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Flashcards in Perio Deck (153):

What is the probing pocket length?

Distance from gingival margin to the tip of the perio probe inserted into the pocket


What is recession?

Distance from ACJ to gingival margin


What is the clinical attachment level (CAL)?

Distance from ACJ to the bottom of the pocket (recession + probing pocket depth)


What should a perio treatment plan consist of?

1. OHI
2. Review oral hygiene status (Gross scale and polis, review OH aiming for turesky <1, repeat as neccessary)
3. RSD on active sites (pockets >4mm)
4. Review OH
5. 3 month review (full mouth perio chart)


What happens if patient becomes stable?

maintenance phase and refer back to GDP


What does healthy gingivae look like

Pink, firm and stippled
Knife edge margin with no bleeding


What is gingivitis?

Reversible inflammation of the gingivae


What are clinical signs of perio?

Redness, loss of stippling (smooth and glossy surface), swelling (softer and pitting tissues), rolling of the gingival margin, loss of interdental papillae, bleeding on gentle probe


What is periodontitis?

Inflammation of tissues supporting the teeth (gingivae, PDL and alveolar bone) = results in progressive destruction that leads to loss of the junctional epithelium, PDL, alveolar bone and teeth


What is the prevalence of periodontitis?

47% of US population >30 yrs have perio (8.5% mild, 30% moderate and 8.5% severe)


What is aggressive perio?

ethnic variation in prevalence with most in african population


How do we classify gingivitis?

Loe and Silness 1963 Gingival index:

4 sites on each tooth are examined and averaged to five a score:
- 0 = normal
- 1 = mild inflammation, slight colour change, no bleeding
- 2 = moderate inflammation, redness, BOP
- 3 = severe inflammation, marked redness, spontaneous bleeding


What are the effects of gingivitis?

Schaetzle et al 2003 2004:
- not all patient who have gingivitis develop periodontal disease
- when gingivitis is consistently present there is likely to be 70% more attachment loss than at healthy sites
- The patient is 46 times more likely to lose the tooth over a 26 year period

Needleman et al 2004:
- Periodontal disease affects peoples QOL


What are the types of gingival disease?

- may be plaque only/ modified by systemic factors (leukaemia, puberty, pregnancy)/ modified by medication (Ca channel blockers)/ modified by malnutrition (vit C)

- specific bacterial, viral (herpes), fungal (candida)
- genetics (hereditary gingival fibrostomatitis)
- manifestation of systemic conditions
- trauma
- foreign body reaction


How do we distinguish between chronic and aggressive forms of perio?

- most pts with plaque induced = chronic
- typical patient with chronics: over 35 y/o with substantial plaque and calculus - and gingival inflammation, perio pockets and attachment loss
- when diagnosing consider: amount, pattern, rate of progress and the patient (age, medical status, familial tendency)


Tell me about necrotising ulcerative gingivitis:

Mostly in 16-30 y/o
Military recruits
In patients with HIV and AIDS (if no other predisposing factors consider they may have this even if not diagnosed yet)


What are the risk factors for NUG

Severe malnutrition
Heavy smoker
Emotional stress
Compromised immune system
Blood Dyscrasias (acute leukaemia)


What is the histology of NUG?

Necrotic surface epithelium and connective tissue
Dense inflammatory infiltration of underlying tissues
Bacteria (spirochetes)
Increased plasma cells, lymphocytes and macrophages


What are the diagnostic features of NUG?

Ulcers at interdental papilla and marginal gingivae
Ulcers = punched out crater like, pseudomembraneous, white/gray slough, bleed readily or spotaneously, painful, short lived (1-3 days with appropriate therapy)
May have slight fever, malaise
Painful gums and 'dead feeling teeth)
Breath odour - footer ex ore
Submandibular and cervical lymphadenopathy


What do you get in NUP that you dont in NUG?

Deep interproximal craters of alveolar bone
Loss of attachment
Sequestration of interdental and possibly buccal/lingual bone


How do we manage NUG/NUP?

Acute phase:
- Irrigation (with ultrasonic)
- Oxygen releasing mouthwash (hydrogen peroxide 1.5% e.g. colgate peroxyl or sodium perborate mouthwash)
- Metronidazole 200 mg TDS for 3-5 days
- Chlorhexidine m/w in short term
- Address predisposing factors

Residual phase (minimise recurrence):
- supra and subgingival debridement
- remove local factors
- gingivoplasty to improve gingival contour
- regular review to ensure good OH
- medical examination blood screen


What is cancrum oris?

Associated with intense poverty, immunosuppression (HIV/AIDS)
Prevalent in subsaharan africa
Diseases commonly preceding it: Measles, malaria, sever diarrhoea, malnourishment, poor sanitation, NUG


What are the early features of Cancrum oris>

Soreness of mouth
Tenderness of lips/cheeks
Would smelling purulent discharge
Blue-black discolouration of the skin area


How do we manage Cancrum Oris?

Rehydration/ nutritional rehabilitation
Antibiotics (penicillin and metronidazole)
Local wound irrigation
Serological test for HIV


What is aggressive perio disease>

A rapidly destructive disease that can affect any age (but usually <30 y/o


What is the prevalence of aggressive perio?

<1% has aggressive perio
0.1-0.2% are caucasians, 2.6% blacks


How was aggressive perio classified in 1993?

Age of patient:
1. Prepubertal
2. Juvenile (puberty - late teens)
3 Rapidly progressive (20s +)


How do we now classify aggressive perio?

localised and generalised


What micro-organisms are present in chronic gingivitis?



What micro-organisms are present in Chronic periodontitis?

Aggregibacter actinomycescommitans (Aa)
P gingivalis


What micro-organisms are present in localised Aggressive periodontitis?

Aggregibacter actinomucescommitans (Aa)


What micro-organisms are present in generalised aggressive periodontitis?

P gingivalis


Whats a key thing to remember about aggressive perio?

Tissue destruction is inconsistent with plaque levels (patient may have excellent OH)


What are the features in localised aggressive perio?

Onset in puberty
Localised to 1st molar and incisor teeth, with interproximal attachment loss at 2 + teeth and NOT involving more than 2 non 1st molar or incisor teeth
Good OH and usually medically fit and well
Often smokers
Tendency in families
BPE = 4
Alveolar bone loss: arc defects on 1st molars and vertical on incisors


What are the features in generalised aggressive perio?

Usually in patients <30 (but may be older)
Generalised interproximal attachment loss in at least 3 permanent teeth ( as well as 1st molars and incisors)
Generalised and severe horizontal bone loss
Subgingival calculus associated with clinical attachment loss
May or may not have gingival inflammation


How do we diagnose aggressive perio?

<35 y/o
Rapid bone loss (over a couple of years)
Localised or generalised
Family history
Usually good oral hygiene


How do we treat aggressive perio?

Good OH
No smoking
Early: debridement of all areas within 1 or 2 visits (within 1 week) accompanied with systemic antibiotics
Supportive: regular monitoring and maintenance on 3 month basis until stable for at least 1 year
Ultrasonic debridement every 3 months


How does smoking link to periodontal disease?

major risk factor: (Kinana and chestnut, 2000)
2.6-6 increased perio destruction than non smokers, more sites with deeper pockets
More likely to get NUG/NUP
reduced healing process
surgical and non surgical RSD outcomes worse


What are the local consequences of smoking?

Reduced gingiva blood flow
Reduced revascularisation of hard/soft tissue
Reduced fibroblast/collagen synthesis
Reduced osteoblast proliferation


What other things affects periodontal health?

Osteoporosis (increased attachment loss)
Pregnancy (increased plaque response = OH and minimal perio tx)
Diabetes (uncontrolled = increased perio -> reduced collagen synthesis, increased perio pathogens in biofilm)
Heart disorder (hypertension linked to worse perio)
Stress (Genco et al., increased level of perio destruction, linked to stress from financial strain and depression)


Which medications are associated with gingival overgrowth?

ANTICONVULSANTs - phenytoin (50% have overgrowth, presents after 1 month and plateus 12-18 months = fibroblast overproduction)

IMMUNOSUPPRESSANTS - Cyclosporin (50% have overgrowth, less common on bone marrow than other organ transplants, enlargement dose dependent = increased collagen)

Ca CHANNEL BLOCKERS - Nifedipine (40% have overgrowth, increased collagen)


What organisms cause periodontitis?

1. SPECIFIC PLAQUE HYPOTHESIS Loesche 1976 -> Aa linked to localised aggressive, P. gingivalis generalisaed aggressive (but also non disease)

2. NON SPECIFIC PLAQUE HYPOTHESIS Loe 1965 Thielade 1986 -> disease from sheer mass of pathogens

3. ENIVORNMENT PLAQUE HYPOTHESIS Haffajee 1991-> pathogenic species required in sufficient numbers in biofilm, species co-dependent

4. MICROBIAL COMPLEXES OF VARYING VIRULENCE Socransky 1998 -> clusters of bacteria discrete microenvironment, increasing virulence associated with gran -ve anaerobic motile bacteria


What happens when we have an increase in plaque?

there is an increase in endotoxin -> increase in complement activations -> higher inflammatory response and gingival tissue damage


How do genetics relate to periodontitis?

38-82% of population variance for gingivitis, probing depth and clinical attachment loss is genetic (Michalowicz et al. 1991)
Likely to be a no. of polymorphisms that predispose to perio (Kornman et al 1997)
Aggressive perio is familial linked, autosomal dominant (kinane and hart 2003)


Whats the causal theory (Heaton and dietrich 2012)?

links causes (smoking, hormones diabetes, stress, biofilm, drugs, genetics etc.) to the periodontium and therefore perio disease


How is nicotine linked with periodontitis?

Increased keratosis and fibrosis


How does diabetes affect perio?

Poor control = increased risk of perio destruction
Wound healing impaired and reduced collagen synthesis
Recurrent lateral abscess (sign of diabetes)


What changes favour plaque accumulation?

Increased salivary cortisol, increased environments for periodontal pathogens (altered immune response)


What is root surface debridement?

The removal of bacterial plaque biofilm and calculus from tooth surfaces, the aim is for cementum conservation, bacterial product removal


What is the rational for RSD?

1. arrest the progress (removes plaque biofilm and plaque retentive calculus deposits)
2. create a healthy environment (allows gingivae to heal and assist maintenance of tissue health)
3. increases effectiveness of patient self care (eliminates areas of plaque retention that are hard to clean)


How long should you allow after RSD for probing?

A minimum of 6 weeks


Whats the advantages of ultrasonic over manual debridement?

-Irrigation of the pocket
- Water cleans working field
- Effective with every movement
- Better access in furcations
- Faster and easier to remove calculus


What are the disadvantages of ultrasonic over manual debridement?

- Expensive
- Noisy
- Risk of damage toe name and dentine
- Dentine hypersensitivity can temporarily increase


What are the contraindications of ultrasonic use?

- Tuberculosis
- Compromised immune system
- Respiratory problems
- Swallowing problems
- Primary teeth
- Newly erupted teeth
- Decalcified enamel
- Pacemakers
- Metal tips used with implants


How effective are ultrasonics?

As effective as manual instrumentation (america acadamy of perio 1996)
20-50% quicker than manual debridement (Drisko 2001) and with appropriate use less cementum removal but best result with combo of both


What is the full mouth single stage debridement rationale?

- subgingival species colonise other niches, persistence of periodontal pathogens cause negative result, treatment reduces bacterial load by 1000 x and decolonisation with smaller no of pathogens within a week
- Quiryen -> elimination of periodontal pathogens from all sites would be best approach
- Apatzidou et al 2004-> sae result from full mouth and staged treatment


What are the side effects perio treatment?

Recession (reduction in gingival inflammation), interproximal dark triangles and sensitivity


What are the risk factors affecting treatment outcomes?

Poor compliance, poor attendance, insufficient debridement, systemic conditions, smoking, persistent deep pockets, molars with furcation involvement


What does BPE stand for?

Basic periodontal exam


When is a BPE recommended?

screening for all new dental patients and those not seen for over a year


What does a BPE of 0 mean?

Coloured band visible (<3.5mm), gingival tissues healthy, no bleeding on probing (no treatment needed, screen in 1 year)


What does a BPE of 1 mean?

Coloured band visible (<3.5mm), no calculus or plaque BUT bleeding on probing (OHI and screen 1 year)


What does BPE of 2 mean?

Coloured band visible (<3.5mm), calculus or defective restoration margin detected (OHI, removal of plaque retentive factor, and screen 1 year)


What does BPE 3 mean?

Coloured band partially visible (3.5-5.5mm) = mild - moderate periodontitis (OHI, RSD/scaling, reassess and repeat scaling and OHI in 3 months)
n.b. if number of pockets score 3 than do full perio assessment


What does BPE 4 mean?

Coloured band hidden (>5.5mm) = moderate- severe periodontitis (full perio assessment, radiographs, OHI, scaling, RSD -> specialist?)


What does BPE * mean?

Furcation involvement


What does a full periodontal assessment show us?

Site specific nature of disease, extent and severity, treatment planning, monitor disease and outcome, patient communication and medico-legal board


What is a mobility score of 0?

None (<0.2mm)


What is a mobility score of 1?

Horizontal mobility <1mm


What is a mobility score of 2?

Horizontal mobility >1mm


What is a mobility score of 3?

Plus vertical mobility


What is an F1?

Furcation can be felt with tip of probe but not entered


What is an F2?

Furcation can be entered (about 1/3 of probe)


What is an F3?

Probe passes all the way through furcation


What are the effects of furcation involvement?

Difficult access, loss of vitality (accessory canals from pulp to furcation), detected with probe


What are the different causes of gingival recession?

Root anatomy, perio, trauma, thin gingivae, orthodontic arch expansion


How s gingival recession classified?

Millers recession classification


What is class 1 recession?

Recession DOESNT extend to mucogingival junction, no alveolar bone loss or soft tissue loss interdentally


What is class 2 recession?

Recession extends to or beyond mucogingival junction , no alveolar bone loss or soft tissue loss interdentally


What is class 3 recession?

Recession extends to or beyond the mucogingival junction, alveolar bone loss and soft tissue loss in interdental area


What is class 4 recession?

Recession extends to or beyond the mucogingival junction, alveolar bone loss or soft tissue loss in the interdental area with gross flattening


What is a turesky 0?

No Plaque


What is a turesky 1?

Separate flecks of plaque at the cervical margin of the tooth


What is a turesky 2?

Band of plaque less than 1mm at the cervical margin of the crown


What is a turesky 3?

Band of plaque wider than 1mm but less than 1/3 of the crown


What is a turesky 4?

Plaque covering between 1/3 and 2/3 of the crown


What is a turesky 5?

Plaque covering more than 2/3 of the crown


What is the response of the periodotium to occlusal trauma?

1) unilateral forces - create pressure and tension zones = hypermobility, normal width of PDL maintained
2) alternating directions (jiggling) - PDL width increases and tooth becomes more mobile

N.b. occlusal trauma at sites with plaque associated perio doesnt initiate gingivitis or perio BUT it can itnitiate bone resorption which may enhance rate of progression of perio


How does periodontal disease affect blood sugar levels in diabetics?

Diabetics with severe perio have higher blood sugar levels than diabetics without perio (even with no diabetes severe perio causes reduced blood sugar control = increased risk of type 2 diabetes)


which haematological conditions affect the periodontium?

Gingival inflammation - acute monocytic leukaemia with thrombocytopenia purpura
Gingival necrosis - paroxysmal nocturnal haemogloburia
Gingival involvement - weighers granulomatosis


What are the effects of pregnancy on the gingivae?

Red, swollen gingiva
Exacerbation of gingivitis


At what point can perio treatment be deferred or declined?

Poor general health, lack of effectiveness of plaque control, patient compliance to OHI, patients wishes, operators decision


What are the advantages of BPE?

well recognised internationally (aids communication)
rapid and easy to complete
requires basic probe only


What are the disadvantages of BPE?

lack of details within sextants (no detail about no./severity of sites)
can't differentiate between true and false pockets
screening only
can't be used on children as clinical crown not fully deeloped


What do you look for in an examination?

- BOP (30% sites with BOP lead to loss of attachment)
- Loss of attachment (sum total of perio destruction, no indication of number of episodes or when occurred)
- Purulence
- Mobility (higher = poorer prognosis)
- Furcation involvement (reduces prognosis, possible pulpal involvement)


Define osseointegration:

direct structural and functional connection between ordered, living bine and the surface of a load carrying implant


What are the implant objectives at placement?

- Primary stability = bicortical fixation, cancellous support with sufficient trabeculae
- correct positioning along the alveolar ridge - consider anatomy and implant dimension
- correct vertical alignment = profile and occlusion of restoration, emergence and anatomical structures
- depth of insertion = available bone depth, vertical positioning the implant per protocol
-adequate bone coverage
- aesthetic soft tissue consideration (crystal tissue and flap design)


What are the implant site complications caused by conventional dental management?

Thin buccal bone (more difficult for primary stability, poor blood supply, prone to breakdown, often fenestrated)
Large coronal area at extraction site (consider bone augmentation/membrane)


How can lack of bone be overcome?

Restorative techniques e.g. over-denture, pink porcelain)
Place implants outside of compromised area
Smaller implants

Compromised site - augmentation can be done AT implant placement or to allow implant placement at a later date


What new row different interventions?

1. lateral ridge augmentation (good success, autogenous bone from drills, suction or adjacent bone or xenograft materials e.g. biogide or bioss or alloplast material - biphasic calcium phosphate or allograft - from another human)
2. vertical ridge augmentation (systematic review 2-8mm vertical gain, mean marginal bone loss 2mm in 1-7 yrs, dental implant survival 92-100%)
3. sinus lift procedures (pjetursson et al 2008, annual failure rate 1.2%, 3 yr survival 96.5%, bone augmentation material not a factor, sinus membrane perforated 19.5% of the time; transalvolar approach had slightly worse prognosis tan et al., 2008)
4. distraction osteogenesis


What is BioOss?

Similar to human cancellous bone
Osteoconductive (scaffold for human bone-> stabilise clot = ingrowth of blood vessels and osteoblasts, new bone laid directly onto the surface of BioOss particles, remodelled to lamellar bone after 6 months with gradual replacement of BiOss by host bone


What is BioGide?

Porcine collagen type 1 and 3
Resorbable barrier membrane, lasts 4- 6 months
Bilayer structure smooth cell occlusive later prevents soft tissue invasion


What are the advantages of sinus elevation?

Suitable for all sites (<5mm bone height)
Increases patient uptake of implants in maxilla


What are the disadvantages of sinus elevation?

Increased timeline for treatment
Prospective audit/clinical studies to validate techniques
Requires per op CT scan


Name some examples of growth factors:

Bone morphogenic protein 2 and 7
Growth differentiation factor 5
Platelet derived growth factor
Parathyroid hormone


Whats the successs criteria for implants?

Buser et al 1990
Absence of persistent complaint (pain, foreign body, dysthesia)
Absence of recurring peri-implant infection with suppuration
Absence of implant mobility
Absene of continuous radiolucency around the implant


What is peri-implant mucositis?

Inflammatory process in the mucosa surrounding a functioning implant with no sign of bone loss -> present of T cells which are limited apically to the barrier epithelium, requires detection by perio probing to identify suppuration or bleeding, radiograph to determine bone levels


What is peri-implantitis?

Inflammatory process in the mucosa which also includes subgigngival biofilm formation and marginal bone loss


What is peri-implantitis characterised by?

cellular infiltrate extension apically, large proportion of plasma cells and lymphocytes present, polymorphonuclear leukocytes and plasma cells in large numbers


What is the recommended periodontal probing force?



What are the risk factors for peri-implantitis?

- history of periodontitis
- smoking
- poor OH
- diabetes history


What is the treatment for peri-implantitis?

Non surgical RSD (difficult due to primary and secondary surface characteristics, access, damage to Ti from curettes)

Antimicrobial therapy: amoxicillin/metronidazole

Access flap surgery (in considerable pocket formation = >5mm n.b. bone grafting and barrier membranes are also important)

Implant surface decontamination (removal of biofilm without modifying implant surface = air polishing units, laser)


What are the different types of bone loss?

Horizontal, vertical (1 wall, 2 wall, 3 wall or circumferential) and interdental crater


What is the treatment of vertical bony defects?

Non surgical debridement/extraction
Surgical treatment - conventional flap surgery + curettage, obturation of defects (bone grafts, synthetic bone substitutes) or guided tissue regeneration


What is the treatment of furcation involvements?

Non surgical debridement/extraction
Tunnel preparation
Obturation of defect (bone graft)
Guided tissue regeneration (reattachment and new attachment)
Root resection (hemisection/amputation)


What is reattachment?

Reunion of connective tissue with root surface which has a viable periodontal ligament


What is new attachment?

Reunion of connective tissue with root surface that has been deprived of its PDL


What is an example of a barrier membrane used?

Goretex (epTFE) = used for vascular grafts, cruciate ligament sutures and patches

(some studies have shown poor results with its use in maxillary molars and class 3 furcations)


What are the two generations of bioabsorbable membranes?

First generation = no secondary surgery, better healing than Goretex, less post op complications, requires stabilising sutures
Second generation (atrisorb) = solid on contact with water or aqueous solutions, no secondary surgery or stabilising sutures



e.g. boomed, periogen, paroguide, biogide, placal
Promote early wound stabilisation
Contains chemotactic chemicals for fibroblasts
Low immunogenicity


Guided tissue regeneration:

Little/ no value for class 3 furcations or interpoximal class 2 maxillary defects
Bioabsorbable membranes > goretex


Enamel matrix protein (Emdogain):

Cochrane review- significant improvement to periodontal attachment levels, when compared to flap surgery

(less clinically relevant -> saviour of periodontically involved teeth not been shown


What does WHO say the prevalence of perio is?

Moderate 2-67%
Advanced 1-79%


Manual vs powered toothbrushing (Cochrane)

Heanue M et al 2003

Powered tooth bruises with rotation oscillation = modest reduction in plaque compared to manual toothbrushing
Cost, reliability and side effects were inconsistently reported

Dorfer et al 2001
Improved interproximal plaque removal where manuals are least effective
Rotation oscillation best results (7% reduction in plaque vs manual)
Battery operated less efficient than powered


How often should teeth be brushed?

2 x day recommended
Effectiveness of brushing is more important than frequency


What is the literature about interdental aids?

Kinane 1998 - reduce prevalence and severity of perio by reducing plaque and gingivitis
Kelly et al 2000 - often motivation, manual dexterity and compliance is low


Floss vs interdental brush:

Interdental brushes more effective (Rosing et al, 2006) (Jackson et al., 2006)
Daily floss significantly removed interdental plaque compared to manual toothbrushing


What is the evidence for tongue scraping?

Cochrane review (Outhouse et al 2006)
Small but significant difference in reduction of volatile sulphur compound levels when tongue scrapers or cleaners are used than toothbrushes to reduce halitosis


What is the evidence for mouthwashes?

Gold standard - chlorhexidine (10ml 0.2% or 15ml 0.12%)
Listerine (essential oils) and triclosan based products are good but not as long lasting as chlorhexidine
24 hour rinsing with chlorhexidine reduces bacteria in saliva by 50-90%


What is a side effect of RSD?

Root sensitivity
Von Troil et al 2002 - root sensitivity occurs in approx 50% of patients following scaling and RSD, intensity of sensitivity increases during first few weeks following therapy after which it decreases


What are the advantages of local (controlled release devices) in perio?

- better concentration profiles (lower total dosage of drug at more controlled concentrations)
- not dependent on compliance
- Reduce unwanted effects and interactions
- site specific
- low total dose


What are the disadvantages of local (controlled release devices) in perio?

- compatibility of delivery vehicle with periodontal tissue
- expense
- time and discomfort of application
- drug clearance in crevicular gingival fluid
- bacterial resistance
- placement and retention


Surgical vs non surgical?

Heitz-mayfield et al 2002
- on pocket depths of 1-3mm (significantly more clinical attachment loss with surgery than scaling and RSD)
- pocket depths 4-6mm (significantly less clinical attachment level gained with surgery than scaling BUT periodontal pocket depth reduces more with surgery than RSD)
- Pocket depths >6mm (significantly more clinical attachment level gained with surgery than scaling and RSD, periodontal pocket depth reduction greater with surgery)
Long term (>1 yr) surgical and non surgical equally effective for perio pocket depth reduction and clinical attachment gain
Insufficient data on furcation


What are the indications for perio surgery?

- deep pockets
- failure of root planing
- bone defects
- furcation involvements (1-3)
- muco-gingival problems
- aesthetics
- short clinical crown height

Surgery should be reserved for inaccessible sites and must facilitate future plaque control by pt and dentist


What are the indications for systemic antimicrobial therapy?

- acute infections (ANUG and abscesses)
- Prophylaxis
- predisposing systemic disease
- deficiency in host immunological response
- aggressive perio
- severe chronic perio


What is the perio pill?

Amoxicillin 500mgs TDS for 7 days
Metronidazole 200mg TDS for 7 days
(allergy to penicillin = ciprofloxacin 250mg bd for 7 days)

the two act synergystically


What is periostat?

Low dose doxycycline 20mg bd for 3 months- 1 yr
Reduces collagenase activity in gingivae and crevicular fluid (inhibits tissue destruction, reduces pocket depth and BOP)


Do systemic antibiotics work?

OH must be excellent
Systemic AB without RSD may change composition of subgingival microbiota (multiple abscesses)


What is gingivoplasty?

Surgical recontouring or remodelling of the gingival tissues


What is a gingivectomy?

surgical procedure in which the pockets are eliminated by removal of gingival tissues (e.g. in drug induced hyperplasia, hereditary hyperplasia)
Is enhanced by gingivoplasty


What is a modified windman flap?

Intracrevecular incision, retract tissues, curettage, eliminate pocket epithelium and granulation tissue for the site and suture


When is the modified windman flap used?

deep pockets, adverse pocket morphology, failure of access with RSD


What are the advantages of the modified windman flap?

No extensive sacrifice of non inflamed tissue
No apical displacement of tissue (close adaption to root surface)
Less exposed root surface (sensitivity and aesthetic benefits)
Minimum trauma to connective tissue and alveolar bone (no recontouring)


List some examples of much-gingival surgery:

Laterally repositioned flap
Free epithelial graft


When is free gingival graft used?

Recession of lower incisors


When is a coronally repositioned flap used>

Recession (flap is cut in gingiva and sutured so meets crown in different way


Root amputation

Depends on tooth (root, defect size, supporting tissue)
- endo first or second
- flap and section root (to enable oral hygiene)
- obturate
Success rate very high 90%


What is recession?

Displacement of the soft tissue margin apical to the cements-enamel junction with exposure of the root surface
n.b. narrow band of gingiva alone doesnt justify surgical intervention


Who is recession common in?

Those with high oral hygiene (buccal surface has wedge shaped notch -> trauma from brushing)
Those with poor oral hygiene (all tooth surfaces affected by perio)


What are the causes of recession?

- Mechanical (vigorous brushing/incorrect technique)
- Localised plaque induced inflammatory lesion (often lower incisors -> subgingival plaque in connective tissue)
- destructive periodontal disease


What is the treatment for recession?

healthy (none)
inflamed and >/= 2mm attached gingiva (OHI)
no attached gingiva or discomfort on chewing/toothbrush-> hypersensitivity or orthodontic movement will cause dehiscence (gingival augmentation procedure)


what is pseudo recession?

The gingival margin is apically positioned when compared to neighbouring teeth (not involved CEJ) = more common in children when eruption is not yet complete


Not all orthodontic tx show formation of root dehiscence, this may be due to:

- the amount of labial tooth displacement
- the force applied
- the presence of plaque and gingival inflammation in the regions subjected to tooth movement
- differences in gingival dimensions
- the thickness of gingiva on the pressure side of the tooth