Periodontology Flashcards
gingival disease can be split into 2 categories
- plaque induced
- non-plaque induced
plaque induced gingival disease
modified by systemic factors - endocrine system i.e. puberty, pregnancy / blood dyscrasias i.e. acute monocytic leukaemia
modified by medication - phenytonin in epilepsy, ciclosporin in immunosuppression, nifedipine in Ca channel blockers
non plaque induced gingival disease
infection - gonorrhoea/syphilis, PHG, gingival candidiasis
genetic - hereditary gingival fibromatosis
manifestation of systemic conditions - lichen planus, toothpaste allergy causing desquamative gingivitis
traumatic lesions - physical / chemical
difference in chronic and aggressive periodontitis
chronic - destruction is consistent with local factors i.e. plaque/disease progresses at a slow or moderate approach
aggressive - clinically healthy ptx but there will be rapid attachment loss and bone destruction. standard pattern follows 6s and incisors
periodontitis as a manifestation of systemic disease
haematological disorders - chronic lymphocytic leukaemia
genetic disorders -cyclic neutropenia (cycles of low neutrophils), papillon lefevre syndrome (autosomal recessive disease cause by deficiency in cathepsin C - rare ectodermal dysplasia)
localised tooth related factors modifying or predisposing plaque induced gingival diseases/periodontitis (4)
tooth anatomical factors i.e. crowding
restoration margins
orthodontic appliances
partial denture
mucogingival deformities & conditions around teeth (5)
gingival recession
lack or keratinised gingivae
aberrant frenal attachment
excessive gingival display
fibrous tuberosities
what is inflammation
the response of living tissue to injury and can be seen as dilation of blood vessels, increased permeability of vessel walls, inflammatory exudate and emigration of white blood cells from vessels to connective tissues
gingivitis
erythema & bleeding on probing, reti pegs on gingival tissues of the junctional epithelium, inflammation in this area but confined to gingivae and there is no loss of attachment
periodontitis
apical extension of gingival inflammation resulting in connective tissue attachment destruction, apical migration of junctional epithelium, bone loss and true pocket formation which all can lead to tooth mobility
what is ANUG and what can it lead to
acute necrotising ulcerative gingivitis can lead to necrotising periodontitis
signs & symptoms of necrotising perio disease
ptx c/o pain, bleeding, halitosis
o/e punched out crater like ulcers covered in grey slough which when wiped away will leave bleeding tissues - caused by necrosis rather than pocketing, erythema, swelling, interdental papilla destroyed
risk factors for necrotising perio disease (3)
impaired immunity e.g. HIV
smoking
stress
pathogenesis of perio disease
in slough itself fusobacterium sp. are the predominant species of bacteria
treponema sp. & p.intermedia also present
will invade tissues unlike other periodontal diseases & produce endotoxins
either the endotoxins produce the damage or the cytokine/neutrophil response
pocketing no produced just actual tissue destruction
treatment of ANUG
effective debridement
chlorhexidine & OHI
use of antibiotics controversial but if lymphadenopathy / systemic symptoms then metronidazole indicated
periodontal abscess & causes
localised acute exacerbation of pre-existing pocket from chronic periodontitis - caused by trauma to pocket epithelium, obstruction at entrance of pocket, post non-surgical treatment as pocket can tighten obstructing flow out of pocket or cause could be unknown
characteristics of periodontal abscess
pain or biting / constant pain
swelling
discharge causing halitosis
bad taste in mouth
o/e - swelling adjacent to periodontal pocket, tooth may be TTP, may be tooth mobility from LoA from inflammation
periapical v periodontal abscess
if there is chronic periodontitis with a pocket adjacent to the swelling then it is likely to be a periodontal abscess especially if tooth is vital
treatment of periodontal abscess
drain abscess (by pocket if possible)
gentle subgingival debridement
hot saline mouthwash
follow up with HPT
surgery if indicated
maintenance
antibiotics for perio abscess
again controversial - unless systemic involvement local measures taken first
amoxycillin 250mg 3-5 days
metronidazole 200mg 3 days
when would you carry out periodontal surgery
only ever indicated when pockets >5mm that persist in presence of excellent OH
must also be at the re evaluation phase 4-6wks after completing non surgical phase
if OH still poor at this stage then supportive care with cause related therapy is indicated
post periodontal surgery
chlorhexidine mouthwash 1-2wks, analgesia for 1-2days, antibiotics may be indicated, after 1wk sutures removed and normal mechanical plaque removal begins
at 2-4wks a long junctional epithelium will attach and probing depth will reduce, gingival recession as a result but gain in clinical attachment levels
infra bony defect & management
bone loss around tooth due to perio disease (may have 1/2/3 bone walls)
3 wall bony defect more likely to heal by repair as they can more easily form a clot and have bony infill from all 3 walls
managed by - closed/open root surface debridement with healing by repair // pocket elimination with osseous resection // regenerative techniques
other forms of periodontal surgery
gingivectomy
mucogingival surgery
crown lengthening surgery
for there to be periodontal regeneration there must be
- formation & maintenance of fibrin clot
- which must adhere to root surface (if not downward growth of epithelium)
- proliferation of progenitor cells
- these reside in PDL and bone
- migration & differentiation of progenitor cells
- formation of bone, PDL & cementum
barriers to periodontal regeneration
- inadequate debridement of root surface leaves smear layer of bacteria which inhibits healing & regeneration as continued inflammation
- not enough space for clot / clot adhesion disrupted will inhibit regeneration - this is caused by suturing clot in too tight, movements such as swallowing/speaking / smiling which can disrupt flap
- inadequate proliferation, migration, differentiation & orientation of progenitor cells; these cells may not work properly due to inadequate signalling molecules
indications for periodontal regeneration
Grade II mandibular furcation defects
Grade II buccal maxillary furcation defects
2 and 3 walled proximal defects
impact on attachment gain different methods have
RSD - 1mm gain
open flap debridement - 2mm gain
bone grafts - 2.5mm gain
emdogain - 3mm gain
guided tissue regeneration - 3.5mm
furcation therapy options
- non surgical debridement
- open flap debridement
- regenerative therapy
- surgical pocket elimination
- root separation or resection
- no treatment / palliative treatment
- XLA
for root resection to be successful
- endo treatment must be successful
- root separation & removal must be feasible
- remaining roots must be hypermobile
- remaining structure must be restorable
alveolar mucosa
dark, red, vascular, loosely attached to underlying bone, very thin & mobile, non keratinised and should move freely in speech & mastication
gingivae
pink, firm, attached to bone & cementum, relatively immobile in comparison to alveolar mucosa, keratinised & designed to resist mechanical stresses
anatomical factors affecting gingival deficiency
crowding
occlusal trauma
orthodontics
tooth position
inflammatory factors affecting gingival deficiency
gingivitis
periodontitis
mechanical factors affecting gingival deficiency
toothbrush
dentures
habits
opposing teeth
subgingival restorations
significance of gingival deficiency
plaque control becomes more difficult especially when marginal soft tissue is into alveolar mucosa
unaesthetic & sensitive
gingival augmentation
does not have to have recession present - creates a functional width of gingiva apical to mucogingival junction instead of alveolar mucosa - technique is called free gingival graft & can be harvested from the palate
root coverage surgery
should be done when recession present & should restore gingivae more coronally - undertaken when need to improve aesthetics, facilitate plaque control and address sensitivity
to work there must be good quality donor tissue, good interdental bone & control of causal factors
miller’s gingival classification
class I - marginal gingival recession does not extend to mucogingival junction; no loss of interdental bone / soft tissue
class II - marginal gingival recession extends to or beyond mucogingival junction; no loss of interdental bone / soft tissue
class III - marginal tissue recedes to or beyond the mucogingival junction there is loss of interdental bone / soft tissue apical to the CEJ but coronal to the apical extent of the marginal tissue recession
class IV - marginal tissue recession extends beyond mucogingival junction, loss of interdental bone extending to a level apical to the extent of the marginal tissue recession
conservative management & prevention of recession in predisposed individuals
avoid hard toothbrushes
reduced brushing to 2x daily
use effective & atraumatic technique
use minimally abrasive toothbrush
disperse paste about all teeth pre brushing
avoid scrubbing
antiseptics
applied topically / subgingival to tooth in conjunction with mechanical therapy
prevent plaque formation but once biofilm produced it can be difficult to penetrate & be effective
available without prescription, good safety record & widely available as mouthwashes
active ingredients in antiseptics
bisbiguanides i.e. chlorhexidine digluconate
phenols & essential oils
stannous fluoride
oxiding agents
detergents
chlorhexidine digluconate
gold standard bisbiguanide with 12hrs substantivity
0.2% 10ml 2x daily
active against gram + & gram - bacteria, yeasts and viruses
only used for specific problems / short term use; post perio / oral surgery when issues with cleaning or in physically / mentally disabled / immunocompromised ptx
safety & side effects of chlorhexidine
may cause staining, taste disturbances, occasionally mucosal erosion with dilute parotid swelling and it interacts with sodium lauryl sulfate
phenols & essential oils
triclosan - used in toothpaste, substantivity of 5hrs decreases plaque / gingivitis by 20-40%
listerine contains these & will reduce plaque by 14-56% & gingivitis by 20-36%
substantivity
persistence of action
to prevent bad breath
exclude smoking & dietary causes
treat caries, gingivitis, perio
treat mucosal sources of infection
exclude psychosomatic & extra oral causes
drink sufficient fluids
avoid garlic / spicy foods
eat regular meals
clean dorsum of tongue on regular basis
for treatment of periodontal abscess
careful subgingival RSD and:
amoxicillin 250mg 3x daily for 3 days OR
metronidazole 200mg 3x daily for 3 days
adv of systemic drug administration
delivered to tissues via serum
can reach reservoirs such as tonsils & tongue
less costly
less time for treatment
smoking & perio disease
less favourable response to treatment
increased likelihood of recurrence
increased disease progression
increased risk of ANUG
smoking & gums
clinically they can look healthy but gingivae will be pale, fibrotic & hyperkeratotic with reducing BoP due to less blood vessels in area, more advanced disease anteriorly & more recession, may have halitosis
host response in smokers
change in function of neutrophils, attachment & proliferation of fibroblasts, decreased GCF cytokines and suppressed response from antibodies
higher prevalence of periodontal pathogens in smokers e.g.
tannerella forsythia
prevotella intermedia
treponema denticola
in summary, smoking causes
increased perio & ANUG
decreased gingivitis
on cessation - rebound gingivitis
decreased perio therapy response
smoking cessation
ask
advice
assess
assist
arrange follow up
at assess stage: if ptx content record & bring up at later date, if ptx concerned, record bring up at further date & give further info, if ptx wanting to stop refer to specialist service
impact of diabetes mellitus on tissue
long term hyperglycaemia / hyperlipidaemia = increased glycosylated haemoglobin leading to increased AGEs (advanced glycation end products) which interact with cell surface receptors increasing endothelial cell permeability and increase adhesion molecules. increase chemotaxis of macrophages which increase production of TNF and IL-6 which increases MMP production and decreases collagen production leading to destruction of tissue
local host response to diabetes mellitus
microangiopathy
impaired neutrophil function
heightened inflammatory response
alteration of collagen metabolism
impaired wound healing
HbA1c
measure of glycated form of haemoglobin to get 3mth average of blood sugar
at risk of type 2 HbA1c should be <42mmol/mol
diabetic HbA1c should be 48mmol/mol or below
helps determine compliance & control
