factors and management Flashcards
What local factors contribute to plaque stagnation, accumulation and perio (anatomical and acquired)
Occlusion (traumatic overbites causing trauma to soft tissues), root grooves (hard to clean), furcations (hard to clean), enamel pearls and cervical enamel projections (stagnation), recession, premature contacts (causing localised bone loss), overcrowding, high labial frenum (hard to clean)
-Overhanging restorations, sub gingival restorations (encroachment of biological width), inadequate contact points, removable appliances, orthodontic appliances, open contacts, root fractures (accumulation and bone loss), root resorption (accumulation and bone loss), orthodontic treatment causing bone resorption
What is biological width and its relevance to restorations. Rough length
= The distance between the most coronal part of JE to the alveolar crest - JE + connective tissue attachment
-it is essential to consider it for maintaining healthy gingiva when doing restorations as enroaching the biological width can cause inflammation
-It is ~3mm. so must keep restoration 3mm clear of alveolar crest
Management of furcations
-calculus/ plaque removal, PMPR, clean with teepee, single tufted brush,
-surgical only for class II or III: furcationplasty, tunnel preparation, RSI with flap surgery for access, guided tissue regeneration, root resection
Management of traumatic incisal relationships. Why it can contribute to perio
-large class II or class III can cause incisors to damage palatal and labial tissues. class II div II can cause shearing trauma
-management: single tufted brush, soft splint to cushion the impact, orthodontic surgery to reposition occlusion, provision of posterior support, anterior restorations to provide occlusal steps, overlay denture to reduce contact of anterior teeth on soft tissues
List potential systemic risk factors for perio
Smoking, diabetes, genetics, age, socioeconomic status, medications, hormones, pregnancy, stress, systemic disease (eg. down’s), poor diet, obesity, alcohol
Why smoking contributes to perio. How more likely are you to have perio if you smoke
-Smokers 4 times as likely to have it than non-smokers.
-Due to changes in immune response. Impaired Neutrophil, lymphocyte, fibroblasts, immunoglobin, cytokines production, function and levels so less effective immune defenses.
-Reducing blood flow to gingiva so reduced oxygen and nutrients to cells and immune cells to area. Altered microflora, more pathogenic as more anaerobic conditions due to impaired vasculature.
-Increased levels of cytokines causes a shift in Pro inflammatory conditions and increased inflammation
How hormones in puberty and pregnancy can affect perio disease
Elevated oestrogen and progesterone increases capillary permeability/ vasodilation/ increased blood flow. Also increases inflammatory and immune responses which aggravates periodontal conditions. Only causes transient gingivitis, so no long-term damage.
What gingival conditions can occur during pregnancy
Pregnancy has increased risk of gingival hyperplasia (benign overgrowths) and pyogenic granuloma (pregnancy tumours) and gingivitis
How stress can lead to perio disease
Could be due to change in behaviours (poorer OH, increased smoking and alcohol). Or physiological changes – reduces leukocyte function, altered cytokines, pro-inflammatory conditions, salivary changes
What 3 drug categories and names can cause gingival overgrowths
-Calcium channel blockers – Nifedipine, amlodipine
-Immunosuppressants – Cyclosporin - immunosupressant for organ rejection. Stimulates fibroblasts so more collagen
– Phenytoin - anti-convulsant for epilepsy. Overproduction of collagen
drug-induced gingival overgrowths: clinical features, management, cause
-Clinical features: diffuse enlargement, vascular lobulated overgrowth. inflammation, swelling, BOP, overgrowth starts at interdental papillae which continues to grow and coalesce. Then starts to affect attached gingiva. Compromises aesthetics and OH.
-Management: Recommend single tufted brush. OHI, debridement. Liase with GP so consider changing meds. surgical excision (gingivectomy) and recontouring (gingivoplasty).
-Causes: Due to proliferation of fibroblasts and increased collagen contact, creating fibrous tissue overgrowths. Highly vascularized tissue with increased inflammatory cells.
How diabetes causes perio. What molecule is the main cause
-Perio and diabetes both chronic inflammatory conditions so linked by a bidirectional relationship.
-Increased glycosylation of proteins in uncontrolled diabetes creates AGEs (advanced glycation end products)
-AGE interacts with RAGE which promotes cytokines (inflammation and local damage), microvascular damage (affecting leukocyte/ nutrient delivery), reduced collagen turnover (reduced periodontal healing), increases collegenase, PMN dysfunction, tissue breakdown
-Impacts immune system so more risk of infection
-AGEs therefore responsible for increasing periodontal disease.
-Anterior more inflamed as diabetes obliterates arteries which worsens perio disease
What marker is used to assess glycemic control.
measuring HbA1c in blood. this is a glycated haemoglobin
-The measurement of plasma glucose
type 1 and 2 diabetes
Elevated glucose. Increased risk if poor glycemic control
-type 1= autoimmune. body attacks beta pancreatic cells so don’t produce enough insulin so cannot store glucose as glycogen
-type 2= metabolic. insulin becomes de-sensitised so body becomes more resistant to it and blood glucose cannot be controlled
Role of dentists when it comes to diabetes
-be aware of bidirectional links of perio and diabetes
-educate patient of links
-regularly update MH of diabetes and level of control
- be aware of HbA1c for measuring plasma glucose
-regular monitoring of these patients
-provide preventative care
-Consider assessing risk of diabetes when suspected and liaising with the medical doctor when there is evidence of increased diabetes risk
-regular review and recall
Ask if it is stable, what was their most recent glucose level, have they eaten, what meds they are on
What is papillon-lefevre syndrome and how it can be linked with perio
mutation in cathepsin C gene, causing impairment in immune response to bacteria. Characterized by lesions on hands and feet, severe generalized periodontal disease, and early loss of primary and permanent teeth
What is ehlers-danlos syndrome and how it is linked with perio disease
defective collagen synthesis. Excessive joint mobility, increased skin fragility, skin extensibility, fragile tissues.
-Type VIII associated with periodontitis. Increased trauma risk in periodontal treatment so caution required to not damage the tissues
What is Down’s syndrome and how it is linked with perio. what chromosome is affected
trisomy chromosome 21 (additional copy)
-Increased prevalence and severity of periodontitis. Due to alterations in immune response, neutrophil chemotaxis, phagocytosis.
-Local factors include restricted access for cleaning, overcrowding, class III, lack of lip seal and mouth breathing causing reduced saliva, high frenal attachments, reduced compliance to OH, lack of dexterity, lack of motivation, shorter roots
How leukaemia linked with perio disease
malignant neoplasm of the bone marrow, causing increased proliferation of white blood cells and their precursors. Reduces the amount of platelets, often causing thrombocytopaenia and gingival bleeding. Gingival swelling due to infiltration of leukaemic cells. Also oral petechiae and oral ulceration
How neutropenia linked with perio
reduced neutrophils, increasing risk of infection. Congenital or acquired.
-Manifestations included ulceration/ necrosis of marginal gingiva, gingival bleeding, generalized severe periodontal disease
How Chidiak-Higashi syndrome and Leukocyte adhesion-deficiency syndrome linked with perio
Chidiak-Higashi syndrome: impaired neutrophil function. Severe perio even at young age, early exfoliation of primary and permanent
Leukocyte adhesion-deficiency syndrome: impaired wound healing, prone to severe infection
What is hypophosphatasia and why it is linked with oral abnormality
error in metabolism. Mutation in gene encoding alkaline phosphatase enzyme important for mineralization of bone and teeth.= impaired bone and tooth mineralization
-Skeletal manifestations (short limbs, bowed legs), early loss of teeth, abnormalities of tooth formation (enlarged pulps, abnormalities in morphology, hypoplasia)
List systemic diseases that perio may cause
diabetes, atherosclerosis, obesity, rheumatoid arthritis, osteoporosis, chronic kidney disease, COPD colon or pancreatic cancer, IBD, adverse pregnancy outcomes (low birth weight), CVD
How perio can cause systemic disease
Highly vascular periodontium and leaky JE means subgingival bacteria, bacterial products (LPS, toxins) and pro-inflammatory molecules can enter the blood and affect distal sites and systems, potentially causing systemic diseases = metastatic infection, inflammation, injury. Trigger immune responses elsewhere.
How perio can cause diabetes
Pathogens and cytokines etc. entering the circulation reduces pancreatic Beta cell function, cause apoptosis, causes insulin resistance, elevated HbA1c levels, exacerbating the diabetic state
-perio therapy has shown to be very effective at reducing HBA1c levels
How perio can be linked with atherosclerosis
P gingivalis, F nucleatum, A actinomycetemcomitans found in atherosclerotic plaques. These pathogens enter the circulation and directly or indirectly induce inflammation
Explain the BSP management pathways that is taken for perio patients (step 1-4)
-Step 1 (OHI, supra PMPR etc.)
-Re-evaluate and those not responding continue with stage 1, and those engaging go to…
-Step 2 (sub PMPR)
-Re-evaluate and those unstable go to step 3, those stable go to step 4
-Step 3 (manage non-responding sites)
-Step 4 (maintenance)
What is involved in step 1 perio pathway and the aims
-Educate about disease, tailored OHI, smoking, remove plaque retentive factors (eg. Overhanging restoration), supragingival PMPR, diabetes control,
-aims= biofilm control, remove plaque retentive factors, address risk factors, reduce gingival inflammation, deliver education, improve patient compliance with advice, ensure patient takes ownership of their role in disease management, improve OH and habits
-Review within 3 months.
How to assess patient engagement. Who stays with step 1 therapy, who moves onto step 2
-Engaging patient= favourable improvement in OH. ≥50% improvement in plaque and BOP scores. OR plaque score ≤20% and BOP ≤30%. OR patient has met targets in care plan made by healthcare practitioner.
-Non-engaging= insufficient improvement in OH. <50% improvement in plaque and BOP scores. OR >20% plaque level and >30% BOP. OR patient wants a palliative approach to perio care
What is involved in step 2 perio therapy. When it needs reviewing and what is involved
-Subgingival PMPR, reinforcing OH, behaviour change and risk factor control, use of adjunctive systemic antimicrobials (mouthwashes)
-6 week review (only at NDH)= assess healing of soft tissues, reinforcing OHI, reassess motivation
-3 month re-evaluation= assessing stability of disease. full perio re-evaluation of gingival health, OH, risk factors, motivation, compliance. OHI, plaque score. Further sub PMPR. PPDs, BOP, CAL, mobility, furcation, recession
-may need further step 2 or referral
When should subgingival PMPR be considered
if active disease diagnosed, for motivated patients complying with advice, patient consents, for pockets ≥5mm or 4mm with BOP. Usually a quadrant by quadrant approach
After step 2, how to assess stability of perio disease and who should go to step 3 and step 4
step 3 for those with active unstable disease
step 4 for those who’s treatment has been successful. stable disease or in remission
stable: BOP <10%. PPD ≤4mm. No BOP at 4mm sites
In remission: BOP≥ 10%. PPD ≤4mm. No BOP at 4mm sites
Unstable: PPD ≥5mm or PPD≥4mm with BOP
If a patient has undergone previous non-surgical perio therapy what pocket depths can they have without BOP to be classified as stable or in remission
5-6mm pockets with no BOP, if previously they had very large pocket depths. As realistically they won’t get smaller than this
If someone is in remission, then take annual indices
What step 3 involves
-for those not responding well to step 2
=management of non-responding sites
-further treatment planning which involves further non-surgical perio therapy (OHI etc.), sub PMPR, adjunctive, possible referral to specialist, perio surgery
-6 week soft tissue review then 3 month review
What step 4 perio therapy involves. aims
-it is the maintenance phase for those responding well to step 2 sub PMPR (stable or in remission)
-reinforce OH, risk factor control, behaviour change, regular PMPR, adjunctive, monitoring motivation and perio/ systemic health
-long-term ongoing care, so patient needs to invest in regular maintenance for life
-aim to prevent relapse, maintain stability, initiate further treatment if progression is detected
When to refer a perio patient to a specialist
-usually after step 3
-only consider after at least 2 round of sub
-when no response to previous optimally completed treatment, deteriorating perio condition after non-surgical management, rapidly progressing perio, medical history that affects clinical management (history of head and neck radiotherapy, bisphosphonates, immunocompromised, bleeding disorder, drug interactions, systemic disease unstable diabetes), complicating anatomical factors affecting prognosis, concurrent mucogingival disease (eg. Pemphigus, MMP, OLP)
2 contraindications for perio surgery
-not normally undertaken following a single phase of non-surgical care - The outcome of the first phase is reviewed and non-surgical care repeated for non-responding sites in engaging patients.
-In non-engaging patients - it will likely fail. attempts should be made to engage patient in behaviour change and establishing optimal levels of OH
The aims of supportive periodontal care. what it involves. What is the recall interval
-it is professional therapeutic measures that support a patient’s own efforts to control periodontal infections and avoid re-infections
-aims of reducing PPDs, BOP, CAL, plaque score, tooth loss, inflammation. Easier for patient to clean when pockets are smaller
-involves: risk factor assessment, OH assessment (eg. Plaque index), sub and supra gingival scaling, RSI + LA of deep sites, indices, radiographs to monitor disease. It can be provided in general dental practice with same outcomes as specialist clinic
-recall frequency 2-4 months
What is calculus
mineralized bacterial plaque. Dental pellicle can also calcify. Secondary cause of periodontitis. Calcium phosphate crystals.
Aims of sub PMPR
it is not 100% necessary to remove it all, as long as it is smooth to disrupt and reduce the biofilm and not make it retentive, and so that PDL can reattach
-removing calculus as it is a plaque retentive factor
-conserve tooth structure
-resolve inflammation
-creating a biologically acceptable root surface
What BOP, tooth loss, systemic factors and PPDs are considered high risk and low risk at perio risk assessment
BOP<10% low risk
BOP >25 % high risk
<4 tooth loss is low risk
>8 tooth loss high risk
diabetes, genetics high risk
PPD >5mm high risk
Furcations high risk
What is considered low, moderate and high risk for smoking
Non-smokers/ former smokers for <5y=low risk
Occasional smokers (<10 a day)= moderate risk
Heavy smokers (one pack a day)= high risk
smoking cessation options
Nicotine replacement therapy (patches, sprays)
Behavioural counselling
Family and friend support
Vaping
What is VBA for smoking cessation, what it involves
-very Brief advice on smoking. Should take 30s
1. Ask about their status -“Do you smoke”
2. Advise how to quit (meds, specialist support)
3. Act: build confidence, give info, refer to local stop smoking service
don’t lecture about why smoking is bad. If not interested let them know where to find support and will keep reassessing
What oral conditions smoking can increase the risks of
-cancer, leukoplakia, periodontitis, ANUG, candida, melanosis, caries (less evidence), dry sockets (impaired healing), staining, halitosis, tooth loss, peri-implantitis, staining, xerosotmia
impaired vasculature, immune impairment, affects microbiota, wound healing impairment,
why vapes may be a good alternative for smokers
-Heats liquid containing nicotine to form a vapor which is inhaled rather than smoke. Doesn’t produce tobacco, or produce tar or CO
-Vaping only poses a small fraction of the risks of smoking, so good option for those wanting to quite smoking, but don’t recommend to non-smokers or young people as addictive
-Increases quitting rates compared to NRT
-E-cigarette use is far less harmful than tobacco cigarettes, although not risk free. Little current knowledge on its damaging effects
Explain the following brushing techniques: horizontal scrub, bass technique, modified stilman, and charter’s technique
-Horizontal scrub= back and forth motion. Simplest method, not as effective
-Bass technique= 45 degree angle of bristles at gumline, back and forth vibrating motion, all 3 tooth surfaces, vertical orientation behind anteriors
-Modified Stillman= involves a rolling stroke coronally to minimise gingival trauma & increase plaque removal
-Charters’ =circular motions. Aids cleaning of abutment teeth, under gingival border of bridges, ortho appliances
Advantages and disadvantages of bass technique
Provides good gingival stimulation
Easy to learn
BUT over brushing can cause gingival injury
can be time consuming
dexterity required may be too high for come patients
vibratory aspect may be ineffective for biofilm removal at gingival margin
Negative outcomes of PMPR
-Gingival recession (due to reduced inflammation. although this is also a positive outcome, resulting in a shallower pocket)
-Root sensitivity (due to recession, cementum removal, calculus removal)
-Aesthetic concerns – black triangles between teeth
Healing stages after sub PMPR
-Within a few hours: acute inflammatory reaction in the pocket wall due to trauma of procedure. Bleeding
-Within 1-2 days: epithelialisation of pocket wall
-1-2 weeks: epithelial re-attachment commences at the base of the pocket, new gingival sulcus forms & gingival recession as a result of inflammation (as inflammation resolves tissues shrink)
-3-6 weeks: formation of functionally-orientated collagen replacing granulation tissue, continued reduction in probing depths
-Over several months: continued maturation of connective tissue, possible bone infill in infra-bony defects
What perio adjunctive treatments are available. when should be considered
Only considered in individual cases when done at least 2 rounds of sub and not responding.
1.CHX mouthwash (poor manual dexterity, xerostomia)
2. Perio chip- local 2.5mg CHX for 7-10 days in non-responding localised sites.*
3.Local antibiotics: for suppurative pockets. eg. doxycycline, minocycline
4. Systemic antibiotics (rare): considered if <45 years old with rapidly progressing perio. GDP don’t prescribe, managed by a specialist
What is a periochip. how long it lasts. Pros and cons
-used as an adjunct to RSD in moderate-severe localised periodontal sites that are not responding to sub. For perio abscesses, resistant disease, furcations, aggressive perio. Sub PMPR needed prior to drug being delivered in pocket to increase its effectiveness
-Releases 2.5mg CHX in the subginigval periodontal pocket at effective levels for 7-10 days
-Disintegrates within 7-10 days due to enzymatic degradation
-Does not stain teeth, no changes in taste, targets high concentration to local area, less adverse systemic effects, antibacterial, removes need for invasive perio surgery
-BUT, does not go into pockets < 5mm, expensive
how chlorhexdine works
-antibacterial, antifungal and perhaps antiviral. Broad-spectrum.
-Bacteriostatic at low concentration, bactericidal at higher concentrations.
-Positively charged molecule destabilised the negatively charged bacterial cell wall causing lysis. Disrupts phospholipid membrae and contents leak out - pops it open
-Substantivity so sticks to surfaces so prolonged action. Should be used at different time to tooth brushing. Check whether known allergy
reasons for using antibiotics as an adjunct for perio therapy. And arguments against
-Bacteria initiate disease, but damage done mainly by host response
-Outcomes of RSD are not always predictable
-Recolonisation occurs
-Bacteria may persist in isolated anatomical niches. >500 species.
-Antibiotics may reinforce traditional therapy by killing persisting microorganisms. Antibiotics only used in adjunct to therapy and not in isolation
Arguments against using antibiotics:
-Bacterial resistance
-Dental plaque is a biofilm. antibiotics useless against undisturbed biofilm
-Are they of any benefit in periodontitis?
-It all comes down to risk/benefit for the individual & society
-Only a small number strongly associated with disease so antimicrobial could unnecessarily kill microbes in the body.
3 mechanisms for gene transfer for antibacterial resistance
-Transformation: uptake of free DNA in the environment (from dead bacterium)
-Transduction: transferred between bacteria via a virus
-Conjugation: direct contact
antibiotic for treating acute periodontal abscess
amoxicillin 500mg 3 times per day for 7 days
then metranidazole
then clindamycin
How doxycycline can be used to treat chronic perio disease
20mg doxycycline 2Xdaily for 3 months to modulate host response by decreasing MMP production and therefore collegenase activity so less tissue breakdown
when to be taking X-ray for perio patients
Only take x-rays if you think sites are worsening, depth increasing by over 1mm. In rapid progressing perio re-take them in a couple of years.
Issues with record keeping and common allegations related to perio disease
-failing to diagnose
-patient unaware of disease severity
-no evidence of perio monitoring or risk assessment
-no or poor treatment carried out
-no management of risk factors
-no referral made or offered when appropriate to do so
That is why it is essential to keep record of all examination, history, consent, perio assessment, discussions (risks/ benefits, options), treatments, follow-up
Reasons for periodontal surgery (types of surgery)
-improve access for RSI -access flap perio surgery
-easier to clean- resective perio surgery
-improve access for guided tissue regeneration,
-excision of gingival hyperplasia (gingivectomy),
-correction of gingival recession (involves tissue graft),
-access subgingival caries
-increase supragingival tissues for restorative procedures
-crown lengthening
-furcation surgery
Patient indications and contraindications for perio surgery
optimized OH, plaque score < 20%, non-surgical management first (OHI, RSI, review), motivated, not immunocompromised, non-smoker, reasonable prognosis of dentition.
Difference between a free gingival graft and connective tissue graft for gingival recession surgery
-free gingival graft= epithelium + lamina properia. creates more keratinized tissue and deepens the sulcus. Split thickness flap raise, removal of overlying epithelium, leaving connective tissue/ periosteum bed, dissection of free gingival graft from hard palate, free gingival graft, sutures
- a connective tissue graft= epithelium + connective tissue. thickens tissue, achieving root coverage. Requires adequate sulcus depth. 3 sides split thickness flap leaving a periosteum and connective tissue bed. Subepithelial dissection of connective tissue graft. Insert of graft. Suture
What is guided tissue regeneration. Name 3 types of biomaterial used for guided tissue regeneration
-Regeneration of lost periodontium in localized vertical defects. Allows direct vision for placement of stable biomaterial into well-constrainted defect. Barrier membranes include:
1. Biogide- prevents ingrowth of epithelium. Osteoblasts populate the wound, producing new bone, cementum and PDL for more stability.
2. Embogain – an enamel matrix derivative to stimulate cementoblasts.
3. Bio-Oss - provides a scaffold for osteoblasts to be layed down around
Reasons for crown lengthening surgery
-to access subginigval caries, increase surface area for restoration, improve aesthetics for an uneven gingival contour (gummy smile)
-if restoration encroaches into biologic width (epithelial attachment) inflammation occurs. So must keep restoration 3mm clear of alveolar crest so may required crown lengthening
Raise flap, remove bone (3mm from proposed new restoration margins)
Reasons for furcation surgery. Why it is not commonly done
improves patient’s ability to maintain OH around lower molar furcation defects
-BUT not commonly done due to the risk of sensitivity or loss of vitality as it requires loss of tissue to achieve this
What is done at the 3 month perio review
-reviewing response to treatment
-periodontal revaluation and re-assessment: post-op PPDs (discuss implications with patient, highlight sites that require further treatment), BOP, mobility, suppuration, furcation lesions, recession. Comment if perio condition is stabilizing
-review OHI and patient motivation: current OH and gingival health, plaque score, further advice, re-assess motivation and compliance, re-asses risk factors
-decision making regarding further treatment: discuss with patient. Document next phase of treatment plan – further PMPR. Adjunctive treatment (mouthwash if poor dexterity), potential referral, supportive periodontal therapy, recall interval defined
-supra or subgingival instrumentation. Record instruments used, sites, if LA, post op advice
-perio indices should be completed on at least an annual basis to allow disease stabilisation to be monitored
Observations that indicate perio treatment success and treatment failure
-Success= reduced pocket depths, BOP, inflammation, recession due to reduced swelling, reduced plaque
-Failure= poor plaque control, persistence of inflammation, ongoing BOP, erythema and swelling, persistent deep pockets or increasing depths, increasing mobility, suppuration
cons of hand scalers and ultrasonic scaler
-hand scalers: remove more cementum than ultrasonic. Can feel things better. Better for hard to reach areas
-ultrasonic- sensitivity issues. More efficient
How ultrasonics work. difference between cavitron and peizon
ultrasonic instruments convert electrical to mechanical energy. electrical current creates alternating magnetic field which causes expansions. contractions which results in vibration of tip
-cavitorn: all sides of tip are active
-piezon: only the lateral surfaces of the tip are active
how to manage chronic erythematous candida
-denture induced
-mechanically clean dentures thoroughly with soft brush and soap
-soak them in chlorhexidine mouthwash or sodium hypochlorite for 15 mins twice daily
-Leave dentures out at night. Leave dentures out as often as possible until resolves. Denture replacement or adjustment
-antifungal therapy if persists
Management of chronic hyper plastic candida
antifungal treatment, advised to stop smoking
- Could develop into oral cancer. It is a premalignant condition.-Would usually refer patient to oral surgery department to take a biopsy.
What are the landmarks for attached and free gingiva
-gingival margin (most coronal aspect of the gingival contour) to the free gingival groove (level of bottom of sulcus)
-Groove to mucogingival junction
How to manage a patient who is not engaging with OH
Move onto a palliative care approach to keep things stable - step 1 perio without sub. Document in notes why you are not moving onto step 2. Don’t use the word palliative in front of a patient as connonations of death. Treatment given every 3 months
