Ver o tópico anterior Ver o tópico seguinte Ir em baixo


Mensagem  Bernardokm em Qua Jan 02, 2013 9:42 am

PERIODONTITIS — Periodontitis is characterized by gingival inflammation accompanied by loss of supportive connective tissues, including alveolar bone. This results in loss of attachment (perda de inserção) of the periodontal ligament to the cementum.

Clinical findings include increased probing depth, bleeding on probing, and tooth mobility. Bone loss is seen on radiographs (picture Cool. Progression of the disease will cause increased mobility and eventual tooth loss. Additionally, systemic disease may result from pathogenic bacterial strains included among the >500 bacterial species harbored in periodontal pockets [32,33].

Moderate periodontitis affects a majority of adults [34,35]. It is estimated that 5 to 15 percent of the population in the United States suffers from severe generalized periodontitis, defined as a loss of attachment exceeding 6 mm.

Periodontitis may be classified as follows [8]:

Chronic periodontitis (most commonly seen in adults)
Aggressive periodontitis (previously known as early onset periodontitis, localized periodontitis, rapid periodontitis, prepubertal periodontitis, most commonly seen in young individuals)
Periodontitis as a manifestation of systemic disease (eg, leukemia, cyclic neutropenia, Ehlers-Danlos syndrome)
Periodontitis associated with pulpal (endodontic) infection
Necrotizing ulcerative periodontitis
Developmental or acquired deformities (eg, gingival recession)

Chronic periodontitis — Chronic periodontitis (once called adult periodontitis, although it may occur in children or adolescents) is the most common form of periodontitis. It is plaque-induced and a major cause of tooth loss throughout the world [6].

The disease usually occurs as a slowly progressive condition, with unpredictable brief episodic periods of rapid progression and attachment loss [36-42]. The triggering mechanism for active bone loss has not been clearly elucidated, but appears to be associated with a shift from a predominantly Gram positive flora to a predominance of anaerobic Gram negative rods. It has been hypothesized that supragingival plaque serves as a reservoir for the pathogenic Gram negative bacteria [43-45]. When the host is overwhelmed, the pathogenic supragingival bacteria migrate subgingivally and form a subgingival biofilm that can be highly detrimental to surrounding periodontal structures.

Host response to the pathogenic flora is variable. Factors contributing to disease progression include cigarette smoking, diabetes mellitus, and emotional stress [46,47]. Disease activity and tissue destruction are modulated through production of inflammatory factors, including interleukins, prostaglandins, and matrix metalloproteinases [48,49].

Chronic (common) periodontitis is graded by increasing severity ranging from slight to severe involvement (table 1). Untreated disease causes architectural defects (craters) in the bone and increased gingival pocket depth.

Treatment includes debridement, scaling and root planing of subgingival biofilm and calculus by a periodontist, general dentist or dental hygienist (O tratamento consiste em raspagens, tratamentos a LASER. e, em casos mais acentuados, cirurgias periodontais). This should be accompanied by improved oral hygiene: brushing two times daily, flossing or interdental cleaning, and adjunctive therapies or host modulating therapies.

Adjunctive therapies to the mechanical removal of calculus and plaque may include the use of topical antibiotic (Atridox® or Arestin®) or antimicrobial (PerioChip®) agents. Systemic antibiotics, such as amoxicillin or metronidazole, may be prescribed for severe and generalized cases. Periostat®, also available in the United States in a generic tablet formulation, is a low dose of doxycycline (20 mg) which may be taken twice a day for up to nine months. Systemic levels do not reach inhibitory concentrations against bacteria. The drug inhibits collagenase activity in vitro and may prevent further breakdown of connective tissue and alveolar bone.

Aggressive periodontitis — Aggressive periodontitis (AP, which includes conditions formerly termed early onset periodontitis, localized periodontitis, rapid periodontitis, and prepubertal periodontitis) is much less common than chronic periodontitis, accounting for only 1 to 2 percent of cases of periodontitis.

Aggressive periodontitis occurs in both localized (affecting the periodontal tissues of first molars and incisors) or generalized (affecting additional teeth) forms. Both conditions affect otherwise healthy patients, although abnormalities in phagocyte function can be identified. Rapid loss of attachment and bone destruction occur, but the condition may be self-arresting [50]. Severity of disease is not related to the amount of bacterial biofilm present, and there is a strong genetic predisposition [51].

Localized aggressive periodontitis usually affects prepubescent individuals, predominantly African-American females [52]. Bone loss around the first permanent molars, mandibular, and maxillary central incisors is seen on radiographs (picture 9). The bone loss may be rapid and severe with few overt clinical signs of inflammation. Untreated lesions will develop into adult periodontitis. (See "Overview of gingivitis and periodontitis in children and adolescents", section on 'Localized aggressive'.)

Generalized aggressive periodontitis (GAP) may affect adolescents and younger adults (ages 25 to 35 years). GAP affects the entire dentition, including teeth other than molars or incisors [50]; heavy accumulations of plaque and calculus may be present. Inflammation may be severe and bone loss is rapid, with a pronounced episodic nature of the destruction. GAP must be treated aggressively with local therapy and systemic antibiotics. Surgery may be required and referral to a periodontist is advised when the diagnosis is made.

Manifestation of systemic disease — Systemic diseases associated with periodontitis include hematologic disorders (leukemia and acquired neutropenia), and genetic disorders (Down syndrome, cyclic neutropenia, Chediak-Higashi syndrome) [53]. Bacterial biofilm is also an important etiologic factor in this category. However, periodontal condition is considered a manifestation of the systemic disease because the underlying host impairment is a major determinant in the development and severity of the periodontitis [52].

Periodontal disease in patients with diabetes mellitus is not described as a distinct disease entity, but the prevalence and overall severity of periodontal disease is increased, particularly when diabetes is not well controlled. Patients with poorly controlled type 2 diabetes have three times the risk of periodontitis [54] and 11 times the risk of progressive alveolar bone loss [55] than patients with diabetes; periodontal morbidity is not increased in patients with well controlled diabetes.

Necrotizing ulcerative periodontitis — Necrotizing ulcerative periodontitis (NUP) involves severe loss of periodontal attachment and alveolar bone. This condition was previously termed "HIV periodontitis", but it is not limited to patients with HIV. It affects patients with HIV infection and CD4 counts less than 400, as well as patients with severe immunosuppression related to cancer chemotherapy [56] or advanced protein-energy malnutrition [57].

The condition manifests as rapid painful soft tissue and bone loss that may appear as necrotic clefts (picture 10). Destruction may be so rapid that denuded bone is visible followed by sequestration.

The microbiologic flora composition is unique; in addition to the Gram negative rods associated with chronic periodontitis, enteric organisms and yeast can be cultured.

Treatment consists of scaling and root/planing (debridement) along with antibiotics and pain medication. Antifungals (nystatin, fluconazole) and antibacterial rinses (chlorhexidine) may also be incorporated into the treatment regimen (picture 11).

Associated with pulpal infection

Periodontal and gingival abscesses — Periodontal and gingival abscess are commonly occurring acute infections of the supporting structures. Patients may be predisposed to abscess formation due to the following:

Deep periodontal pockets [58,59]
Incomplete removal of subgingival calculus after a professional scaling and root planing [59,60]
Occlusion of the pocket orifice by foreign bodies (ie, popcorn kernel) [59,61]
Inadequate treatment of periodontitis (eg, administration of antibiotics in the absence of scaling or planing mechanical therapy) [62]
Poorly controlled diabetes

Dental abscesses are classified in one of three categories [63,64]:

Periodontal abscess — Localized within the tissues adjacent to the periodontal pocket. These are the most common.
Gingival abscess — Confined to the marginal gingival and interdental papilla.
Pericoronal abscess — Develop within tissue surrounding the crown of a partially erupted tooth (ie, third molars, also known as wisdom teeth).

The abscess usually presents as a painful swelling of the buccal or lingual/palatal gingiva/mucosa, but may be asymptomatic. Teeth in the affected region may be painful and sensitive to mastication. The patient may have lymphadenopathy and fever. A productive sinus tract fistula may be evident when palpating the fluctuant area.

Abscesses cause rapid alveolar bone resorption, which can be confirmed radiographically. However, prompt treatment often leads to repair. The prognosis is dependent upon the presence of other endodontic complications. Treatment consists of incision and drainage followed by antibiotic therapy. (See "Complications, diagnosis, and treatment of odontogenic infections".)

Associated with endodontic lesions — An existing periapical infection may spread to a periodontal pocket or an infection from the periodontal pocket may spread to the apex of the tooth and join a periapical lesion. The existence of endodontic and periodontal infections has been named combined periodontal-endodontic lesions [65].

Developmental or acquired deformities

Periimplantitis — Periimplantitis refers to bone infection secondary to dental implants. The tissues surrounding the implant may become painful and the implant itself may loosen. Dental radiographs display periimplant radiolucency (bone destruction). The bacteria associated with periimplantitis are similar to those in chronic periodontitis. Treatment ranges from antibiotic therapy and bone grafting to surgical removal of the implant [66,67].


Anesthesia — Teeth with associated periodontal disease can present a significant problem for the anesthesiologist. Intubation and extubation may dislodge teeth, calculus, and prostheses. All have the potential to act as a source of infection and/or obstruction. Careful presurgical screening and dental consultation may prevent many of these complications.

Hematogenous seeding — Odontogenic infections in any individual may disseminate hematogenously to seed native or prosthetic heart valves, joint replacements, or other prosthetic devices. Antibiotic prophylaxis is essential prior to any invasive dental procedure. (See "Antimicrobial prophylaxis for bacterial endocarditis".)

Routine examination of the oral cavity should be considered prior to elective prosthetic heart valve implantation or artificial joint replacement [33].

Diabetes mellitus — Poorly controlled diabetes may be a risk factor for increased severity of periodontitis and poor response to periodontal treatment. Patients may present with xerostomia, candidiasis, and caries as well as periodontal disease. Consensus guidelines for dental and medical providers have been developed by an expert panel to aid in recognizing diabetes and providing appropriate attention to dental and gingival health in patients with diabetes [68].

Patients with poor control of diabetes and severe periodontitis may show improvement in their A1c levels, as well as decrease in periodontal inflammation, with treatment of the periodontitis [69,70]; not all studies confirm improvement in glycemic control, however [71-73]. To date, there is no strong scientific evidence on the effects of periodontal treatment on glycemic control and systemic inflammation[74]

[img:af5a]][/URL] [/img][img:af5a]][/URL] [/img][img:af5a]][/URL] [/img][img:af5a]][/URL] [/img]

1) UptoDate:


Mensagens : 14
Data de inscrição : 18/11/2012

Ver perfil do usuário

Voltar ao Topo Ir em baixo

Importância da periodontite

Mensagem  Bernardokm em Qua Jan 02, 2013 9:52 am

Pessoal, acho que o mais importante para nós é saber identificar a gengiva e o periodonto alterado para encaminharmos corretamente ao dentista e às vezes até fazendo a profilaxia adequada com antibioticos. Por isso, devemos reconhecer os principais sinais da doença periodontal como mobilidade e mudança de posição dos dentes, sangramento gengival principalmente ao exame físico, alteração do paladar, sensibilidade dental, dores e desconfortos gengivais, alteração da cor dos dentes, mau hálito e tártaro. Em muitos casos, os dentes da frente podem se projetar para fora e pode haver acúmulo de pus.

É importante também sabermos que algumas doenças tem relação com a periodontite: artrite reumatóide, doenças renais, diabétes, osteoporose, infarto agudo do coração, partos prematuros, infecções pulmonares e úlceras.
Fumo, bruxismo, deficiências nutricionais, medicamentos e doenças emocionais podem potencializar os efeitos da periodontite.



Mensagens : 14
Data de inscrição : 18/11/2012

Ver perfil do usuário

Voltar ao Topo Ir em baixo

Ver o tópico anterior Ver o tópico seguinte Voltar ao Topo

Permissão deste fórum:
Você não pode responder aos tópicos neste fórum