Specific bacterial infections affecting oral cavity
Oral Lichen Planus (OLP)
1. Oral Lichen Planus
Department Of Oral Medicine & Radiology, IDST
Under the Guidance of:
Dr. Shalu Rai
Dr. Rohit Malik
Dr. Deepankar Misra
Dr. Sapna Panjwani
Dr. Sankalp Verma
Ashish Angural
Roll. 17
2. Oral Lichen Planus
Aka Lichen Rubber Planus
First described clinically :-
1869 – Wilson
First described histologically by:-
1906 - Dubreuilh
3. Erasmus Wilson (1869)
-Mixed non Scrapable Red and
white lesion in the mouth
-Can occur individually or with skin
lesions
*Lichen in Greek – tree moss
*Planus in Latin - flat
4. Epidemiology
• 1% of general population is
affected
• 0.14-0.8% worldwide
• 2/3rd of cases occur in middle age
• No racial predilection reported
although some authors claims a
predilection in blacks
• Increased in the month of Jan-July
& Dec-Jan
5. • Male: Female - 1:1
• 20% females with oral lesions have
genital involvement
• 2/3rd of the cases are symptomatic
• 40%- of patients have both Oral &
Cutaneous lesions
• 35%- of patients have Cutaneous
lesions only
• 25%- of the cases presents with
mucosal lesions only
6. Etiology
• Etiology is unknown.
• Immune System has a primary role in
the development of this disease.
• Genetic background
• Dental materials- metallic & non metallic
restoration
• Drugs & chemicals
• Infectious agents
• Autoimmunity
• Chronic liver disease
• Immunodeficiencies
8. Dental materials:
• Both metallic and nonmetallic
• Silver amalgam fillings
• Electrogalvanic reactions
• Copper and mercury
• Composite have also been implicated
10. Infectious agents
• Gm –ve anaerobic bacillus & spirochetes.
• increased prevalence of Candida species in
both mycological and histological studies of
oral lichen planus.
• In HIV + ve patients.
• Human papilloma virus in oral lichen planus
lesions.
• HCV is a virus that has high rate of mutation.
This results in a repeated activation of immune
cells increasing the likelihood of cross reaction
with self tissues and therefore increasing the
risk for developing autoimmune diseases.
11. Habits
• Smoking as an etiologic factor in some
Indian communities
• There is an increased prevalence of
betel nut chewing among lichen planus
patients
• Plaque type of lichen planus is most
commonly seen in smokers & less of
reticular and atrophic variety.
12. Trauma:
Chronic trauma from a improper restoration or tooth
itself is considered as a risk factor for the
development of oral lichen planus.
Diabetes & Hypertension:
impaired glucose metabolism in a high percentage of
lichen planus patients
in a diabetic individual lingual involvement & erosive
forms are more common.
Grinspan 1966-described association of
diabetes, hypertension with oral lichen planus and
called it as Grinspan syndrome
13. Stress
• Any stress causes activation of adrenal
medullary system.
• This leads to secretion of
catecholamines like adrenaline and
noradrenaline.
• These hormones have got
immunosuppressive activity which
results in lichen planus like lesions
14. Pathogenesis
• TARGET :- Epithelial basal cells
-Cell mediated immune process involving
Langerhans cells, T-lymphocytes, &
macrophages
-T lymphocytes become cytotoxic for
basal keratinocytes.
15. Definition
Lichen planus is a unique common inflammatory
disorder that affects the skin, mucous
membrane, nails and hair.
Oral lichen planus is a relatively common chronic
inflammatory immunologic reaction in which
epidermal or epithelial basal cell damage
produces mucocutaneous lesions of various
types
Oral lichen planus is a common chronic
immunologic inflammatory mucocutaneous
disorder that varies in appearance from keratotic
(reticular/plaque like) to erythematous or
ulcerative
16. Oral Lichen Planus
clinical features
• Disease of middle age
• Males = Females
• Children rarely affected
• Severity of disease often parallels
patient’s level of stress
• 2/3 are asymptomatic
• Usually present bilaterally
• Most common site: posterior buccl
mucosa
• Other locations: tongue, gingiva,alveolar
mucosa, palate, lip(mucosal side)
• Characteristic feature: Wichams striae.
17. Lichen Planus
Extra oral features
• Characteristic 4p’s- purple, polygonal,,
pruritic, papule- characteristic Cutaneous
lesions
• Wickhams striae
• The classic appearance of skin lesions
consists of erythematous to violaceous
papules that are flat topped and
occasionally polygonal in form. A network
of white lines often overlies the papules.
18. • Koebners phenomena- it refers to
development of papules along the line of
trauma in a linear fashion. Most commonly
seen on skin.
• Penogingival syndrome- male analog of
vulvovaginal gingival syndrome- rare in males
• vulvovaginal gingival syndrome- Association
of Vulva, vagina & gingiva as the
• Lichen planopilaris is the involvement of the
scalp & hair follicles by lichen planus which
results in scarring alopecia
• Symptoms like burning, pain, vaginal
discharge- erosive & erythematous types
19. Types of
Oral Lichen Planus
1.Reticular form
2.Papular type
3.Plaque- like
4.Bullous
5.Erythematous or Atrophic
6.Ulcerative
21. 1.Reticular form
• Characterised by fine white lines or
striae.
• striae may forma network or show
annular patterns.
• Often displays a peripheral erythematous
zone reflecting sub epithelial
inflammation.
• Most frequently observed in buccal
mucosa (bilaterally)
• Rarely on lips (mucosal side)
• May also be seen on Vermillion border.
24. 2.Papular type
• Usually present in intial phase of
disease
• Characterised by small white dots
• Minute white papules
• These gradually enlarge to form
either a reticular, annular, or plaque
pattern.
In most occasions it intermingles with
Reticular form.
27. 3.Plaque type
• Shows a homogenous well demarcated
white plaque oftenly but not always,
surrounded by striae.
• Simultaneous presence of Reticular &
Papular structures seen
• Most oftenly seen in smokers.
• Confluent white patches similar to oral
keratoses
32. 4.Bullous Form
• This form of OLP is quite rare.
• May appear as Bullous structure
surrounded by a reticular network.
• The intraoral bullae rupture soon after they
appear, resulting in the classic
appearance of erosive OLP.
35. 5.Erythematous or
Atrophic form
• Characterised by homogenous red area
• In buccal mucosa or palate, striae are
seen at periphery
• May exclusively affect attached gingiva
• May occur without any papules or striae
and presents as Desquamative Gingivitis
• Can be very painfull
• Red lesions often with a whitish border.
• May cause erosions.
45. 1. Hyperorthokeratosis/Hyperparakeratosis
2. Acanthosis
3. Thickening of the granular cell layer
4. Basal cell liquefaction
5. Saw tooth configuration of the rete pegs
6. Band like dense inflammatory cellular
infiltrate in the upper lamina propria
46. Differential diagnosis
• Squamous Cell Carcinoma
• Lichenoid reaction contactant-history
• Pemphigus vulgaris-microscopic examination
of acantholysis
• Candidasis-pseudomembrabe can be rubbed
• Chronic cheek biting / chewing
• Dermatitis Herpetiformis
• Discoid lupus erythematosus-not in fine
reticular pattern
• Leukoplakia-men more,in LP Wicham’s straie
• Atrophic glossitis in tertiary syphilis-red centre
with raised margin
48. Systemic retinoids:
• It can also be used at a starting dose of Etretinate of
1.6 to 0.6 mg/day/kg for 2 months followed by
maintenance dose of Etretinate of 0.3mg/kg/day or
0.1%
• Tretinoin in a adhesive base applied topically twice
daily similarly systemic Isotretinoin (13-cis-retinoic
acid) can be used in dosage of 10-60mg/day for 2
months
Topical retinoids:
• Topical Tretinoin 0.1% in an adhesive gel (4 times a
day for 2 months)
• Topical Isotretinoin 0.1% (2 times a day for 2 months)
also appears to be effective in 85% of patients.
• A new topical retinoid Tazarotene has been found to
be used in the treatment of oral lichen planus and
demonstrated to be helpful in hyperkeratotic oral lichen
planus.
49. • Immunosuppressive agents:
• Azathioprine: It is used in the dose of 75-
150mg/day for about 1-2 months. Long term use
may increase the risk of internal malignancy.
• Cyclosporine: It is used in the dose of 6mg/kg/day.
The adverse side effects include is most
importantly renal dysfunction and hypertension.
• Topical cyclosporine can also be used. Mouth
rinses (450-1500mg/day for 8-12 weeks) and
finger applications of base of solution (100mg/day
for 4 weeks) or a cellulose base preparation of
cyclosporine (48mg/day for 8weeks) produce
significant improvement in oral lichen planus with
no side effects and little systemic absorption.
50. • Tacrolimus: Topical tacrolimus seems to penetrate
better than topical cyclosporine. Local irritation is
the most common side effect. It is used as a dose
of 0.1% topical ointment.
• Dapsone: it has been used to treat the various
inflammatory and infectious dermatoses.
Significant side effects like headache and
haemolysis have been reported.
• Antibiotics: 2% aureomycin mouthwash.
Tetracyclines has also been proved to be useful in
the treatment of gingival lesions in some reports.
• Glycyrrhizin: the successful treatment of oral
lichen planus with chronic hepatitis C infection has
been reported in patients on use of glycyrrhizin. It
is given intravenously.
51. • Interferon: topically applied gel containing human
fibroblast interferon( HuFN-β ) and interferon α cream may
improve oral erosive lichen planus. Systemic interferon can be
used in the dose of 3-10 million IU thrice weekly.
• Levamisole: it is used as an immunomodulator in oral lichen
planus. It is used in the dose of about 150mg/day for 3 days in
a week for 3 consecutive weeks. However levamisole itself can
induce lichen planus like lesions.
• Mesalazine: it is 5 aminosalicylic acid is a relatively new drug
widely used in the treatment of inflammatory bowel disease.
Topically it is as effective as that of steroid. It itself can induce
lichen planus.
• Phenytoin & Reflexotherapy are the other modes of treatment
used.
52. • PUVA:
• ultraviolet irradiation along with the psoralens may suppress the cell
mediated immunoreactivity in epermental animal models and
humans.
• PUVA treatment usually begins with the Methoxpsolaren- 0.6mg/kg
or equivalent taken 2hr prior to UV irradiation.
• An apparatus for Light cured dental fillings can be used as an
irradiation source to deliver a beginning dose of 0.75J/sq.cm
initially and a total dose ranging from 11.6-16.5J/Sq.cms.
• Oncogenic potential is a serious side effect thought to be caused
due to use of PUVA.
• Extracorporeal photochemotherapy
• use of 308 nm UVB excimer laser in th treatment of lichen planus.
• Surgery:
• Excision – although this is not the first treatment of choice. It is done
in cease of refractory for the rest of the treatment.
• CO2 laser
• Cryosurgery
53. Complications
• Malignant change is found in about 0.4-
3.5% over a period of 0.5-20 yrs.
• Commonly malignant transformation is
seen with the variants such as-
erosive/atrophic/ulcerative variant
• 1% of oral lichen planus shows
malignant transformation.
54. Conclusion
• Oral lichen planus is a complex and poorly
understood clinical condition which cannot
be cured. A definitive diagnosis and
careful, conscientious follow-up are
imperative. Symptoms and complications
are common and challenging but may be
managed with a variety of therapies
including orally administered and systemic
medications as well as lifestyle alterations
and reduction of precipitating factors.
55. References
• Burket’s 11th edition
• Woods & Goaz, differential diagnosis
• Internet
• WIKIPEDIA
• www.mndental.org
• www.emedicinemedscape.com
• www.dermnetnz.org
• www.rxdentistry.com
• Google photos
• Vincent, S.D., Fotos
• Wilson, E.: On lichen planus. J Cutan Med Dis
Skin
