The predominant microorganisms are polymicrobial Gram-negative rods, particularly 'red complex pathogens' like P. gingivalis, T. forsythia, and Treponema spp.
Patient expectations, treatment expectations, esthetics, finances, and patient compliance.
Restorative factors including faulty restorations, extensive caries, crown:root ratio, and the need for post core + crown.
Brush twice a day with a small soft-head brush (electric preferred over manual), use fluoride-containing toothpaste, and use interdental cleaning aids more than once a day.
To adjust tooth length and contour.
Subject level risk assessment categorizes individuals as LOW risk (all low), MODERATE risk (at least 2 moderate), or HIGH risk (at least 2 high).
Initial treatment includes drainage, debridement of the root surface, and possibly extraction if there is severe damage.
Control of acute/painful conditions such as abscesses and necrotising diseases, including potential extractions.
Aid to diagnosis, help determine prognosis and treatment, reveal alterations to calcified tissue, show past effects on bone, aid diagnosis and classification initially, and track changes in bone levels over time during SPT.
Necrosis and ulcers of the free gingival margin, spontaneous gingival bleeding, rapid onset pain, pouch appearance, marginal erythema, pseudomembrane (whitish/yellow), halitosis, lymphadenopathy, fever, and discomfort.
Rapid necrotising destruction of periodontal tissues, significant pain, rapid tissue necrosis and ulceration, and susceptibility in immunocompromised patients.
Tissue response including color, form, tissue tone, and bleeding, along with resolution of inflammation and reduced probing depth.
Inflammation of the periodontium with attachment loss, characterized by swelling, erythema, bleeding, deep pockets, gingival recession, and bone/attachment loss.
Antibiotics should be prescribed only for systemic symptoms, with options including Penicillin, Metronidazole, Amoxicillin, and Clindamycin.
Systemic diseases can compromise the health of periodontal supporting tissues, leading to conditions such as periodontitis.
Disruption of plaque or biofilm on a regular basis to prevent accumulation + disease
Systemic conditions, modifying factors, diabetes, IL-1 genotype, smoking, plaque, and BOP.
Supportive periodontal therapy, prevention of recurrence, examination, oral hygiene instruction, root surface debridement, fluoride application, and re-evaluation of future needs.
The pathogenesis involves bacterial invasion into the pocket, an inflammatory process with PMN influx, pus production, connective tissue destruction, and encapsulation of the infection.
Symptoms include fatigue, infections, alteration in vision, pruritis, polyphagia, polyuria, hyperglycaemia, and weakness.
Periodontal treatment may increase metabolic control in diabetes by changing HbA1c levels, potentially reducing the burden of complications, but requires increasing the frequency of SPT to every 3 months.
To open furcation to allow cleaning, usually performed on mandibular molars.
An acute periodontal abscess is a localized collection of inflammatory cells and pathogens in periodontal tissues, associated with pain and rapid tissue breakdown.
Aetiologic factors such as calculus, perio re-treatment, root proximity, surgery bone dimensions, and root canal treatment.
SPT, or Supportive Periodontal Therapy, is done during the maintenance phase and involves regular maintenance, evaluation, and surveillance to prevent recurrence and tooth loss.
Extraction is indicated when there is a hopeless prognosis, particularly in Grade III cases.
Analgesics for discomfort, periodontal debridement under local anesthesia, CHX mouth rinse, and metronidazole as an adjunct treatment.
Treatment options include root surface debridement (RSD) and scaling and root planing (SRP), with considerations for PD increase or reduction.
1) Exam, re-evaluation, Dx; 2) Motivation, reinstruction, instrumentation; 3) Treatment re-infected sites; 4) Polishing, fluorides, determine future SPT.
GTR stands for Guided Tissue Regeneration, which is the direct growth of new tissue.
To determine diagnosis and identify who is at risk, as well as to determine prognosis and likely response to treatment.
Bleeding, suppuration, pain, halitosis, and difficulty eating.
Tooth position within arch, furcation involvement, iatrogenic factors (overhangs, open contacts etc.), residual periodontal support, mobility.
Attain sustained high levels of achievement in personal plaque control (absence BOP), absence of increased attachment loss, probing depths no greater than 5mm + no horizontal probing of furcations >5mm.
1) Bleeding on probing (BOP), 2) Residual pockets >4mm, 3) Tooth loss, 4) Bone loss/age, 5) Systemic disease, 6) Smoking.
Bone loss severity is classified as Mild (<1/3 root), Moderate (<2/3 root), and Advanced (>2/3 root).
There is some association between periodontal disease and adverse pregnancy outcomes, including premature birth and low birth weight, although no RCT evidence.
To remove deposits/biofilm from the root surface without removing cementum, create an environment compatible with periodontal health, remove endotoxins, and preserve cementum for healing.
It is the surgical removal of all or part of a root to eliminate furcation, mainly performed on molars with severe bone loss around the root.
Key clinical symptoms include discomfort, pain, tenderness, swelling, tooth mobility, and sensitivity to palpation.
Grade 1: <1/3 through furcation; Grade 2: >2/3 but not completely through; Grade 3: completely through furcation.
Mucogingival deformities refer to conditions that affect the relationship between the gingiva and the mucosa, impacting the periodontal supporting tissues.
Tooth position, function, stability; degree of furcation involvement; amount of periodontal support; endodontic conditions; anatomy; patient functional, financial, and esthetic demands/resources; oral hygiene capacity.
1) Removal of pre-disposing factors, 2) Oral hygiene instruction, 3) Debridement of supra/subgingival calculus.
Resolution of signs of inflammation (oedema + suppuration).
Military service, students, smoking, HIV, malnutrition, and stress.
Remission is characterized by maintenance and monitoring, with either a decrease in PD and positive BoP or the same PD with negative BoP.
Systemic inflammation model where periodontal disease contributes to systemic inflammation.
Other determinants such as smoking, systemic conditions, bisphosphonates, and clinical skill.
Periodontal treatment affects circulating levels of endotoxin, CRP, and TNF-a, leading to long-term improvement in endothelial function.
Diabetics have a 3x higher prevalence of periodontitis, with contributing factors including age, metabolic control, and the presence of inflammatory cytokines.
AGEs activate RAGE on various cells, leading to increased inflammatory cytokines and direct cell damage, which compromises healing.
Less than 10% visible plaque and less than 10% BOP.
The three levels are: 1) Subject level - individual risk factors; 2) Tooth level - factors about the tooth; 3) Site level - factors about the site.
Stability is defined as maintenance with a decrease in probing depth (PD) and no bleeding on probing (BoP).
Periodontal infection may increase systemic inflammation and induce insulin resistance, while increased cytokine levels can affect the efficacy of insulin receptors, contributing to poor glycemic control.
Degree of bone loss (% or mm), pattern/type (horizontal vs vertical), presence of subgingival calculus, furcations, and other factors like endo-perio lesions and widened PDL.
Evaluate treatment and assess healing response, compare pre and post-treatment clinical parameters, review and reinforce oral hygiene instruction, and assess tissue characteristics.
Formation of long junctional epithelium (JE), reduced pocket depth, regeneration of cementum and periodontal ligament (PDL), and maturation of connective tissue.
Advanced bone loss, uncontrolled environmental/systemic conditions.
Direct infection by periodontal bacteria through ulcerated junctional epithelium (JE) into the bloodstream, leading to bacteremia.
BOP (30% is threshold), CAL, pocket depths, suppuration.
Patient education, training in personal oral hygiene, counselling on control of risk factors, removal of defective restorations, and scaling and root debridement.
It involves creating a surgical flap to access the area and debride it.
Bacterial invasion into epithelium and connective tissue, particularly by spirochetes like Treponema and Fusobacterium, along with activation of host response leading to periodontal destruction.
Plaque can be detected visually (dry direct vision) or using plaque disclosing solutions such as erythrosine, fuschine, or fluorescine dye.
Furcation involvement, including furcation class, interproximal bone level at entrance, root anomalies, and root resection.
Increased circulating levels of pro-inflammatory cytokines such as IL-1, IL-6, and TNF-a.
By showing the amount of remaining bone rather than bone lost, with normal being 1.5-2mm from CEJ to alveolar crest, and evaluating the distribution and pattern of bone loss.
Break in continuity of lamina dura, bone loss with widening PDL space, wedge-shaped radiolucency at M-D, reduced height of interdental bone and septa, and irregular areas of reduced density in interdental craters.
Clinical prevention involves proper and regular plaque elimination, professional support at regular intervals, continuous scaling and root debridement, and specific treatments for gingivitis and periodontitis.
Subgingival probing shows depth reduction and absence of bleeding on probing (BOP).
Periodontal abscesses may lead to tooth loss and pose a potential risk of bacteraemia.
Common etiological factors include untreated periodontitis, incomplete periodontal debridement, systemic microbial intake, and uncontrolled diabetes.
Instability is indicated by further treatment needs, with an increase in PD, positive BoP, and clinical attachment level (CAL) increase, or the same PD with positive BoP and CAL increase or same.
Periodontal disease severity, including probing depth, mobility, recurrent perio abscess, bone loss, and bone defect morphology.
Evaluating systemic status (e.g., diabetes, smoking), managing risk factors, providing oral hygiene instruction and education, and conducting a clinical exam.
PA (Periapical), BW (Bitewing), and OPG (Orthopantomogram).
Progression to the periodontal ligament and alveolar bone, with necrosis and ulcers extending to these areas, attachment loss, open interdental papillae, and exposed interdental bone.
1. Attain sustained high level of personal plaque control, BOP <10%. 2. Absence of increase in attachment loss. 3. Probing depths <5mm, horizontal furcations <5mm. 4. Tooth mobility should not impair patient's plaque control.
LOW – 6-12 months, MOD – 6 months, HIGH – 3 months.
Probing depth and CAL are tooth-related factors that indicate the severity of periodontal disease and influence prognosis.
An Excellent prognosis is characterized by no bone loss, excellent gingival condition, good cooperation, and no systemic or environmental factors.
A Poor prognosis includes moderate to advanced bone loss, mobility, Grade II or III furcation involvement, doubtful cooperation, and the presence of systemic or environmental factors.
Factors affecting periodontal prognosis include anatomical factors, tooth-related factors, prosthetic factors, local factors, and overall clinical factors.
Local factors include plaque and calculus.
The levels of periodontal prognosis are Excellent, Good, Fair, Poor, and Questionable.
Anatomical factors include short tapered roots, root proximity, furcation involvement, enamel pearls, grooves/concavities, and cervical enamel projections.
Patient compliance is an overall clinical factor that can significantly influence the prognosis, with better cooperation leading to improved outcomes.
