Complete physical, mental, and social well-being.
Oral epithelium
Sulcus < 3mm, pink, firm, scalloped outline, no bleeding, stippled, knife-edge margin.
SRD stands for Scaling and Root Debridement, and it should ideally be performed at the first appointment, depending on the patient's pain level.
Corrective treatments include gingivectomy, gingivoplasty, and regenerative/respective surgery.
Yes, microbes are consistent between endodontic infections and deep periodontal pockets.
Fibroblasts, cementoblasts, osteoblasts/clasts
Alveolar crest fibres, horizontal fibres, oblique fibres, (peri)apical fibres
Sanitary, (Modified) Ridge lap, Ovate, and Conical.
Debridement with surgery.
Plasma cells predominate (>50%).
Whether the tooth is needed for removable partial dentures (RPDs) or other functional and aesthetic demands.
The chronic and aggressive classifications from Armitage 1999 were merged into a single classification called 'periodontitis'.
Lamina densa and Lamina lucida
Slow if bone surgery is involved, and rapid if orthodontic extrusion is combined with fibrectomy.
Increased hydrostatic pressure and vascular permeability leading to exudate into CT and increased GCF flow.
Leucocyte adhesion deficiency
Hypophosphatasia
3-monthly recall for prophylaxis and oral hygiene instruction (OHI) for 3 years, followed by a life-long commitment. Only scale if there’s calculus to avoid unnecessary gum irritation.
An inflammatory lesion resulting from interactions between the dental plaque biofilm and the host’s immune-inflammatory response, which remains contained within the gingiva and does not extend to the periodontal attachment beyond the mucogingival junction.
No, endodontic lesions rarely involve the marginal periodontium unless abscessed.
Fibromas, papillomas, peripheral and central granulomas, leukoplakia, gingival cyst.
Remove overhang, avoid convexities, reduce occlusal table, and use a metal finishing line.
Tunnel preparation, open flap debridement, root resection, guided tissue regeneration (especially for mandibular molars).
Management steps include draining the abscess through the pocket by compression or incision, or extraction if the tooth is hopeless, debriding the pocket, and irrigating with water or 0.2% solution.
Multilayer and parakeratinised with rete pegs.
Hemidesmosomes attach to the tooth, and desmosomes attach to other epithelial cells.
The periodontium is intact and exhibits complete physical, mental, and social well-being.
The prognosis is poor to hopeless.
Neutrophils, lymphocytes, macrophages
They anastomose with alveolar bone and PDL vessels.
Loss of collagen, fibroblast degeneration, rete peg proliferation in coronal JE, clinical signs like BOP and marginal erythema.
They are modifying factors, not diagnoses.
Vessels in dento-gingival plexus remain dilated, increased vascular proliferation with looping and activation of previously inactive capillary beds.
To ensure ongoing oral health and prevent disease progression.
Two layers: basal and suprabasal.
To establish and maintain oral health.
Intrinsic fiber cementum contains primarily intrinsic fibers produced by cementoblasts, oriented parallel to the cementum surface. It is predominantly located at sites undergoing repair following surface resorption and plays no role in tooth anchorage.
Mixed fiber cementum contains a mixture of extrinsic and intrinsic fiber cementum.
H2O2 (Hydrogen Peroxide)
In furcal areas.
Grade B is the default.
48 hours (Rincon says 24-48, eTG says 48-72)
The part of the fibres embedded in cementum and bone
Bleeding on probing (BOP), increased oedema, and changes in color and contour indicating moderate to severe inflammation.
Apical down-growth of biofilm, increasingly anaerobic environment, irreversible damage, pocket deepening (≥ 5mm), JE migrates apically from the CEJ, extensive damage to collagen fibers, and loss of connective tissue attachment.
Triangular shape, wider coronally.
No, if the bone is thick; Yes, if the bone is thin.
This condition can be corrected with periodontal surgery.
Placement of margins, considering the base of the sulcus as the top of the attachment.
Supracrestal attached tissues.
They found that systemic antimicrobial therapy using a combination of amoxicillin and metronidazole can enhance the clinical benefits of non-surgical periodontal therapy, with a full-mouth weighted mean change for PD improvement of 1.41 mm and CAL gain of 0.94 mm.
The epithelial attachment is the attachment apparatus, including the internal basal lamina and hemidesmosomes, that connects the junctional epithelium to the tooth surface.
Gentle removal of plaque and necrotic debris, ultrasonic debridement, local irrigation with 0.2% chlorhexidine mouthwash or 3% H2O2, elimination of causative factors (e.g., smoking cessation, stress), antibiotic therapy (e.g., Metronidazole: 400 mg orally, 12-hourly for 5 days), analgesics (e.g., 400-600 mg ibuprofen orally, 4-hourly; alternate with 1000 mg paracetamol orally, 4-hourly), oral hygiene instructions (OHI)
1-3 mm.
Experienced clinicians achieve better outcomes compared to those with minimal experience.
Bone loss is categorized as <30% (mild), 30-65% (moderate), >65% (severe).
Furcation involvement is classified as: I (incipient), II (moderate), III (severe).
The distinction is mainly based on the complexity of management, such as a high level of mobility indicating Stage IV.
Because it can lead to recession of papillae and margins.
Papillion-Lefèvre Syndrome
PMNs predominate, infiltrate 15% of CT, lymphocytes and plasma cells appear.
4.5-5 mm on average.
Horizontal, vertical, and angular bone loss.
The presence of calculus is associated with periodontal disease, except in cases of aggressive periodontitis.
> 70% bone loss with Grade III furcation
> 0.8 mm of residual bone.
It alters the charge and free energy of the tooth surface, increasing bacterial adhesion.
Gram-positive cocci, such as Oral streptococci (e.g., S. sanguis, S. gordonii, S. oralis).
Less than 4 teeth.
Advanced bone loss, doubtful cooperation, tooth mobility, Grade II/III furcation, inaccessible areas, and systemic/environmental factors
Further bacterial proliferation occurs, late colonizers arrive, and an intermicrobial matrix develops, composed of bacterial lysates, GCF, and salivary components.
Interproximal CAL is less than or equal to buccal CAL
IV bisphosphonates have a higher risk of complications compared to oral bisphosphonates.
Adequate bone support, patient cooperation, control of aetiological factors, and manageable systemic or environmental factors.
1.
3.
Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium.
Rate of disease progression, risk of further progression, potential responsiveness to standard therapy, and effect on general health.
Superior/inferior dental artery, dental artery, intraseptal artery, rami perforantes.
It tells you where the bone is by measuring the level of the bottom of the pocket (depth in relation to soft tissue) relative to the cementoenamel junction (CEJ).
Naber’s probe.
Non-surgical debridement with ultrasonic tools.
There is an increase in GCF flow.
Because it provides more surfaces for possible bone formation.
50-70% bone loss with Grade II furcation
Improvement in soft tissues and oral hygiene.
Long-term survival if successful; retreatment required if failed.
The extent of the caries and the condition of the restoration.
Moderate to advanced bone loss, doubtful cooperation, tooth mobility, Grade I/II furcation, difficult to maintain, and systemic/environmental factors
Extracting hopeless teeth, caries control, endodontic treatment, and oral hygiene instruction (OHI).
F. nucleatum acts as a bridge between initial colonizers and later colonizers, forming corn-cob-like structures as filamentous bacteria adhere to the oral streptococci.
Factors include initial assessment of patient expectations, treatment expectations (short-term and long-term), aesthetics, financial status, and patient compliance.
Crown-lengthening, which includes protocols like gingivectomy and apically repositioned flap with ostectomy/osteoplasty.
The layers of oral epithelium are the basal layer, prickle cell layer (stratum spinosum), granular cell layer (stratum granulosum), and keratinized cell layer.
Clinician’s skill level, initial pocket depth, predisposing factors, tooth morphology, tooth type, time, and patient’s compliance.
Junctional epithelium ulceration.
0.
To address issues that non-surgical methods cannot reach, such as pockets deeper than 5.5 mm, through procedures like gingivectomy, open flap debridement, grafting, regenerative surgery, implant placement, endodontic surgery, and extraction of non-responding teeth.
It seems to be low.
Bone to cementum
Some PMNs in JE and sulcus, lymphocytic infiltrate 5% of CT, pro-inflammatory cytokines leading to vasodilation.
Scaling and root debridement (ultrasonic), odontoplasty (reshaping crown).
The percentage of plaque present in the mouth.
Extrinsic fiber cementum contains primarily extrinsic fibers, such as Sharpey's fibers, which are continuous with the principal fibers of the periodontal ligament. These fibers are oriented perpendicularly to the cementum surface and play a major role in tooth anchorage.
Not diagnostic of active periodontal disease, no indication of cellular activity, shows less bone loss than actual, crestal lamina dura not related to clinical inflammation, angulation can influence detection, shallow palate can distort CEJ and alveolar crest, may not show interdental defects, thick bone can hide defects.
35% overall
OHI (smoking cessation, tooth brushing, and interdental cleaning), SRD (± LA, e.g., ultrasonic cleaning and/or hand scaling), and periodontal surgery if advanced (OFD ± bone recontouring).
They found significant CAL gain (WMD = 0.21; 95% CI = 0.02 to 0.4; P <0.05) and PD reduction (WMD = 0.43; 95% CI = 0.24 to 0.63; P <0.05) in favor of SRP + AMX/MET.
Initial phase therapy, local therapy, hygiene phase, non-surgical phase, or host-related phase.
Cellular intrinsic fiber cementum is found in resorption lacunae at the apex of the tooth, at sites of cemental repair. It contains cementocytes, which are cementoblasts in the matrix that have lost their secretory ability, and it plays no role in tooth anchorage.
It indicates a shortened dental arch.
Uncontrolled systemic conditions worsen the prognosis, while controlled conditions improve it.
A tooth with recurrent periodontal abscess generally has a hopeless prognosis.
4-6 weeks after initial debridement.
Thin phenotype: probe visible (< 1 mm); Thick phenotype: probe invisible (> 1 mm)
No sign of enlargement
2.
Severity of disease and anticipated complexity of management.
Histological perfection is a theoretical concept with no infiltrate and continuous sparse neutrophil migration into the coronal JE and crevice.
Sublingual, Mental, Buccal, Facial, Greater palatine, Intraorbital, Posterior superior dental artery.
Squamous Cell Carcinoma (SCC)
A periodontal abscess is a localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus due to an inflammatory process that attracts PMNs.
No, there are no unique phenotypic features unique to diabetic periodontitis.
Langerhan’s cell histiocytosis
Less than 10% bleeding on probing (BOP) and probing depth of ≤ 3 mm. It also assumes biological and inflammatory markers compatible with homeostasis, with health being predominantly neutrophilic infiltrate for immune surveillance.
The types of oral mucosa are masticatory, lining, and specialized mucosa.
Uncontrolled diabetes (HbA1c <6.5%), immunosuppression, acute infections, and medication-related issues.
Bisphosphonates, cyclosporine, and amlodipine.
Managing acute conditions such as pain (e.g., abscesses), rapid bone loss, and ANUG.
They form reversible attachments via van der Waals and hydrogen bonding interactions, and then irreversible attachments via specialized surface adhesins and receptors.
Patients are responsible for compliant oral maintenance and elimination of undesirable habits such as smoking.
Smokers have a worse prognosis compared to non-smokers.
They found a small additional benefit in terms of reductions in mean PD and mean percentage of BoP, with significant effects favoring SRP plus antibiotic for reductions in mean PD (-0.22 mm) and mean percentage of BoP (4%). There was no significant effect for CAL gain and plaque index reduction.
Root anomalies include enamel projections, pearls, grooves, etc., and they can complicate periodontal treatment and affect prognosis.
25%.
Enlargement confined to interdental papilla
It indicates aggressive periodontitis with a molar-incisor pattern.
Factors include the cause, level of attachment loss (LOA), healing response, oral hygiene, supportive periodontal therapy (SPT) compliance, restoration longevity, and skill of the clinician.
Carcinoma (e.g., squamous cell carcinoma), melanoma.
The JE detaches from the tooth, forming pocket epithelium that is ulcerated and more permeable, allowing further apical migration of biofilm.
Rolled flap, Pouch graft, (Combined) Onlay graft, and GBR.
Interproximal embrasures, tooth contact, and papilla.
Plasma cells (10-30% infiltrate) and B cells increase.
Pedicle graft, Semilunar coronally positioned flap, and Envelope.
The endodontic condition of the tooth, including a pulp test.
Aids diagnosis, helps determine prognosis and treatment, adjunct to clinical assessment, reveals altered calcification, shows past effects on bone, detects systemic skeletal conditions.
Most had 50-70% attachment
Only non-restorable teeth, those with concurrent endo-perio lesions with grade III mobility, and 8s with poor accessibility or furcation involvement
Supra-crestal connective tissue attachment (1.07 mm) and junctional epithelium (0.97 mm).
Specialized mucosa is found on the dorsum of the tongue.
The prognosis should be re-evaluated after Initial Periodontal Therapy (IPT) based on the response to treatment and control of local, systemic, and environmental factors.
0.12% chlorhexidine, 15 mL, rinse for 1 minute, 8 to 12-hourly, for a maximum of 2-3 weeks
Interproximal CAL is greater than buccal CAL
Greater than 4 mm.
Because periodontal disease may be related to occlusal overload.
Reduced pocket depths, reattachment/repair via formation of long junctional epithelium, resolution of inflammation, reduced bleeding on probing, elimination of exudates, and gingival recession.
Vertical bone filling, very little horizontal bone gain, and possible sensitivity due to debridement.
30% of the connective tissue is infiltrated.
Causes include foreign body impaction, bacterial invasion, and underlying systemic diseases such as diabetes.
Tooth-related factors such as mobility, probing depth (PD), sound tooth remaining, occlusal antagonisms/tooth position, and endodontic condition.
Alveolar bone loss begins.
The periodontium includes the gingiva, periodontal ligament, cementum, and alveolar bone.
The reduced enamel epithelium and the basal layer of oral epithelium increase mitotic activity and migrate into the underlying connective tissue, forming an epithelial mass that prevents bleeding.
The junctional epithelium (JE) covers these portions.
It is replaced by the junctional epithelium, which becomes continuous with the oral epithelium and provides the attachment between the tooth and gingiva.
The mucogingival line is the boundary between the attached gingiva and the alveolar mucosa, present only on the buccal mucosa.
Prognosis is the prediction of a disease’s probable course duration and outcome, established after diagnosis and before treatment.
No recession
To remove plaque, bacterial by-products, and calculus while preserving cementum to aid in healing.
Tooth mobility indicates the severity of periodontal disease: 0/1 (normal or slight), 2 (moderate), 3 (severe).
Underlying osseous support, bioform (scalloping), and tooth morphology
Incomplete treatment and requires further therapy.
Deep, narrow bone defects generally have a better prognosis compared to superficial, wide (horizontal) bone defects, which are associated with poorer outcomes.
Healing may take 9-12 months for deeper sites.
Enlargement covers three-quarters of the crown
1.5 – 2 mm
It forms after amelogenesis when ameloblasts become reduced in height, produce a basal lamina that contacts enamel, and epithelial cells communicate via hemidesmosomes.
Smoking, metabolic factors (e.g., hyperglycemia), nutritional factors (e.g., scurvy), pharmacological agents (e.g., phenytoin, cyclosporine, nifedipine), hormonal changes, and hematological conditions (e.g., leukemia, myelodysplasia, thrombocytopenia, clotting-factor deficiencies).
Developmental/genetic factors, infections, immune conditions, reactions, neoplasms, endocrine diseases, trauma, etc.
They have an increased risk of recurrent periodontitis even if there is no current disease and can go through periods of exacerbation. They are still considered periodontitis cases if inflammation is present.
Bone loss
1) Recession if thin phenotype, leading to an apical shift of JE and loss of periodontal supporting tissue. 2) Persistent inflammation if thick phenotype, creating space for biological width without changing bone levels.
They found that the evidence for an additional benefit of adjunctive antibiotic therapy in smokers with chronic periodontitis is insufficient and inconclusive.
Oral epithelium is keratinized stratified squamous epithelium.
Gradients for oxygen, pH, and nutrients develop, with the biofilm becoming increasingly anaerobic in deeper areas.
Pocket depth reflects disease severity as follows: <5 mm (mild), 5-7 mm (moderate), >7 mm (severe).
No adequate zone of attached gingiva, supracrestal attachment < 3 mm, improve bone architecture, and recontouring periodontal defects.
They found that adjunctive therapy may improve the efficacy of SRP in reducing PD in diabetic subjects, with a WMD in PD reduction of -0.15 mm favoring antibiotic use. However, WMDs in CAL gain, PI, and BOP reductions did not favor adjunctive antibiotic use.
It is effective in removing plaque and calculus, flushes out bacteria and by-products, is anti-bacterial via cavitation, and causes less fatigue for the clinician.
Success and periodontal stability.
To guide the growth of new periodontium using barrier membranes, preventing gingiva from interfering with bone and periodontal ligament (PDL) regeneration.
Proximal convexity at CEJ level
Plaque-retentive factors and oral dryness.
Masticatory mucosa is found on the hard palate and gingiva.
The gingival margin, also known as free gingiva, has a dull surface, a rounded and scalloped outline, and is firm.
Attached gingiva extends from the sulcus to the mucogingival line and is stippled, while free gingiva is the gingival margin with a dull surface and rounded outline.
Less than adequate bone support, patient cooperation, some tooth mobility, Grade I furcation, and SPT possible
Cellular mixed stratified cementum is found in the apical 1/3 of the tooth and furcation areas. It is composed of mineralized extrinsic collagen (Sharpey's fibers) that are more irregular than in acellular cementum, and it includes a combination of intrinsic and extrinsic fibers with trapped cementoblasts.
Extension beyond the gingiva and bone denudation through alveolar mucosa, osteitis, and bone sequestra (generally only in severely immunocompromised patients)
Gingival recession with no interproximal clinical attachment loss (CAL)
No bone loss, good cooperation, excellent gingival condition, and no systemic/environmental factors.
Triangular teeth
High probability of periodontal health.
Identify the cause, which may require further instrumentation or periodontal surgery, and possibly refer to a specialist.
Gingivectomy, open flap debridement, grafting, regenerative surgery, implant placement, endodontic surgery, and extraction of non-responding teeth.
Corrective orthodontics, final restorations, fixed and removable prosthetics, and evaluation of restorative and periodontal conditions.
It is parallel to the CEJ projection.
Chief complaint, medical history, extraoral exam, intraoral exam, occlusion, and mobility assessment.
Salivary proteins (e.g., mucins, antibodies, slatherin, enzymes) and lipids.
Superficial bacterial zone, Neutrophil-rich zone, Necrotic zone, Spirochaetal/bacterial infiltration zone
Papilla necrosis, ulcers, bleeding on probing (BOP), pain, halitosis, pseudomembrane formation, lymphadenopathy, fever
The presence of extensive caries.
No, there is no evidence suggesting problems if the patient maintains adequate oral hygiene.
Probing.
Host immune impairment
Painless, slow-growing discrete, sessile or pedunculated masses ballooning of papilla and margin
Mouth-breathing, systemic conditions, idiopathic (rare, congenital fibromatosis)
4.
Marked bone loss.
An abscess.
Unless periodontal disease extends all the way to the tooth apex, the dental pulp is capable of surviving significant insults, and the effect of periodontal disease and treatment on the dental pulp is negligible.
An osteon is comprised of lamellae, which are concentric layers of compact bone surrounding the central Haversian canal. The blood supply is facilitated by Volkmann’s canals that communicate with Haversian canals to connect osteons and supply nutrients to the bone.
Acellular extrinsic fiber cementum is located in the cervical 2/3 of the tooth, including the coronal and midroot areas. It is characterized by well-defined collagen type I fibrils, specifically Sharpey's fibers.
A favourable ratio is less than 1:1; an unfavourable ratio is greater than 1:1.
They found a 0.5-millimeter average improvement in CAL with SRP, and combinations of SRP with assorted adjuncts resulted in CAL improvements between 0.2 and 0.6 mm over SRP alone. Four adjunctive therapies were judged beneficial with moderate certainty: systemic subantimicrobial-dose doxycycline, systemic antimicrobials, chlorhexidine chips, and photodynamic therapy with a diode laser.
Impaired oral function.
Advanced bone loss, non-maintainable areas, extraction indicated, and uncontrolled systemic and environmental factors
It can slow the rate of bacterial recolonization and prevent more pathogenic bacteria from emerging and causing disease progression.
The main cell types in oral epithelium are keratinocytes, melanocytes, Langerhans cells, Merkel's cells, and inflammatory cells.
The biofilm becomes more anaerobic, attracting Gram-negative strict anaerobes such as spirochetes and Aggregatibacter actinomycetemcomitans (Aa).
The lamina propria is the underlying connective tissue of the oral epithelium.
If the distance is 5 mm, the papilla is present in 98% of cases; if 7 mm, it is present in only 27% of cases.
Reduced quantity of plaque and a shift in composition towards gingival health, with less Gram-negative anaerobic bacteria and more Gram-positive aerobic bacteria.
Organize frequent reviews to ensure they are ready to progress or manage palliatively.
Primary molars have a more coronal CEJ height.
1-3 mm pockets: 0 mm reduction, 4-6 mm pockets: 1.3 mm reduction, >7 mm pockets: 2.2 mm reduction.
Enlargement involves papilla and margin
Periodic recall to assess plaque/oral hygiene, bleeding on probing (BOP), clinical attachment level (CAL), pockets, restorations, new caries, occlusion, mobility, and other pathological conditions.
Cancer screening, saliva, halitosis, and gingiva.
They are irregular reduced radiopacity areas.
Accessory canals connect the root canal system's neurovasculature with that of the periodontal ligament, and they are more common in molars than in premolars or anteriors.
They are normal despite looking suspicious.
Horizontal and vertical bone loss.
Red gingiva indicates inflammatory vascular changes.
Oedema in the gingiva appears as puffy or spongy tissue.
Phenytoin stimulates fibroblasts and epithelial cell proliferation, leading to gingival overgrowth in approximately 50% of patients.
Furcation arrows.
A positive pulp test indicates that the lesion is not endodontic in origin, unless there is necrobiosis in multi-rooted teeth.
500 mg phenoxymethyl penicillin qid for 5 days OR 300 mg clindamycin 8-hourly for 5 days.
Localized or generalized periodontal disease.
It is a continuous white line, though its appearance can vary depending on beam angulation.
Cyclosporin suppresses T cell function and can cause more vascularized gingival enlargement.
They are indicative of periodontal disease.
Host defense mechanisms can’t reach far into the canals of necrotic pulps to combat infection, leading to a chronic inflammatory zone unless treated.
Diabetes, arthritis, cardiovascular disease, pregnancy, genetic conditions, blood disorders, blood-borne infections, and autoimmune conditions.
Normal gingiva color is coral pink.
Yes, pulpal disease can cause periodontal changes.
Advanced periodontitis can allow bacteria to gain access to the pulp via accessory canals or the apex of the root and lead to infection of the pulp.
Normal pulps are observed in the majority of teeth with advanced periodontal disease.
A labial or lingual defect.
No, the absence of the lamina dura is not predictive of health or disease.
Reduced height and possible angular defects.
Grey discoloration suggests necrotizing gingivitis, metal deposition, or amalgam tattoos.
No, the effect of periodontal disease on the pulp is not clear-cut.
Firm and resilient gingiva with a stippled texture indicates healthy connective tissue projections.
Via a widened periodontal ligament (PDL).
It is not always diagnostic, but its presence indicates health.
To corroborate probing depths.
The innate immune responses include increased vascular permeability, PMN migration, and nerve fiber sprouting in adjacent pulp.
