosis[edit]

Periodontitis and associated conditions are recognised as a wide range of inflammatory diseases that have unique symptoms and varying consequences. In order to identify disease, classification systems have been used to categorise periodontal and gingival diseases based on their severity, aetiology and treatments.[39] Having a system of classification is necessary to enable dental professionals to give a label to a patient's condition and make a periodontal diagnosis. A diagnosis is reached by firstly undertaking thorough examination of the patient's medical, dental and social histories, to note any predisposing risk factors (see above) or underlying systemic conditions. Then, this is combined with findings from a thorough intra and extra oral examination. Indices such as periodontal screening record (PSR) and the Community Periodontal Index of Treatment Needs (CPITN) are also used in making a diagnosis and to order or classify the severity of disease.[40]

If disease is identified through this process, then a full periodontal analysis is performed, often by dental hygienists, oral health therapists or specialist periodontists. This involves full mouth periodontal probing and taking measurements of pocket depths, clinical attachment loss and recession. Along with this other relevant parameters such as plaque, bleeding, furcation involvement and mobility are measured to gain an overall understanding of the level of disease. Radiographs may also be performed to assess alveolar bone levels and levels of destruction.[41]

Treatment[edit]

Phases of Periodontal Therapy[edit]

Contemporary periodontal treatment is designed based on the ‘Trimeric Model’, and is performed in 4 phases. These phases are structured to ensure that periodontal therapy is conducted in a logical sequence, consequently improving the prognosis of the patient, in comparison to indecisive treatment plan without a clear goal.

Phase I Therapy (Initial Therapy – Disease Control Phase)[edit]

Non-surgical Phase[edit]

The non-surgical phase is the initial phase in the sequence of procedures required for periodontal treatment.[42] This phase aims to reduce and eliminate any gingival inflammation by removing dental plaque, calculus (dental), restoration of tooth decay and correction of defective restoration as these all contribute to gingival inflammation, also known as gingivitis.[42] Phase I consists of treatment of emergencies, antimicrobial therapy, diet control, patient education and motivation, correction of iatrogenic factors, deep caries, hopeless teeth, preliminary scaling, temporary splinting, occlusal adjustment, minor orthodontic tooth movement and debridement (dental).[42]

Re-evaluation Phase[edit]

During this phase, patients after 3–6 weeks from initial therapy; it is required to re-evaluate the steps carried out after the phase I therapy.[42] Usually 3–6 weeks re-evaluation is crucial in severe cases of periodontal disease. The elements which are required to be re-evaluated are the results of initial therapy (Phase I Therapy), oral hygiene and status, bleeding and plaque scores and a review of diagnosis and prognosis and modification of the whole treatment plan if necessary.[43]

Phase II Therapy (Surgical Phase)[edit]

After post Phase I, it is necessary to evaluate the requirement of periodontium for surgery.[43] Factors identifying the Surgical phase is required are: periodontal pocket management in specific situations, irregular bony contours or deep craters, areas of suspected incomplete removal of local deposits, degree II and III furcation involvements, distal areas of last molars with expected mucogingival junction problems, persistent inflammation, root coverage and removal of gingival enlargement.

Phase III Therapy (Restorative Phase)[edit]

During this phase, any defects need to be restored with removable or fixed through dental prosthesis, prosthodontics, or other restoration process.[42]

Phase IV Therapy (Maintenance Phase)[edit]

The last phase of Periodontal Therapy requires the preservation of periodontal health. In this phase, patients are required to re-visit through a scheduled plan for maintenance care to prevent any re-occurrence of the disease.[43] The maintenance phase constitutes the long-term success for periodontal treatment, thus contributes to a long relation between the oral health therapist/dentist/periodontist and the patient.[43]

Periodontal and Restorative Interface[edit]

The prognosis of the restorative treatment is determined by the periodontal health. The goals for establishing periodontal health prior to restorative treatment are as follows:

  1. Periodontal treatment should be managed to assure the establishment of firm gingival margin prior to tooth preparation for restoration. Absence of bleeding tissue during restorative manipulation provides accessibility and aesthetic outcome.[43]
  2. Certain periodontal treatment is formulated to increase sufficient tooth length for retention. Failure to accomplish these methods prior restorations can lead to the complexity or risk of failure of treatment such as impression making, tooth preparation and restoration.
  3. Periodontal therapy should follow restorative method as the resolution of gingival inflammation may result in the repositioning of teeth or in soft tissue and mucosal changes.[43]

Standard of Periodontal Treatment[edit]

Non-surgical therapy is the golden standard of periodontal therapy which consists of debridement (dental) with a combination of oral hygiene instructions and patient motivation. It mainly focuses on the elimination and reduction of putative pathogens and shifting the microbial flora to a favourable environment to stabilise periodontal disease.[44] Debridement (dental) is thorough mechanical removal of calculus and dental biofilm from the root surfaces of the tooth.[45] Debridement (dental) is the basis of treatment for inflammatory periodontal diseases and remains the golden standard for surgical and non-surgical treatment in the initial therapy. It is conducted by hand instrumentation such as curettes or scalers and ultrasonic instrumentation.[46] It requires a few appointments, depending on time and clinician skills for effective removal of supragingival and subgingival calculus (dental), when periodontal pocket is involved. It can assist in periodontal healing and reduce periodontal pocketing by changing the subgingival ecological environment.[46] Prevention of periodontal disease and maintenance of the periodontal tissues following initial treatment requires on the patient's ability to perform and maintain effective dental plaque removal.[46] This requires patient to be motivated in improving their oral hygiene and requires behaviour change in terms of tooth brushing, interdental cleaning, and other oral hygiene techniques.[47] Personal oral hygiene is often the considered an essential aspect of controlling chronic periodontitis Research has shown that it is important to appreciate the motivation of the patient behaviour changes that has originated from the patient.[47] Patients must want to improve their oral hygiene and feel confident that they have the skills to do this. It is crucial for the clinician to encourage patient changes and to educate the patient appropriately. Motivational interviewing is a good technique to ask open-ended questions and express empathy towards the patient.

Role of the Oral Health Therapist[edit]

An Oral Health Therapist is a member of the dental team who is dual qualified as a Dental Hygienist and Dental therapist. They work closely with Dentists and a number of Dental Specialists including Periodontists. It is common for the Oral Health Therapist to be involved in the treatment of gingival and periodontal diseases for patients. Their scope of practice in this area includes oral health assessment, diagnosis, treatment and maintenance and referral where necessary. They also have expertise in providing oral health education and promotion to support the patient to maintain their at home oral care.[48] Oral Health Therapists are employed into the dental team to share the responsibilities of care. They are an important asset as they have been uniquely and specifically trained in preventative dentistry and risk minimisation. This allows the dental team to work more competently and effectively as Dentists can manage more complex treatments or significantly medically compromised patients.[49]

Periodontist[edit]

A periodontist is a specialist dentist who treats patients for periodontal related diseases and conditions. They are involved in the prevention, diagnosis and treatment of periodontal disease. Periodontists receive further specialist training in Periodontics after completing a dental degree. Periodontists provide treatments for patients with severe gingival diseases and/or complex medical histories. Periodontists offer a wide range of treatments including root scaling and planing, periodontal surgery, implant surgery and other complex periodontal procedures.[50]

Dental-implant

List of procedures performed by a periodontist:[50]

  • Non-Surgical Treatments
  • Gum Graft Surgery
  • Laser Treatment
  • Regenerative Procedures
  • Dental Crown Lengthening
  • Dental Implants
  • Pocket Reduction Procedures
  • Plastic Surgery Procedures

Patient's are able to access treatment from a specialist periodontist with an appropriate referral from a dental practitioner. The Dental Hygienist, Oral Health Therapist or Dentist will decide upon whether or not the patient requires further treatment from a Periodontist. The practitioner will then fill out a referral form outlining both patient and practitioner concerns, needs and wants.[citation needed]

Training[edit]

Before applying to any postgraduate training program in periodontology, one must first complete a dental degree.

Europe[edit]

Although each European country has its own independent system, an umbrella organisation—the European Federation of Periodontology (EFP)—has the ability to accredit post-graduate programs according to specific guidelines. The EFP awards a certificate of specialized training in periodontology, periodontics and implant dentistry to every successful European candidates after 3 years of full-time training in an accredited post-graduate program. The EFP organizes bi-annual meetings around Europe under the title EuroPerio where many thousands of dentists attend the sessions featuring over 100 of the world's top perio speakers.[51][52] The graduate programs that have been approved are the following: Academic Centre for Dentistry Amsterdam [nl], University of Bern, Sahlgrenska University Hospital, Institute for Postgraduate Dental Education Jönköping, UCL Eastman Dental Institute, University of Louvain (UCLouvain), University Complutense in Madrid, University of Dublin, Trinity College, University of Strasbourg in France, Paris Diderot University at Rothschild hospital.[citation needed]

Australia[edit]

Australian programs are accredited by the Australian Dental Council (ADC) and are 3 years in length and culminate with either a Master's degree (MDS) or a Doctor of Clinical Dentistry degree (DClinDent). Fellowship can then be obtained with the Royal Australasian College of Dental Surgeons, FRACDS (Perio).[citation needed]

Canada[edit]

Canadian programs are accredited by the CDAC[53] and are a minimum of three years in length and usually culminate with a master (MSc or MDent) degree. Graduates are then eligible to sit for the Fellowship exams with the Royal College of Dentists of Canada (FRCD(C)). Dentistry is a regulated profession. To become a licensed dentist in Canada you must have a BDS/DDS/DMD degree and be certified by the NDEB.[54] To further specialise into periodontics, accredited dentists are required to undertake a specialty core knowledge examination and complete a postgraduate degree.[citation needed]

India[edit]

Periodontics is offered as a specialization field of dentistry in India. Periodontists attend a Master of Dental Surgery (M.D.S.) program affiliated with dental schools in India. The minimum qualification required for the M.D.S. degree is a Bachelor of Dental Surgery. A majority of dental schools in India offer M.D.S. degrees specializing in Periodontology. The course is three years and students are trained for implantology as well as diagnosis and treatment of peri implant diseases along with Periodontology.[citation needed]

United Kingdom[edit]

The British Society of Periodontology exists to promote the art and science of periodontology. Their membership includes specialist practitioners, periodontists, general dentists, consultants and trainees in restorative dentistry, clinical academics, dental hygienists and therapists, specialist trainees in periodontology and many others.[citation needed]

Specialist training in periodontics in the UK is either a three-year full-time or four years at three days per week. At the end of the training, candidates are awarded a Master of Clinical Dentistry (MClinDent) before being entered on the specialist list held by the General Dental Council.[citation needed]

United States[edit]

UCLA School of Dentistry periodontics graduate clinic

The American Dental Association (ADA) accredited programs are a minimum of three years in length. According to the American Academy of Periodontology, U.S.-trained periodontists are specialists in the prevention, diagnosis and treatment of periodontal diseases and oral inflammation, and in the placement and maintenance of dental implants.[55] Many periodontists also diagnose and treat oral pathology. Historically, periodontics served as the basis for the specialty of oral medicine. Following successful completion of post-graduate training a periodontist becomes Board eligible for the American Board of Periodontology examination. Successful completion of board certification results in Diplomate status in the American Board of Periodontology.[citation needed]

Maintenance[edit]

After periodontal treatment, whether it be surgical or non-surgical, maintenance periodontal therapy is essential for a long term result and stabilization of periodontal disease. There is also a difference in the maintenance of different types of periodontal disease, as there are different types, such as:[56]

Gingivitis[edit]

The reversible inflammation of the gums, is easily maintained and easily done by patients alone. After the removal of the inflammatory product, usually plaque or calculus, this allows the gums room to heal. This is done by patients thoroughly cleaning teeth every day with a soft bristle toothbrush and an interdental aid. This can be floss, flosset, pikster or what is preferred by patient. Without patient compliance and constant removal of plaque and calculus, gingivitis cannot be treated completely and can progress in to periodontitis that is irreversible.[57]

Necrotising ulcerative gingivitis (NUG)[edit]

Also Acute necrotising ulcerative gingivitis and necrotising ulcerative periodontitis, a type of periodontal disease, different than many other periodontal diseases, clinical characteristics of, gingival necrosis (break down of the gums), gingival pain, bleeding, and halitosis (bad breath), also has a grey colour to the gingiva and a punched out appearance. It is treated through debridement usually under local aesthetic due to immense pain. To maintain and treat the condition completely, a Chlorhexidine mouth wash should be recommended to the patient to use twice daily, oral health instruction should be provided, using a soft bristle toothbrush twice a day or an electric toothbrush and an interdental cleaning aid, such as floss or piksters which cleans the areas that the toothbrush cannot reach. Patient should also be educated on proper nutrition and diet, and also healthy fluid intake, also to complete cease disease smoking cessation should be done not just to completely eradicate disease but also for health od patient. Pain control can be done through ibuprofen or Panadol. In the case of an immunocompromised patient antibiotics should be prescribed. Assessment of treatment should be done after 24 hours of treatment and continued to do so every 3–6 months until signs and symptoms are resolved and gingival health and function restored.[58]

Chronic periodontitis[edit]

The inflammation of the gums and irreversible destruction of the alveolar bone and surrounding structures of the teeth, usually slow progressing but can have bursts. Local factors explain presence of disease, such as, diet, lack of oral hygiene, plaque accumulation, smoking etc. Characterised by pocket formation and recession (shrinkage of the gums) of the gingiva. Treatment and maintenance are important in stopping disease progression and to resolve the inflammation, treatment usually consist of scaling and root planning, surgical therapy, regenerative surgical therapy. After treatment, patient care and regular maintenance check ups are important to completely eradicate disease and present reappearance of the disease. This is done through patient effective plaque control and removal, done through daily toothbrushing of twice a day and interdental cleaning once a day, chlorhexidine mouthwash can also be effective. Patient should also present to dentist for maintenance check ups at least every three-months for in office check-up and if necessary, plaque control.[59]

Aggressive periodontitis[edit]

Involves inflammation of the gingiva and rapid and severe destruction of the periodontal ligament, alveolar bone and surrounding structures, different to chronic periodontitis often happens in patients with good oral health and plaque control and can be genetic. Patients generally appear clinically healthy. It can be localised, which generally has a circumpubertal onset, and generalised which usually occurs in individuals above the age of 35. Treatment is determined on the severity of the disease and the age of the patient. Usually supra gingival (above gums) and sub gingival (under gums) debridement and antibiotics are sometimes necessary. To maintain the treatment and prevent reoccurrence of disease patient care is necessary, such as oral hygiene, like all other forms of periodontitis and gingivitis, brushing twice a day and interdental cleaning is a necessity in maintaining a healthy periodontium and preventing the continuation of periodontal destruction. Regular periodontal check ups are also necessary, every 3–6 months.[citation needed]

Periodontitis as a manifestation of systemic disease[edit]

Periodontitis that is caused by systemic disease, there are currently at least 16 systemic diseases that have been linked with periodontal disease, such as, diabetes mellitus, haematological disorders such as acquired neutropenia and leukemia, down syndrome etc. Treatment and preventions are a very important concept in the management and maintenance of periodontitis as a manifestation of systemic disease. Treatment can consist of either surgical or non surgical treatment depending on severity. After treatment patient compliance is important which includes oral hygiene which is tooth brushing twice a day, interdental brushing at least once a day and chlorohexidine mouth wash may also be helpful.[citation needed]

See also[edit]

  • Bone grafting
  • Chronic periodontitis
  • Dental implant
  • Gingival graft
  • Gingival recession
  • Journal of Periodontology
  • Periodontitis
  • Scaling and root planing
  • Sinus lift

References[edit]

  1. ^ "What is a Periodontist? | Perio.org". www.perio.org. Retrieved 2019-10-21.
  2. ^ "Anatomy of the Periodontium | An Overview of Dental Anatomy | CE Course | dentalcare.com". www.dentalcare.com. Retrieved 2019-10-21.
  3. ^ a b Clerehugh, V., Tugnait, A., & Genco, R. J. (2009). Periodontology at a glance. Chichester: John Wiley & Sons Ltd[page needed]
  4. ^ a b c d e Cope, Graham; Cope, Anwen (1 July 2011). "The periodontium: an anatomical guide". Dental Nursing. 7 (7): 376–378. doi:10.12968/denn.2011.7.7.376.
  5. ^ a b Newman, M., Takei, H. Klokkevold, P. R., Carranza, F. A. (2015). Carranza’s Clinical Periodontology (12th ed.). St. Louis: Elsevier Inc[page needed]
  6. ^ a b c d Weinberg, M., Westphal, C., Froum, S. J., Palat, M. P., & Schoor, R. S. (2010). Comprehensive Periodontics for the Dental Hygienist (3rd ed.). Upper Saddle River, N.J.: Pearson Education[page needed]
  7. ^ a b c d e Gehrig, J., & Willmann, D. E. (2011). Foundations of Periodontics for the Dental Hygienist (3rd ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health.[page needed]
  8. ^ "Search the Glossary - AAP Connect". members.perio.org. Retrieved 2019-10-21.
  9. ^ de Vries, Kevin (July 2015). "Primary care: Gingivitis". The Australian Journal of Pharmacy. 96 (1141): 64.
  10. ^ a b Highfield, J (September 2009). "Diagnosis and classification of periodontal disease". Australian Dental Journal. 54: S11–S26. doi:10.1111/j.1834-7819.2009.01140.x. PMID 19737262.
  11. ^ Lee, Jae-Hong; Oh, Jin-Young; Choi, Jung-Kyu; Kim, Yeon-Tae; Park, Ye-Sol; Jeong, Seong-Nyum; Choi, Seong-Ho (October 2017). "Trends in the incidence of tooth extraction due to periodontal disease: results of a 12-year longitudinal cohort study in South Korea". Journal of Periodontal & Implant Science. 47 (5): 264–272. doi:10.5051/jpis.2017.47.5.264. PMC 5663665. PMID 29093985.
  12. ^ McCaul, L. K.; Jenkins, W. M. M.; Kay, E. J. (June 2001). "The reasons for extraction of permanent teeth in Scotland: a 15-year follow-up study". British Dental Journal. 190 (12): 658–662. doi:10.1038/sj.bdj.4801068. PMID 11453155.
  13. ^ "Periodontology: an overview". Retrieved 17 September 2018.
  14. ^ Hasan, A.; Palmer, R. M. (25 April 2014). "A clinical guide to periodontology: Pathology of periodontal disease". British Dental Journal. 216 (8): 457–461. doi:10.1038/sj.bdj.2014.299. PMID 24762896.
  15. ^ a b c "Gum Disease: Causes, Prevention, & Treatment of Gum Disease". Colgate® Australia.
  16. ^ a b Genco, Robert J.; Borgnakke, Wenche S. (June 2013). "Risk factors for periodontal disease". Periodontology 2000. 62 (1): 59–94. doi:10.1111/j.1600-0757.2012.00457.x. PMID 23574464.
  17. ^ Caton, Jack G.; Armitage, Gary; Berglundh, Tord; Chapple, Iain L.C.; Jepsen, Søren; Kornman, Kenneth S.; Mealey, Brian L.; Papapanou, Panos N.; Sanz, Mariano; Tonetti, Maurizio S. (June 2018). "A new classification scheme for periodontal and peri-implant diseases and conditions - Introduction and key changes from the 1999 classification" (PDF). Journal of Periodontology. 89: S1–S8. doi:10.1002/JPER.18-0157. PMID 29926946.
  18. ^ Hasan, A.; Palmer, R. M. (25 April 2014). "A clinical guide to periodontology: Pathology of periodontal disease". British Dental Journal. 216 (8): 457–461. doi:10.1038/sj.bdj.2014.299. PMID 24762896.
  19. ^ a b c d e f Marsh, P. D.; Zaura, Egija (March 2017). "Dental biofilm: ecological interactions in health and disease". Journal of Clinical Periodontology. 44: S12–S22. doi:10.1111/jcpe.12679. PMID 28266111.
  20. ^ O'Toole, George; Kaplan, Heidi B.; Kolter, Roberto (October 2000). "Biofilm Formation as Microbial Development". Annual Review of Microbiology. 54 (1): 49–79. doi:10.1146/annurev.micro.54.1.49. PMID 11018124.
  21. ^ a b c Gurenlian, JoAnn R. (31 December 2007). "The Role of Dental Plaque Biofilm in Oral Health". American Dental Hygienists' Association. 81 (suppl 1): 116.
  22. ^ Kinane, Denis F. (February 2001). "Causation and pathogenesis of periodontal disease". Periodontology 2000. 25 (1): 8–20. doi:10.1034/j.1600-0757.2001.22250102.x. PMID 11155179./
  23. ^ a b c Van Dyke, Thomas E.; Dave, Sheilesh (2005). "Risk Factors for Periodontitis". Journal of the International Academy of Periodontology. 7 (1): 3–7. PMC 1351013. PMID 15736889.
  24. ^ a b AlJehani, Yousef A. (2014). "Risk Factors of Periodontal Disease: Review of the Literature". International Journal of Dentistry. 2014: 182513. doi:10.1155/2014/182513. PMC 4055151. PMID 24963294.
  25. ^ Chahal, GurparkashSingh; Chhina, Kamalpreet; Chhabra, Vipin; Chahal, Amna (2017). "Smoking and its effect on periodontium – Revisited". Indian Journal of Dental Sciences. 9 (1): 44. doi:10.4103/ijds.ijds_96_16.
  26. ^ Rivera-Hidalgo, Francisco (October 1986). "Smoking and Periodontal Disease: A Review of the Literature". Journal of Periodontology. 57 (10): 617–624. doi:10.1902/jop.1986.57.10.617. PMID 3534210.
  27. ^ Grossi, Sara G.; Zambon, Joseph J.; Ho, Alex W.; Koch, Gary; Dunford, Robert G.; Machtei, Eli E.; Norderyd, Ola M.; Genco, Robert J. (March 1994). "Assessment of Risk for Periodontal Disease. I. Risk Indicators for Attachment Loss". Journal of Periodontology. 65 (3): 260–267. doi:10.1902/jop.1994.65.3.260. PMID 8164120.
  28. ^ Grossi, SG; Zambon, J; Machtei, EE; Schifferle, R; Andreana, S; Genco, RJ; Cummins, D; Harrap, G (May 1997). "Effects of smoking and smoking cessation on healing after mechanical periodontal therapy". Journal of the American Dental Association. 128 (5): 599–607. doi:10.14219/jada.archive.1997.0259. PMID 9150643.
  29. ^ Tezal, Miné; Grossi, Sara G.; Ho, Alex W.; Genco, Robert J. (February 2001). "The Effect of Alcohol Consumption on Periodontal Disease". Journal of Periodontology. 72 (2): 183–189. doi:10.1902/jop.2001.72.2.183. PMID 11288791.
  30. ^ Neiva, Rodrigo F.; Steigenga, Jennifer; Al-Shammari, Khalaf F.; Wang, Hom-Lay (July 2003). "Effects of specific nutrients on periodontal disease onset, progression and treatment". Journal of Clinical Periodontology. 30 (7): 579–589. doi:10.1034/j.1600-051x.2003.00354.x. PMID 12834494.
  31. ^ Brogden, K., & Guthmiller, J. (2002). Polymicrobial diseases (p. Chapert 8 – Periodontal diseases). [Washington, D.C.]: ASM Press.[page needed]
  32. ^ Izumi, Aki; Yoshihara, Akihiro; Hirotomi, Toshinobu; Miyazaki, Hideo (May 2009). "The Relationship Between Serum Lipids and Periodontitis in Elderly Non-Smokers". Journal of Periodontology. 80 (5): 740–748. doi:10.1902/jop.2009.080584. PMID 19405827.
  33. ^ Hugoson, A.; Ljungquist, B.; Breivik, T. (March 2002). "The relationship of some negative events and psychological factors to periodontal disease in an adult Swedish population 50 to 80 years of age". Journal of Clinical Periodontology. 29 (3): 247–253. doi:10.1034/j.1600-051x.2002.290311.x. PMID 11940145.
  34. ^ Michalowicz, Bryan S.; Diehl, Scott R.; Gunsolley, John C.; Sparks, Brandon S.; Brooks, Carol N.; Koertge, Thomas E.; Califano, Joseph V.; Burmeister, John A.; Schenkein, Harvey A. (November 2000). "Evidence of a Substantial Genetic Basis for Risk of Adult Periodontitis". Journal of Periodontology. 71 (11): 1699–1707. doi:10.1902/jop.2000.71.11.1699. PMID 11128917.
  35. ^ Van Dyke, T. E.; Serhan, C.N. (13 December 2016). "Resolution of Inflammation: A New Paradigm for the Pathogenesis of Periodontal Diseases". Journal of Dental Research. 82 (2): 82–90. doi:10.1177/154405910308200202. PMID 12562878.
  36. ^ Taylor, Barbara Anne (1 February 2003). "Management of drug-induced gingival enlargement". Australian Prescriber. 26 (1): 11–3. doi:10.18773/austprescr.2003.007. PMID 11709926.
  37. ^ Kinane, DF; Marshall, GJ (March 2001). "Peridonatal manifestations of systemic disease". Australian Dental Journal. 46 (1): 2–12. doi:10.1111/j.1834-7819.2001.tb00267.x. PMID 11355236.
  38. ^ Laine, Merja Anneli (2 July 2009). "Effect of pregnancy on periodontal and dental health". Acta Odontologica Scandinavica. 60 (5): 257–264. doi:10.1080/00016350260248210. PMID 12418714.
  39. ^ Highfield, J (September 2009). "Diagnosis and classification of periodontal disease". Australian Dental Journal. 54: S11–S26. doi:10.1111/j.1834-7819.2009.01140.x. PMID 19737262.
  40. ^ Armitage, Gary C. (February 2004). "Periodontal diagnoses and classification of periodontal diseases". Periodontology 2000. 34 (1): 9–21. doi:10.1046/j.0906-6713.2002.003421.x. PMID 14717852.
  41. ^ Preshaw, Philip M (15 September 2015). "Detection and diagnosis of periodontal conditions amenable to prevention". BMC Oral Health. 15 (S1): S5. doi:10.1186/1472-6831-15-s1-s5. PMC 4580822. PMID 26390822.
  42. ^ a b c d e Duarte, Poliana Mendes; da Rocha, Marcelo; Sampaio, Eduardo; Mestnik, Maria Josefa; Feres, Magda; Figueiredo, Luciene Cristina; Bastos, Marta Ferreira; Faveri, Marcelo (July 2010). "Serum Levels of Cytokines in Subjects With Generalized Chronic and Aggressive Periodontitis Before and After Non-Surgical Periodontal Therapy: A Pilot Study". Journal of Periodontology. 81 (7): 1056–1063. doi:10.1902/jop.2010.090732. PMID 20192617.
  43. ^ a b c d e f Mohd-Dom, Tuti; Ayob, Rasidah; Mohd-Nur, Amrizal; Abdul-Manaf, Mohd R; Ishak, Noorlin; Abdul-Muttalib, Khairiyah; Aljunid, Syed M; Ahmad-Yaziz, Yuhaniz; Abdul-Aziz, Hanizah; Kasan, Noordin; Mohd-Asari, Ahmad S (20 May 2014). "Cost analysis of Periodontitis management in public sector specialist dental clinics". BMC Oral Health. 14 (1): 56. doi:10.1186/1472-6831-14-56. PMC 4033493. PMID 24884465.
  44. ^ Mordohai, N.; Reshad, M.; Jivraj, S.; Chee, W. (27 January 2007). "Factors that affect individual tooth prognosis and choices in contemporary treatment planning". British Dental Journal. 202 (2): 63–72. doi:10.1038/bdj.2007.23. PMID 17255985.
  45. ^ Oshman, Sarah; El Chaar, Edgard; Lee, Yoonjung Nicole; Engebretson, Steven (25 July 2016). "Effect of patient age awareness on diagnostic agreement of chronic or aggressive periodontitis between clinicians; a pilot study". BMC Oral Health. 17 (1): 27. doi:10.1186/s12903-016-0258-0. PMC 4960759. PMID 27456238.
  46. ^ a b c Allen, E; Ziada, H; Irwin, CR; Mullally, B; Byrne, PJ (2 April 2008). "Periodontics: 10. Maintenance in Periodontal Therapy". Dental Update. 35 (3): 150–156. doi:10.12968/denu.2008.35.3.150. PMID 18507223.
  47. ^ a b Martinez-Canut, Pedro; Llobell, Andrés; Romero, Antonio (June 2017). "Predictors of long-term outcomes in patients undergoing periodontal maintenance". Journal of Clinical Periodontology. 44 (6): 620–631. doi:10.1111/jcpe.12730. PMC 5519943. PMID 28419497.
  48. ^ "Guidelines for scope of practice". Dental Board of Australia. Retrieved 8 May 2019.
  49. ^ Nash, David A. (October 2012). "Envisioning an oral healthcare workforce for the future". Community Dentistry and Oral Epidemiology. 40: 141–147. doi:10.1111/j.1600-0528.2012.00734.x. PMID 22998319.
  50. ^ a b American Academy of Periodontology. (2019). What is a periodontist?. Retrieved from https://www.perio.org/consumer/what-is-a-periodontist
  51. ^ "EuroPerio Congress – EFP". efp.org. 2019-12-23.
  52. ^ PERIO PEOPLE. "PerioPeople Home". efp.org.
  53. ^ CDAC. (2013). Retrieved from https://www.cda-adc.ca/cdacweb/en/
  54. ^ Becoming a licensed dentist in Canada | The National Dental Examining Board of Canada. (2019). Retrieved from https://ndeb-bned.ca/en/requirements
  55. ^ "What is a Periodontist?". Perio.org. American Academy of Periodontology. Retrieved 2015-01-26.
  56. ^ Hou, Yue; Wang, Xin; Zhang, Cong-Xiao; Wei, Yu-Dan; Jiang, Li-Li; Zhu, Xiao-Yu; Du, Yu-Jun (1 September 2017). "Risk factors of periodontal disease in maintenance hemodialysis patients". Medicine. 96 (35): e7892. doi:10.1097/MD.0000000000007892. PMC 5585499. PMID 28858105.
  57. ^ Azaripour, Adriano; Weusmann, Jens; Eschig, Carl; Schmidtmann, Irene; Van Noorden, Cornelis J. F.; Willershausen, Brita (23 May 2016). "Efficacy of an aluminium triformate mouthrinse during the maintenance phase in periodontal patients: a pilot double blind randomized placebo-controlled clinical trial". BMC Oral Health. 16 (1): 57. doi:10.1186/s12903-016-0214-z. PMC 4878033. PMID 27216479.
  58. ^ Dufty, J; Gkranias, N; Donos, N (2017). "Necrotising Ulcerative Gingivitis: A Literature Review". Oral Health & Preventive Dentistry. 15 (4): 321–327. doi:10.3290/j.ohpd.a38766. PMID 28761942.
  59. ^ Furuta, Michiko; Fukai, Kakuhiro; Aida, Jun; Shimazaki, Yoshihiro; Ando, Yuichi; Miyazaki, Hideo; Kambara, Masaki; Yamashita, Yoshihisa (2019). "Periodontal status and self-reported systemic health of periodontal patients regularly visiting dental clinics in the 8020 Promotion Foundation Study of Japanese Dental Patients". Journal of Oral Science. 61 (2): 238–245. doi:10.2334/josnusd.18-0128. PMID 31217373.

External links[edit]

  • AAP Directory of Periodontists
  • American Academy of Periodontology's (AAP) article on Periodontal Disease
  • British Society of Periodontology
  • Canadian Academy directory of Periodontists
  • Dental Council of India
  • European Federation of Periodontology
  • The National Institute of Cranialfacial Research's article on Periodontal Disease
  • South African Society for Periodontology