They affect susceptibility to disease, plaque microbiota, clinical presentation, disease progression, and response to treatment.
Hormones suppress the immune response to plaque, leading to depressed PMN chemotaxis, phagocytosis, antibody, and T-cell responses.
Histology
1. Autogenous 2. Allografts (other humans) 3. Xenografts (e.g. Bio-oss from bovine bone) 4. Alloplasts (synthetic)
Class II/III furcation involvement, severe bone loss around ≥ 1 root(s), root fracture, perforation, resorption, adequate bone structure around remaining roots (and good crown:root ratio), sound restorative prognosis, and minimal mobility ≤ grade 1.
Cellular cementum.
Periodontal surgery should be considered for patients with deep pockets, impaired access for debridement, and when there is a need to regenerate lost tissues.
Indications include being medically healthy, psychologically sound, a non-smoker, having good oral hygiene, and pockets greater than 5 mm.
Contraindications include poor patient cooperation, impaired access for debridement, and certain medical conditions like arterial hypertension and anticoagulant use.
Moderate risk
Attached gingiva augmentation if gingiva is too thin.
A longer root trunk length (from CEJ to fornix) is associated with a lower chance of furcation involvement.
High risk for recurrent disease
Cells from PDL, epithelial cells, gingival CT cells, and bone-derived cells.
Factors include the width of the periodontal ligament, the number and width of periodontal fibers, and the density of alveolar bone.
Poor crown:root ratio, inadequate bone support on roots to be retained, long root trunks, fused roots (hence the need for CBCT prior to treatment), poor restorative/endo prognosis, poor surgical access, and poor oral hygiene.
Increased risk of post-surgical infection and impaired wound healing.
Sustained hyperglycaemia leads to impaired immunity and poorer healing response, particularly affecting neutrophil function.
Impaired neutrophil function results in reduced adherence, chemotaxis, and phagocytosis, allowing bacteria to persist in the periodontal pocket and leading to common periodontal abscesses.
Overhangs in dental restorations.
Existing gingiva preserved, marginal alveolar bone exposed for identifying morphological defects, preserved oral epithelium, and generally less unpleasant post-op period compared to gingivectomy.
Evidence is limited and indirect; surrogate measures like CRP and IL-6 generally decrease following treatment, but the impact on CVD risk remains uncertain.
Osteoplasty creates physiologic form without removing supporting bone, while ostectomy involves the removal of bone.
<10%
BOP (bleeding on probing), probing depth, and LOA (loss of attachment).
Hormonal influences affect the physiological response, vascular system, inflammatory response, and immune system.
Better bone gain and improvement of +1 mm.
Diabetes
It is dose-dependent; heavy smokers (>20/day) are at high risk.
Techniques are sensitive, making case selection important.
Probing inside developmental fissures is crucial to detect disease and facilitate debridement, preventing bone loss.
Increased gingivitis, with 35-100% of pregnancies showing increased bleeding on probing, gingival crevicular fluid, and probing depth.
Ectopic teeth exposure.
Greater short-term pocket reduction, but mixed long-term response regarding pockets and attachment.
Acute traumatic occlusion is characterized by pain/sensitivity to percussion and increased tooth mobility due to abrupt occlusal impact from biting on hard objects or restorations.
Polishing, fluorides, and determination of future supportive periodontal therapy.
Plaque-induced inflammation with a well-defined inflammatory infiltrate rich in vascular structures, plasma cells, and lymphocytes, without extension into the supracrestal CT zone.
Increased recurrence leads to a greater need for re-treatment and antibiotics.
Smoking leads to less gingivitis and bleeding on probing due to nicotine-induced vasoconstriction.
>1%
After 6 months to a year if there is reduced gingival inflammation, reduced bleeding, and compliance with recall appointments.
Bleeding, swelling, discomfort, bruising, and root sensitivity.
The rationale includes eliminating pockets, improving access for debridement, and potentially regenerating lost tissues.
It is validated as a tool for predicting disease progression and tooth loss.
Root coverage procedures.
Pathogens like P. gingivalis, T. Forsynthia, and A. actinomycetemcomitans produce virulence factors that activate the host immune response, leading to the recruitment of inflammatory cells such as PMNs and macrophages.
Injury of the attachment apparatus/tooth due to excessive occlusal forces that exceed the adaptive capacity of tissues.
Altered direction of loading can change the orientation of the periodontal ligament fibers, impacting the response of the periodontium.
Capnocytophaga species are predominant in T1DM patients, while T2DM is associated with Prevotella intermedia, Campylobacter recuts, Porphyromonas gingivalis, and Aggregatibacter actinomycetemcomitans.
Duration, diabetes (long-short term), puberty, pregnancy, and menopause.
MSCs consistently promoted increased PDL and cementum regeneration in animal models.
No additional benefits were detected in certain defect models, but superior histological results were observed in others.
Root concavities can be identified on radiographs and are likely found on lower molars, making them a risk factor for periodontal disease.
Raised estradiol levels in females lead to inflammation, papillary/interdental bleeding, and possibly pocketing.
A well-organized professional care regime every 3-6 months helps maintain probing depths and attachment levels.
Closer root proximity can lead to a thin bone septum, making it harder for patients and periodontists to remove plaque.
Waerhaug’s concept indicates that angular defects are not consistent with trauma and occur equally in traumatised and non-traumatised teeth.
Possible infection or periodontal disease.
Primary aetiology involves adaptive mobility with normal support, while secondary aetiology involves progressive mobility requiring splinting due to inadequate support from conditions like active periodontitis.
Bone surgery is required.
Bleeding on probing (BOP), possible erythema, swelling, and suppuration.
1. JE must < 2 mm 2. New, functionally oriented, CT (Sharpey’s) fibres to insert into previously exposed bone to reproduce PDL 3. New acellular extrinsic fibre cementum on previously exposed root 4. Alveolar bone height restored to within 2 mm of CEJ
AGEs lead to increased collagen cross-linking, greater stability of collagen, and accumulation in tissues due to resistance to enzyme degradation and tissue turnover.
RAGE is upregulated in type 2 diabetics, leading to increased inflammatory load and altered homeostatic transport across membranes, which can impair oxygen diffusion and metabolic waste elimination.
1. Direct bacterial effects on platelets, 2. Bacterial invasion into cells, 3. Autoimmune response, 4. Inflammatory response.
Epithelialisation takes about 7-14 days, with complete healing taking 4-5 weeks.
Periodontal infection increases systemic inflammatory load, which elevates cytokines that affect the efficacy of insulin receptors, particularly TNF-a, which inhibits autophosphorylation of the receptor tyrosine kinase.
Periodontal treatment costs between $900 and $2500, while open heart surgery costs less than $180,000.
They should be biocompatible and consider allergies and plaque retention.
Orthodontic force creates pressure on one side leading to undermining resorption and tension on the other side causing PDL widening and apposition.
Motivation, re-instruction, instrumentation.
Implants have a greater failure rate, especially in the maxilla, and a higher incidence of peri-implantitis.
Improved glycaemic control with a 1% reduction in HbA1c, associated with a 25% reduction in diabetes-related deaths.
There are increased percentages of spirochetes and motile rods and decreased cocci associated with poor glycaemic control.
Open contact can lead to plaque retention and requires restoration. Uneven marginal ridges and opposing cusps can also contribute to debris accumulation.
Smoking alters neutrophil chemotaxis, phagocytosis, and oxidative burst, leading to increased collagenase and elastase in gingival crevicular fluid (GCF).
Smokers show less healing and less reduction in subgingival T. forsythia and P. gingivalis after treatment, leading to regression in pocket depth reduction and attachment gain over time.
Supra/equi-gingival to avoid interfering with supracrestal attachment.
Glickman’s concept suggests that occlusal forces do not initiate plaque-induced gingival disease or periodontitis, but this is incorrect as shown by Waerhaug’s studies.
Non-traumatised teeth exhibit horizontal bone loss, while traumatised teeth show angular bone loss.
The study found no migration of connective tissue attachment due to periodontal conditions or excessive occlusal forces, and no good evidence that it contributes to periodontal disease.
Jiggling trauma is a combination of pressure and tension that increases the width of the PDL and causes inflammatory changes.
Treatment of re-infected sites.
Tissue repair is affected by hormonal influences on the immune response.
There is a positive relationship between the number of cigarettes smoked per day and the probability and severity of periodontal disease, including deeper probing depths and more sites affected.
They cause significant changes, particularly in the presence of pre-existing, plaque-induced gingival inflammation.
Estrogen and progesterone.
It leads to a 50% reduction in IL-6, increased capillary permeability, and increased gingival exudate.
Neglecting SPT leads to ineffective periodontal treatment and a higher progression of disease.
Root contour and conform to furcation anatomy.
It can lead to increased tooth mobility and inflammatory response.
They are hard to clean.
Peri-implant health may have deeper pockets, shorter interproximal papillae, and histological differences such as a 3-4 mm height of the junctional epithelium and less vascularity compared to the periodontium.
No, occlusal trauma does not initiate periodontal destruction, but removal of the trauma may reduce tooth mobility without stopping further periodontal breakdown.
Foam cell formation, leading to stenosis of the artery lumen and potential rupture of plaque from arterial walls, which can cause a thrombotic event.
Peri-implantitis lesions are larger than mucositis sites and progress faster than periodontitis.
Patients with periodontal disease have a high risk of reinfection, necessitating regular long-term maintenance.
Smokers experience increased calculus, greater colonization of pockets, greater species diversity, and an increase in pathogenic organisms such as P. gingivalis and T. forsythia.
Cervical enamel projections can lead to plaque retention and periodontal issues, especially in the furcation area of lower molars.
Through parameters such as percentage of bleeding on probing (BOP), number of pockets greater than 4 mm, and tooth loss.
Severe periodontal disease is associated with a 6-fold increase in poor glycaemic control, a 3.5-fold increase in cardio-renal disease mortality, and a 2.5-fold incidence of renal disease complications.
To improve bone architecture, expose subgingival caries, or for prosthetic reasons.
Ovate, conical, ridge-lap, modified ridge-lap, and sanitary.
Oxidative stress is increased by interactions between host immune cells and invading microorganisms, leading to systemic circulation of reactive oxygen species (ROS) and stimulating various functions at atheroma sites.
It is classified into acute and chronic. Acute involves abrupt occlusal impact, while chronic involves gradual changes in occlusion due to factors like tooth wear and parafunction.
Waerhaug’s concept states that angular defects occur equally in disease and non-disease stages, indicating they are not solely caused by occlusal trauma.
Surgery may cause disease to progress more rapidly, lead to greater furcation deterioration, complications with membranes for guided tissue regeneration, less success with bone replacements, and an increased incidence of tooth loss post-surgery due to recurrence.
Low risk
Every 3-4 months, as the RBC lifespan is 100-120 days.
Poor dental health has been correlated with heart attacks and is considered a risk factor for CVD.
Pockets extending beyond the mucogingival border, furcation involvement, treatment of bony defects, more residual subgingival calculus in closed debridement of pockets > 5 mm, and recurrent abscesses.
CRP is a plasma protein involved in the acute phase response to infection and inflammation, mediating macrophages’ uptake of LDL, and is a predictor of heart disease risk. Levels are consistently high in patients with periodontal disease compared to controls, and periodontal treatment can reduce CRP levels.
Patients should be informed that surgery may be required at the start to avoid misconceptions about the dentist's competence.
More recession in the long- and short-term, with no difference in pocket depth reduction compared to closed debridement.
The Theory of Co-destruction describes a zone of irritation of marginal gingiva due to plaque and a zone of co-destruction of PDL, cementum, and alveolar bone due to both plaque and trauma.
Management includes plaque control, occlusal adjustment (enameloplasty), occlusal splints, and splinting to control mobility using composite, orthodontic wires, RPD, fixed bridges, or cross-arch splints.
Clinical signs include mobility, thermal sensitivity, excessive wear, migration, discomfort or pain on chewing, and fractured teeth.
The presentations include signs of injury to the periodontal attachment apparatus, which can be observed both clinically and through radiographic imaging.
Therapeutic measures include surgical methods to treat complex periodontal problems, tissue reconstruction, and addressing deep pockets that may require surgery.
Elimination of bacteria, patient oral hygiene, and regular interceptive professional support therapy.
Continuous diagnostic modeling at recall appointments, requiring objective criteria for assessing individual risk.
Complications include retinopathy (blindness), neuropathy (amputations), nephropathy (end-stage renal disease), and a 2- to 4-fold increase in cardiovascular mortality and stroke.
P. gingivalis can invade cardiac endothelial cells, leading to an inflammatory response and the formation of foam cells, which are hallmarks of early atherosclerotic lesions.
Suprabony pockets and abscesses, elimination of gingival enlargement, and gingival deformities.
Diabetics experience less collagen production, elevated collagenases, decreased osteoblast proliferation, and increased apoptosis of fibroblasts and osteoblasts, leading to poor healing of the periodontium.
Reproduction or reconstruction of cementum, PDL, and alveolar bone to completely restore architecture and function.
Pockets ≥ 6 mm, infrabony defects (3-wall more likely to regenerate), and furcation defects (Grade 3 unpredictable).
Chronic traumatic occlusion involves gradual changes in occlusion due to tooth wear, drifting, extrusion, and parafunction, and is more common and significant than acute.
To use a barrier membrane to block the epithelial and CT cells from causing healing, allowing PDL cells to repopulate the affected root surface.
>96% of teeth retained over >10 years (Cortellini et al., 2004)
Endogain
Low risk
Avoid surgery as there is no difference in attachment and only a greater short-term reduction in pocket depth.
The PDL space widens in response to occlusal forces, and the tooth may show non-progressive increased mobility, but the PDL can return to normal width following occlusal adjustment.
Constant pressures are more injurious than intermittent forces, and more frequent application of intermittent forces increases injury to the periodontium.
