Periodontal therapy involves the diagnosis and treatment of plaque-associated diseases as well as non-plaque related conditions like desquamative gingivitis. Desquamative gingivitis presents as erythema, desquamation, and ulceration of the gingiva and can be caused by conditions like lichen planus, pemphigoid, and pemphigus vulgaris. The pathogenesis involves autoimmune responses against epithelial antigens that disrupt cellular junctions and cause separation of the epithelium from the underlying connective tissue. Management consists of treating the underlying cause, improving oral hygiene, and using topical or systemic corticosteroids.
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
REFERENCES TAKEN FROM CARRANZA'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND LINDHE'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY. CONTAINS ENOUGH AND MORE DETAILS OF THIS TOPIC FOR BDS STUDENTS.HOPE THIS PRESENTATION WILL HELP U GAIN SOME KNOWLEDGE ABOUT PERIODONTAL PLASTIC AND ESTHETIC DENTISTRY.
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
The periodontal examination should be systematic, starting in the molar region in either maxilla or mandible and proceeding around the arch. It is important to detect the earliest signs of gingival and periodontal disease.
REFERENCES TAKEN FROM CARRANZA'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND LINDHE'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY. CONTAINS ENOUGH AND MORE DETAILS OF THIS TOPIC FOR BDS STUDENTS.HOPE THIS PRESENTATION WILL HELP U GAIN SOME KNOWLEDGE ABOUT PERIODONTAL PLASTIC AND ESTHETIC DENTISTRY.
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
The periodontal examination should be systematic, starting in the molar region in either maxilla or mandible and proceeding around the arch. It is important to detect the earliest signs of gingival and periodontal disease.
Necrotising periodontal diseases, Necrotising periodontal diseases as a manifestation of systemic diseases.
By Dr. Ritam Kundu, MDS PGT, Dr. R. Ahmed Dental College & Hospital, Kolkata, India.
Eosinophilic Ulcer of the Oral Cavity, Approach, and Differential Diagnosissemualkaira
Benign ulcerations of the oral mucosa may have a similar appearance to malignant lesions [1, 2]. There are several conditions, both local and systemic, that can manifest as oral ulcers, and that can correspond, on many occasions, to both infectious and autoimmune causes. Probable etiology can often be determined by a complete medical history and a careful physical examination. However, on several occasions, an exhaustive diagnostic study will be necessary, counting on a range of diagnostic suspicions
Mucocutaneous Involvement in Behcets Diseasenavasreni
Behçet’s disease is a chronic inflammatory disease characterized by its clinical polymorphism associating mucocutaneous involvement to systemic manifestations. The mucocutaneous lesions are considered the hallmark of the disease, being the most common symptoms presenting at the onset of disease. Our objective was to determine the characteristics of this skin involvement during Behçet’s disease. We conducted a descriptive study over a period of 30 years, having collected all patients with Behçet’s disease.
Mucocutaneous Involvement in Behcets Diseasepateldrona
Behçet’s disease is a chronic inflammatory disease characterized by its clinical polymorphism associating mucocutaneous involvement to systemic manifestations. The mucocutaneous lesions are considered the hallmark of the disease, being the most common symptoms presenting at the onset of disease. Our objective was to determine the characteristics of this skin involvement during Behçet’s disease
Mucocutaneous Involvement in Behcets Diseasesemualkaira
Behçet's disease is a chronic inflammatory disease characterized by
its clinical polymorphism associating mucocutaneous involvement
to systemic manifestations. The mucocutaneous lesions are
considered the hallmark of the disease, being the most common
symptoms presenting at the onset of disease. Our objective was
to determine the characteristics of this skin involvement during
Behçet's disease. We conducted a descriptive study over a period
of 30 years, having collected all patients with Behçet's disease.
These were 98 patients. A male predominance was observed in
our studied population with a Sex Ratio of 2.5. The mean age at
diagnosis was 34 years. Mucocutaneous involvement was observed
in all patients. Oral aphthosis was constant and genital ulcers, were
observed in 81 cases. The other mucocutaneous manifestations
were: pseudofolliculitis (61 cases), erythema nodosum (7 cases),
skin ulcers (4 cases), acneiform lesions (2 cases), perianal ulcers (1
case), skin ulceration (1 case) and erythema multiforme. (1 case).
All of our patients were treated with colchicine. Corticosteroids
and non-steroidal anti-inflammatory drugs were each indicated in
one case for resistant forms.
Mucocutaneous Involvement in Behcets Diseasekomalicarol
Behçet's disease is a chronic inflammatory disease characterized by
its clinical polymorphism associating mucocutaneous involvement
to systemic manifestations. The mucocutaneous lesions are
considered the hallmark of the disease, being the most common
symptoms presenting at the onset of disease. Our objective was
to determine the characteristics of this skin involvement during
Behçet's disease. We conducted a descriptive study over a period
of 30 years, having collected all patients with Behçet's disease.
These were 98 patients. A male predominance was observed in
our studied population with a Sex Ratio of 2.5. The mean age at
diagnosis was 34 years. Mucocutaneous involvement was observed
in all patients. Oral aphthosis was constant and genital ulcers, were
observed in 81 cases. The other mucocutaneous manifestations
were: pseudofolliculitis (61 cases), erythema nodosum (7 cases),
skin ulcers (4 cases), acneiform lesions (2 cases), perianal ulcers (1
case), skin ulceration (1 case) and erythema multiforme. (1 case).
All of our patients were treated with colchicine. Corticosteroids
and non-steroidal anti-inflammatory drugs were each indicated in
one case for resistant forms
Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
Similar to Desquamative gingivitis 5th seminar (20)
Introduction
History
Types of immunity
Tissues of immunity
Cells of immunity
Basic aspects of immunology
Major histocompatibility complex
Cytokines
Disorders of immune system
Immune responses in periodontal pathogenesis
Periodontal vaccine
Host modulation
Conclusion
References
seminar on gingiva
contents:
Introduction
Definition
Development of gingiva
Macroscopic anatomy
Microscopic anatomy
Blood supply
Lymphatic drainage
Nerve supply
Correlation of clinical and microscopic features
Repair/healing of gingiva
Age changes
Gingival diseases
Clinical considerations
Conclusion
References
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
5. Periodontal therapy involves not only the tx of plaque induced diseases
but also varous nonplq induced conditions. And one of those conditions
is desquamative gingivitis.
Periodontal therapy involves not only the diagnosis and treatment of
plaque associated diseases but also various non plaque related diseases.
The International workshop for classification of periodontal diseases
and conditions noted that the periodontist may be called upon to
manage these non-plaque related mucocutaneous disorders either
alone or as a part of treatment team consisting of physicians, dentists or
other allied health care professionals. Among the oral manifestations
which have long baffled dentists, chronic desquamative gingivitis is one
of the most interesting and persistent
6. • Desquamation
from Latin desquamare, 'to scrape the scales off a fish‘
skin peeling,
shedding of the outermost membrane or layer of a tissue, such as
the skin or mucosa.
6
7. DEFINITIO
N
• “A peculiar condition characterized by intense erythema,
desquamation, and ulceration of the free and attached gingiva.”
- Prinz (1894)
• McCarthy and colleagues (1960) suggested that “desquamative
gingivitis was not a specific disease entity but rather a gingival
response associated with a variety of conditions.”
7
8. HISTOR
Y
Tomes & tomes, 1894: Described for the first time.
Goodby, 1923: mentioned in his book
Prinz, 1932: coined the term “chronic diffuse
desquamative gingivitis”
Meritt, 1933: a disease of unknown etiology
Stoloff, 1933 : “Periodic transitory meno-gingivitis"
Ziskin and Zegarelli, 1942: discussed the clinical and
microscopic features of chronic desquamative
gingivitis.
8
9. Schour & Massler, 1947: gave the term gingivosis in
anemic hospitalized children of postwar Italy.
McCarthy et al, 1960: Not a specific disease entity
but a gingival response associated with a variety
of conditions.
Hosiosky, et al, 1961: suggested treatment of
DG by improving cervical oral hygiene.
Glickman and Smulow, 1962: studied the
histopathology and histochemistry. Two basic
microscopic types recognized: a bullous type, and
a lichenoid type.
Glickman and Smulow, 1964: advocated a treatment
regimen of systemic corticosteroid therapy and
removal of local irritants.
9Oles, R.D. Chronic desquamative gingivitis. J Periodont 38:485 Nov-Dee
11. CLASSIFICATI
ON
Based on etiological considerations, desquamative gingival lesions are
classified as (modified classification of McCarthy and others)
Dermatoses
Lichen planus
Cicatricial
pemphigoid
Bullous
pemphigoid
Pemphigus vulgaris
Psoriasis
Linear IgA
disease
11
12. Endocrinal
imbalance
Estrogen deficiency in females
(menopause, following
hysterectomy and oopherectomy)
Testosterone deficiency in males
Chronic
infections
Tuberculosis
Chronic candidiasis
Histoplasmosis
12
15. EPITHELIAL
BIOLOGY
The integrity of oral epithelium is mainly dependent on the cells and the
cellular junctions.
Cellular junctions:
1. Occluding junctions
2. Communicating junctions
3. Anchoring junctions:
• Cell-cell:
Desmosomes
Adherens junction
• Cell-matrix:
Hemidesmosomes
Focal adhesions
KV Arun. Molecular biology of periodontium. 1st Ed. 2010.
16. Desmosomes:
• Cadherins: desmoglein, desmocollin
• Catenins: desmoplakin, plakoglobin, plakophillin
Garrod et al. Desmosome structure, composition and function. Biochimica et Biophysica
Acta 1778 (2008) 572–587
17. Hemidesmosomes
Mihai et al. Immunopathology and molecular diagnosis of autoimmune bullous diseases. J.
Cell. Mol. Med. Vol 11, No. 3, 2007 pp. 462-481
18. ETIOLOGY
• Various etiological factors contribute to the development of
desquamative gingivitis.
• Encompass autoimmune/immune mediated, infectious,
neoplastic, hematologic, reactive, nutritional and idiopathic
causes.
• Approximately, 50% of oral mucosal diseases are localized to
gingiva causing desquamative gingivitis, although other
intraoral and extraoral sites may be involved.
S. Sangeetha et al. The molecular aspects of oral mucocutaneous diseases: A review. International
Journal of Genetics and Molecular Biology Vol. 3(10), pp. 141-148, November 2011
19. R. J. Nisengardt and R. S. Rogers. The Treatment of Desquamative Gingival
Lesions. 19
20. PATHOGENESI
S
• An immunologic phenomenon has been recognized as an
important pathogenic mechanism responsible for the
initiation and/or progression of autoimmune diseases such
as mucocutaneous lesions. Epitope spreading.
• Epitope spreading the development of immune
responses to endogenous epitopes secondary to the release
of self antigens during a chronic autoimmune or inflammatory
response.
S. Sangeetha et al. The molecular aspects of oral mucocutaneous diseases: A review.
International Journal of Genetics and Molecular Biology Vol. 3(10), pp. 141-148, November 2011
22. Subepithelial lesions
Proteins Diseases
BP 230 Cicatricial pemphigoid
BP 180 Cicatricial pemphigoid,
bullous pemphigoid
α6, β4 Cicatricial pemphigoid,
junctional epidermolysis bullosa
Laminin 5 (epiligrin) Cicatricial pemphigoid,
junctional epidermolysis bullosa
Type VII collagen Epidermolysis bullosa dystrophica,
Epidermolysis bullosa acquisita
Target antigens of hemidesmosomes implicated in subepithelial blistering
disorders (Bagan, 2005).
23. Intrepithelial/subepithelial clefts
acantholysis/dissolution of ep-
basal lamina junc.
Activates immune system
(complement, attracts immune
cells).
Formation of Ag-Ab complexes
intercellulary or at the ep-basal
lamina interface.
Auto-antibodies formed against
self-Ag.
24. CLINICAL
PRESENTATION
24
• 1.5–2.5% of population.
• females > males.
• 3rd or 4th decade of life (can be seen in younger
individuals).
• Asymptomatic; when symptomatic their complaints range
from burning sensation to severe pain.
26. Moderate Form
Patchy distribution of
bright red and gray
areas.
Smooth, shiny, soft
gingiva.
Burning sensation,
sensitivity to
temperature.
Inhalation of air may be
painful.
Massaging the gingiva
results in peeling of the
epithelium with bleeding
on brushing. 26
27. Severe Form
Wide areas of the
oral cavity involved.
Surface epithelium
appears shredded.
Blowing of air
causes a bubble in
gingival epithelium.
Very painful.
Constant dry,
burning sensation.
27
29. Lichen Planus
31
Immunologically mediated mucocutaneous disorder, T-cells
trigger apoptosis of epithelial cells.
Mostly seen: Middle aged & older women.
The skin lesions of LP appear as small , angular, flat topped
papules.
Oral lesions:
1. Reticular
2. Patch
3. Atrophic
4. Erosive
5. Bullous
most common reticular & erosive
30. Reticular:
•Asymptomatic & B/L.
•Has interlacing white lines on
erythematous background.
Whickams striae
•Involves buccal mucosa,
lateral & dorsal aspects of
tongue, hard palate, alveolar
ridge, gingiva.
Erosive:
•Painful
•Atrophic, erythematous &
ulcerated areas with fine
white radiating striae at the
borders,
•Sensitive to heat, acid & spicy
foods.
32
31. Gingival Lesions:
Approx. 7% to 10% of patients with OLP.
Four distinctive patterns:
Keratotic lesions:
raised white
lesions,
papules/ linear-
reticular lesions/
plaquelike
configurations.
Erosive/ ulcerative
lesions:
Extensive
erythematous
areas
patchy
distribution focal
or diffuse
Vesicular / bullous
lesions:
raised, fluid-filled
lesions
uncommon and
short lived
quickly rupture
Atrophic lesions:
Atrophy of tissues
epithelial thinning
erythema confined
to the gingiva.
32. Histopathology:
• Hyperkeratosis,
• Hydropic degeneration of
the basal layer,
• Saw-tooth rete pegs;
• Lamina propria exhibits
dense, bandlike infiltrate
primarily of T lymphocytes;
• Civatte bodies colloid
bodies seen at ep.-CT
interface
• E/M: separation of basal
lamina from basal layer
33. Immunopathology:
DIF: linear fibrillar (“shaggy”) deposits of
fibrin in the basement membrane zone,
• scattered immunoglobulin staining cytoid
bodies in the upper areas of the lamina
propria.
IIF: negative.
Differential Diagnosis:
• Lichenoid mucositis
• Oral lichen planus of gingival tissues without white striations MMP, PV
• less common possibilities linear IgA disease and chronic ulcerative
stomatitis.
34. • Mild cases: use of vacuum-formed custom trays
Rx: Lidex (0.05% fluocinonide) gel
Rx: Nystatin oral pastilles (100,000 IU)
• Recalcitrant cases:
Rx: Protopic (0.1% tacrolimus) ointment
• Severe or refractory cases: Intralesional injections of triamcinolone
acetonide (10 to 20 mg) or short-term regimens of 40 mg prednisone
daily for 5 days followed by 10 to 20 mg daily for an additional 2 weeks.
Antifungal therapy.
Treatment
35. Pemphigoid
The term pemphigoid number of cutaneous, immune mediated,
subepithelial bullous diseases that are characterized by a separation of the
basement membrane zone.
1. Bullous pemphigoid NON-SCARRING
2. Mucous membrane pemphigoid SCARRING
3. Pemphigoid (herpes) gestations
36. Bullous
Pemphigoid:
38
• Chronic, autoimmune, subepidermal
bullous disease with tense cutaneous
bullae that rupture and become
flaccid.
• Oral Lesions:
Reported to occur secondarily in
up to 40% of cases.
Gingiva- Erythematous and
Desquamate
Painful.
Negative Nikolsky sign
Coalescing cutaneous bullae
Rupture serpiginous ulcers.
37. 39
• Subepithelial clefting with
epithelial separation from
the underlying lamina
propria, leaving an intact
basal layer.
• No evidence of
acantholysis.
Histopathology: • Characterized by:
1. Immunoglobulin G (IgG)
Complement 3 (C3) immune
deposits along the epithelial
basement membranes.
2. Circulating IgG antibodies to
the epithelial basement
membrane.
• DIF + in 90% to 100% of
patients
• IIF + in 40% to 70% of patients.
Immunofluorescence:
38. Treatment:
Designed to control its signs and symptoms.
Primary Tx moderate dose of systemic prednisone.
Steroid-sparing strategies
• prednisone plus other immunomodulatory drugs
• used when high doses of steroids are needed or when the
steroid alone fails to control the disease.
For localized lesions high-potency topical steroids or
tetracycline with or without nicotinamide can be effective.
39. Mucous Membrane Pemphigoid
(Cicatricial Pemphigoid):
41
• A chronic vesiculo-bullous autoimmune disorder of unknown
cause.
• Predominantly affects women, fifth decade of life.
• Rarely been reported in young children.
• Involves the oral cavity, the conjunctiva, mucosa of the nose,
vagina, rectum, esophagus, and urethra. 20% cases showed skin
involvement.
• Five subtypes:
1. oral pemphigoid,
2. anti-epiligrin pemphigoid,
3. anti-BP antigen mucosal pemphigoid,
4. ocular pemphigoid,
5. multiple-antigens pemphigoid.
40. Pathogenesis of the lesion
Attraction of PMNs to the area
Elaboration of chemotactic factors
Complement activation
Antigen/antibody complexing at the BMZ
Release of proteolytic enzymes that ultimately dissolve or cleave
the basement membrane zone, usually at the lamina lucida level
(Eversole, 1994).
2 major antigenic determinants: bullous pemphigoid 1 and 2 (BP1 and BP2).
epiligrin (laminin-5), and β4 integrins.
41. Ocular Lesions:
• The initial lesion is characterized
by unilateral conjunctivitis that
becomes bilateral within 2 years.
• Symblepharon: adhesions of
eyelid to eyeball.
• Ankyloblepharon: Adhesions
the edges of the eyelids may
leading narrowing of the
palpebral fissure.
• Small vesicular lesions may
develop on the conjunctiva, which
may eventually produce scarring,
corneal damage, and blindness.
42. • Presence of desquamative
gingivitis, typically with areas of
erythema, desquamation,
ulceration, and vesiculation of
the attached gingiva.
• The bullae tend to have a
relatively thick roof
• Rupture within 2 to 3 days,
leaving irregularly shaped areas
of ulceration.
• Healing of these lesions may
take 3 weeks or more.
Oral Lesions:
Lesions are confined to the
gingival tissues, where they
produce a typical desquamative
gingivitis appearance
43. • Subepithelial clefting with
epithelial separation from the
underlying lamina propria,
leaving an intact basal layer.
• A mixed inflammatory
infiltrate (i.e., lymphocytes,
plasma cells, neutrophils, and
scarce eosinophils) is observed
in the underlying fibrous
connective tissue.
Histopathology: Immunofluorescence
• DIF: Linear deposits of C3
with or without IgG at the
basement membrane zone in
almost all cases.
• C3 deposits confined along
the basement membrane.
• IIF: Basement membrane
zone (IgG) antibodies in 10%
of cases
44. Treatment:
• Mild cases:
• Rx: Lidex (0.05% fluocinonide) gel
• Rx: Temovate (0.05% clobetasol propionate) TID for 6 months.
• Severe or refractory cases: Refer to dermatologist for management
with prednisone (20 to 30 mg/day);
• concomitant use of azathioprine may be needed; dapsone,
sulfonamide, and tetracycline are other alternatives
• High risk: IV ig
45. Pemphigus Vulgaris
• A group of autoimmune bullous disorders that produce
cutaneous and mucous membranes blisters.
• Other types:
pemphigus foliaceus,
pemphigus vegetans,
pemphigus erythematosus.
• potentially lethal chronic condition 10% mortality rate.
• Female predilection, after 4th decade.
• Also been reported in unusually young children and
newborns.
46. Pathogenesis of PV
• Circulating autoantibodies are responsible for disruption of
intercellular junctions and loss of cell-cell adhesion.
• Auto antibodies directed against desmoglein 3ORAL;
DSG1CUTANEOUS.
• Early studies implicated complement in the acantholysis which
follows antibody binding (Jordan et al., 1974; Kawana et al.,
1984,1985).
• Plasminogen activator (PA) production by keratinocytes has
been implicated in acantholysis. (Hashimoto et al., 1983;
et al., 1985),
Pemphigus foliaceus-Antibodies directed against Dsg 1 (Hashimoto
al., 1990; Calvanico et al., 1991)
Drug-induced pemphigus.Penicillamine and captopril can produce.
Paraneoplastic pemphigus antigenically distinct from pemphigus
vulgaris, and it is associated with underlying malignancies
47. Intraoral
manifestations
• Intraepithelial separation
• Bullae soon rupture-Painful
erosions with ragged
borders.
• Gingival lesions can occur
and, along with other oral
lesions, may represent the
first manifestations of the
disease.
• Positive Nikolsky’s sign
Orlowski WA et al, J Periodontol 1983, Markitziu A et al Oral Surg Oral Med OralPathol 1983
48. Histologic Features
• Intraepithelial clefting”
• Acantholysis and suprabasilar
bullae formation.
• Basal cells lining the floor of
the bullae-"tombstone"
pattern
• Acantholytic keratinocytes
(Tzank cells) - blister fluid.
• Dense mononuclear
lymphocytic infiltration.
49. Immunofluoroscence:
DIF
• Intercellular deposits in
the epithelium; IgG in all
cases and C3 in most
cases.
• Chicken wire” or “fish
net” appearance.
IIF
• Less sensitive
• Helpful in monitoring
the disease
50. D/D:
If the oral lesions of pemphigus vulgaris are restricted to the gingival
tissues, then erosive lichen planus, pemphigoid, LAD, and chronic
ulcerative stomatitis should be ruled out.
Treatment:
51. Chronic Ulcerative Stomatitis
first reported in 1990.
clinically presents with chronic oral ulcerations.
predilection for women during 4th decade of life.
Oral Lesions:
• Painful
• solitary small blisters and
erosions with surrounding
erythema
• mainly on the gingiva and the
lateral border of the tongue.
• The buccal mucosae and hard
palate may also present
similar lesions
52. Histopathology:
• Hyperkeratosis,
acanthosis, liquefaction
of the basal cell layer
with areas of
subepithelial clefting.
• The underlying lamina
propria exhibits a
lymphohistiocytic
chronic infiltrate in a
bandlike configuration.
Immunofluorescence:
DIF
• typical stratified epithelium–specific
antinuclear Ab.
• nuclear deposits of IgG with a
speckled pattern, basal cell layer
of epithelium.
• fibrin deposits at the epithelial-
connective tissue interface.
IDIF
• presence of stratified epithelium–
specific antinuclear antibodies.
53. Treatment:
• Mild cases
topical steroids (e.g., fluocinonide, clobetasol
propionate)
topical tetracycline
• For severe cases a high dose of systemic
corticosteroids
• Recalcitrant cases Hydroxychloroquine sulfate
200-400 mg/ day
54. Linear Immunoglobulin A Disease
• linear IgA dermatosis
• Uncommon mucocutaneous disorder with female predilection.
• Etiology:
drug-induced LAD triggered by ACE inhibitors has been
reported.
• Clinical presentation:
Pruritic vesiculobullous rash.
Characteristic plaques/ crops with an annular presentation
surrounded by a peripheral rim of blisters affect the skin.
Mucosal involvement ranges from 50% to 100% of the
cases published.
Mimic lichen planus both clinically and histologically.
55. 57
Oral Lesions:
• vesicles, painful ulcerations or
erosions, and erosive gingivitis or
cheilitis.
• Hard and soft palates > tonsillar
pillars > buccal mucosa > tongue
> gingiva.
• Rarely, oral lesions may be the
only manifestation of LAD.
• oral lesions of LAD have been
clinically reported as
desquamative gingivitis.
56. Immunofluorescence:
Linear deposits of IgA are observed at the epithelial–connective
tissue interface.
Differential Diagnosis:
includes erosive lichen planus, chronic ulcerative stomatitis,
pemphigus vulgaris, bullous pemphigoid, and lupus
Microscopic examination and immunofluorescence studies are
necessary to establish the correct diagnosis.
Treatment:
The primary treatment
combination of sulfones and dapsone.
Small amounts of prednisone (10 mg/day to 30 mg/day).
OR
tetracycline (2 g/day) + nicotinamide (1.5 g/day).
Refractory ulcerations Mycophenolate (1 g twice daily) +
prednisolone (30 mg daily).
57. Dermatitis Herpetiformis
• chronic condition that usually develops in young adults
between the ages of 20 and 30 years.
• Male predilection
• Currently, evidence indicates that it is a cutaneous
manifestation of celiac disease.
• Etiology:
tissue transglutaminase seems to be the
autoantigen in the intestine, the skin, and sometimes
the mucosae celiac disease.
58. Clinically:
Bilateral and symmetric
pruritic papules/vesicles
Oral lesions:
range from painful ulcerations
preceded by the collapse of
ephemeral vesicles or bullae to
erythematous lesions.
59. Histopathology:
focal aggregates of
neutrophils and eosinophils
among deposits of fibrin at
the apices of the dermal
pegs.
Immunofluorescence:
DIF IgA and C3 are present at the dermal papillary apices.
80% of patients have anti-endomysial and gliadin antibodies.
Treatment:
A gluten-free diet celiac disease and dermatitis herpetiformis.
Oral dapsone to alleviate symptoms promptly.
60. Lupus Erythematosus
Lupus erythematosus is an autoimmune disease with three
different clinical presentations:
1. systemic,
2. chronic cutaneous,
3. Subacute cutaneous.
61. Systemic Lupus Erythematosus:
• Females 10 : 1
• Affects kidneys, skin and
mucosa
• Fever, weight loss and
• arthritis
• Oral lesions are present in
up to 40% of patients.
• malar area with a
distribution rash
62. Oral lesions:
• hyperkeratotic plaques
reminiscent of lichen planus
appear on the buccal
and palate.
Immunofluorescence:
• Ig and C3 deposits at the
dermal–epidermal interface.
• Antinuclear antibodies
of cases,
• deoxyribonucleic acid and
extractable nuclear antigen
antibodies 50% of patients
63. • Has no systemic signs or
symptoms, lesions limited to
the skin / mucosa.
• chronic scarring, atrophy-
producing lesion that may
develop into hyper/hypo
pigmentation or of the
healing area.
• In the oral cavity, lichen-
planus–like plaques on the
palate and the buccal
mucosa.
• The gingiva may be affected
and present clinically as
desquamative gingivitis.
Chronic Cutaneous Lupus Erythematous/ DLE:
65. Subacute Cutaneous Lupus Erythematosus:
• similar to DLE but lack the development of scarring and atrophy.
66. Treatment:
• depends on the severity and extent of the disease;
• range from topical steroids to NSAIDS,
• For chronic cutaneous lupus erythematosus:
topical steroids cutaneous and oral lesions.
• for severe systemic organ involvement:
moderate to high doses of prednisone.
Immunosuppressive drugs (e.g., cytotoxic agents such
as cyclophosphamide and azathioprine)
plasmapheresis alone or with steroids.
rituximab long-term remissions.
• For patients who are resistant to topical therapy:
systemic antimalarial drugs may be used, with good
results
67. Erythema Multiforme
Acute bullous and macular inflammatory mucocutaneous disease.
young adults (20 and 40 years)
Etiology:
Allergic/hypersensitivity reactions.
Medications
Bacterial or viral infections
Other triggers-Benign and malignant tumours, Crohns disease,
sarcoidosis and infective mononucleosis
Etiopathology:
Deposition of immune complexes in the superficial
microvascular supply of skin and mucosa (type II Immune
reaction) / Cell mediated immunity (type IV).
Complement fixation→ Leukocytic destruction of vascular walls
and small vessel occlusion.→ Ischemic necrosis of the epithelium
& connective tissue.
68. Clinical features:
• mild condition (EM minor)
• severe and possibly life-
threatening condition (EM
major or Stevens–Johnson
syndrome).
• An underdiagnosed type of
erythema multiforme is the
oral form
• Target or “iris” lesions with
central clearing are the
hallmark of erythema
multiforme.
69. Oral lesions:
• multiple large, shallow, painful
ulcers with an erythematous
border.
• chewing and swallowing are
impaired.
• buccal mucosa > tongue > labial
mucosa > floor of the mouth >
hard and soft palates > gingiva.
• Lesions confined to gingiva
presenting as DG are rare.
• Hemorrhagic crusting of the
vermilion border of the lips may
occur.
70. Histopathology:
• liquefaction degeneration of
ep.
• intraepithelial microvesicles
• without the acantholysis
(pemphigus).
• hyperplasia, and necrotic
keratinocytes
• Degenerative changes
basement membrane.
• lamina propria is indistinct
because of a dense
inflammatory cell infiltrate &
Edema
71. Immunofluorescence:
NEGATIVE
Treatment:
no specific treatment for erythema multiforme.
For mild symptoms
systemic and local antihistamines
topical anesthetics
debridement of lesions with an oxygenating agent are
adequate.
In patients with bullous or ulcerative lesions and severe
symptoms
corticosteroids are considered the drug of choice,
although their use is controversial and not completely
accepted
72. Drug Eruptions
• Drug allergen:sensitizes the tissues.
• Stomatitis medicamentosa: Eruptions in the oral cavity that
result from sensitivity to drugs that have been taken by mouth
or parenterally.
• Stomatitis venenata / contact stomatitis: The local reaction
from the use of a medicament in the oral cavity (e.g.,
stomatitis as a result of topical penicillin use).
• Manifestations: multiform.
Vesicular and bullous lesions
pigmented / nonpigmented macular lesions
Erosions deep ulceration with purpuric lesions.
seen in different areas of the oral cavity, with the gingiva
often being affected.
73. • Development of gingival lesions caused by contact allergy:
Mercurial compounds in dental amalgam.
Pyrophosphates and flavoring agents like cinnamon in tartar
control toothpastes.
• Intense erythema of the attached gingival tissues Comparitive
of plasma cell gingivitis.
Management:
• clinical history source of the gingival disturbance.
• Elimination of the offending agent resolution of the gingival
lesions within a week,
• If removal of the offending medication is not possible, topical
corticosteroids and topical tacrolimus can be used to treat the
lesions.
74. Miscellaneous Conditions that
Mimic
Desquamative GingivitisHeterogeneous conditions that may masquerade as
desquamative gingivitis.
Factitious lesions,
candidiasis,
Graft versus- host disease,
Wegener’s granulomatosis,
foreign body gingivitis,
Kindler syndrome,
squamous cell carcinoma
75. Effect of desquamative gingivitis on periodontal status
• From a theoretic point of view, disorders causing DG may have potential
harmful outcomes on the development and progression of plaque-
related periodontal disease.
• These potential injuries may be related to both direct and indirect
relationships.
Indirect effect: symptomps associated with DG prevent proper
oral hygiene plaque periodontal disease.
Direct effect: may also be plausible based on the possible shared
pathogenetic mechanisms ⁄ mediators.
• Ramon-Fluixa et al, 1999: observed that no significant differences
were present between an OLP group of patients and a control group
with regard to different periodontal indices.
• Akman et al, 2008: periodontal status is worse in patients affected by
pemphigus vulgaris (PV).
L Lo Russo et al. Effect of desquamative gingivitis on periodontal status: a pilot study.
Oral Diseases (2010) 16, 102–107.
76. Diagnosis of Desquamative Gingivitis:
A Systematic Approach
• Desquamative gingivitis is only a clinical term and not a
diagnosis per se.
• The following discussion represents a systematic approach to
elucidate the disease that is triggering desquamative
gingivitis:
Clinical History
Clinical Examination
Biopsy microscopic examination
immunofluoroscence
Management
77. Clinical History
Complete data regarding symptoms associated with the condition
as well as historical aspect.
• When did it start (acute or chronic)?
• Aggrevating & alleviating fators?
• Are the lesions recurrent? If yes, how often do they recur?
• How long does it take for each lesion to heal?
• Extraoral involvement?
• has patient had fever, malaise, lymphadenopathy? (positive
response may indicate an infections agent)
• are there are any other systemic problems?
• Medications being used?
• Family history
78. Clinical Examination
• Recognition of pattern of disease: focal/multifocal
• If only gingiva involved other areas also.
Nikoliskys sign –slight rubbing of the skin results in exfoliation of
the outermost layer, forming a blister within minutes.
+ Pemphigus, MMP
- lichen planus, BP
Asboe-Hansen sign: extension of a blister to adjacent unblistered
skin when pressure is put on the top of the bulla.
Kobners phenomenon: appearance of lesion along the line of
trauma/injury.
LP, SLE, Psoriasis
Auspitz sign: Psoriasis
79. Biopsy
• Incisional biopsy is best to begin microscopic and
immunological evaluation.
• A perilesional biopsy should avoid areas of ulcerations
because necrosis and epithelial denudation hamper diagnostic
process.
• Mostly perilesional tissues also show immunoflourescence.
• In some lesions such as lichen planus, subacute lupus
erythematosus only lesion tissue can be used.
80. H&E staining and light microscopic
Immunoflourescence
For direct Immunoflourescence :
Unfixed frozen sections are incubated with a variety of
flourescein labelled anti - human serum (antiIgG, antiIgA,
anti IgM, anti- fibrin, anti- c3 etc.,)
Indirect Immunoflourescence :
Unfixed frozen section from oral or esophageal animal
mucosa are first incubated with the patients serum to allow
attachment of any serum antibodies to mucosa
MICROSCOPIC EXAMINATION
81. After the diagnosis is established, the dentist must choose
the optimum management for the patient.
This is accomplished in accordance with three factors:
(1) the practitioner’s experience;
(2) the systemic impact of the disease;
(3) the systemic complications of the medications.
Overview Of Management
Elimination of
potential factors
Suppressing the
inflammatory
reaction
Using specific
therapies for the
underlying diseases
Management of lesions by:
82. Drug therapy has included
corticosteroids
Antibiotics
Immunosuppresive agents
Intravenous Immunoglobulis
Hormonal therapy
Vitamins
83. Corticosteroids:
Impair immunological competence.
Suppress hypersensitisation and allergic phenomena
Suppress recruitment of leucocytes at sites of contact with Ag.
Regulation of protein synthesis
Transcription of specific mRna
binding to specific sites on the chromatin
Migration into the nucleus
Structural changes in steroid receptor complex
Binds to a high affinity cytoplasmic receptor protein
Corticosteroid penetrates cells
MOA at cellular level
84. Topical Corticosteroids :
Triamcinolone, Fluocinonide ,Clobetasol gel Beclomethasone
dipropionate spray (inhaler) Hydrocortisone hemi succinate
Topical creams or pastes in suitable customized tray or veneer
(Carozzo et al;Northwood:Sci reviews 1996)
Systemic corticosteroids
Prednisone 10-40 mg.
Long-term complications (steroid)
Osteoporosis, impaired wound healing
Premature cataract formation
Behavioral changes
Chemically-induced diabetes mellitus, HTN
Infections
Myopathy and muscle wasting, weight gain
Gastric ulceration and bleeding.
Suppression of HPA axis adrenal crisis impaired stress
response
85. Immunosuppressive agents :
Cyclosporine, Griseofulvin, Azathioprine , Methotrexate,
Cyclophosphamide (Lever WF.et al . Am J Dermatopathol 1979;
GorlinRJ et al . Gerodontics 1985)
Drug Combinations
Prednisone + Azathioprine or cyclophosphamide.
Additional immunoregulatory benefit & Steroid-sparing properties
Tetracycline
Anticollagenase effects
Inhibit PMN chemotaxis and random PMN migration.
Inhibit complement-induced inflammatory responses to BM antigen-
antibody complexes
Help maintain the cohesion of the epithelial connective tissue junction.
Systemic doxycycline improves Dg in LP (Ronbeck Oral surg Oral Med
Oral Path oral radiol Endodontic 1990)
86. Intravenous Immunoglobulins:
• Proved successful and safe in steroid-resistant PV. (Mobini et al., 1995;
Bewley and Keefe, 1996; Bystryn and Steinman, 1996; Sibaud et al., 2000)
Hormonal therapy:
• Ziskin, 1937: established the ability of estrogen to stimulate connective
tissue & to produce hyperkeratinization and hyperplasia of the oral
epithelium.
• He also showed that testosterone propionate produces a stimulating
action on epithelium and connective tissue with a resultant benefit to the
gums.
• Yih et al: do not support the use of estrogen in the treatment of
idiopathic CDG, might be because the ER expression in the gingiva is
probably not related to the presence or absence of estrogen as well as the
side effects of estrogen.
Other Drugs:
• Gold (Penneys et al., 1976; Salomon and Saurat, 1986),
• Etretinate (Orfanos and Bauer, 1983),
• prostaglandin E2 (Morita et al., 1995),
87. Plasmapheresis:
Selective removal of large volumes of plasma which includes
antibodies.
used for tx of bullous pemphigoid, epidermolysis bullosa
acquisita, lupus erythematosus, and pemphigus.
Photopheresis:
Extracorporeal photopheresis involves the exposure of the
patient's mononuclear cells to 8-methoxypsoralen and ultraviolet
A light to induce apoptosis of the T-cells.
88. Other tx:
- proteinase inhibitors (Dobrev et al., 1996),
-chimeric molecules for specific recognition and elimination of
the autoimmune B-cells (Proby et al., 2000),
-suggestions for targeting Dsg 3-specific T-cells for the
eventual modulation of the T-cell-dependent production of
pathogenic autoantibodies (Hertl and Riechers, 1999),
-suggestions for a novel avenue for the development of a
steroidal treatment for using the anti-acantholytic activity
cholinergic agonists (Grando, 2000)
89. Control of dental plaque and local irritants (Damoulis PD et al J
Periodontol 2000).
Oral hygiene maintainance using soft brush with gentle brushing,
use of floss or waterpik, & antiseptic mouth rinses.
Caustic mouthwashes avoided.
Dietary changes with avoidance of spicy food.
Emphasis on oral hygiene, along with frequent SRP
Multidisciplinary consultation
Periodontal therapy :
during periods of remission or if condition is not vesicular.
Doubling of systemic steroid therapy to avoid adrenal shock
during stressful periodontal treatment.
Prophylactic antibiotics must be prescribed.
Antifungals to prevent candidiasis
Periodontal Management
90. TREATMENT OF DESQUAMATIVE
GINGIVITIS WITH FREE GINGIVAL
GRAFT
97
Comparison of surgical side(rt)
with medication therapy side (lt)
Recurrence of desquamation
After 9 months
Mehdi Vatankhah et al. Treatment of Desquamative Gingivitis with Free
Gingival Graft: A Case Report. Dent Res Dent Clin Dent Prospect 2010; 4(1):33-36
91. Treatment of DG with tissue engineered
human cultured gingival epithelial sheets.
Okuda K1, Momose M, Murata M, Saito Y, lnoie M, Shinohara C, Wolff LF, Yoshie H. Treatment of chronic
desquamative gingivitis using tissue-engineered human cultured gingival epithelial sheets: a case
report. Int J Periodontics Restorative Dent. 2004 Apr;24(2):119-25.
92. Yilmaz HG, Kusakci-Seker B, Bayindir H, Tözüm TF. Low-Level Laser Therapy in the Treatment of Mucous
Membrane Pemphigoid: A Promising Procedure. J Periodontol. 2010 Aug;81(8):1226-30.
Treatment of DG with
LLLT• A patient presented with MMP was successfully treated with the application
of local corticosteroids and LLLT using an 810-nm diode laser.
• The lesions were treated by LLLT over a period of 7 days using a
continuous waveform for 40 seconds and an energy density of 5 J/cm2.
Clinical condition at 12
months after LLLT.
Clinical condition at 1 week after
at the first visit
LLLT may improve healing after the application of a local corticosteroid for a period of 12
months.
93. CONCLUSIO
N
In patients with suspicious desquamative lesions of the gingiva,
it is imperative to establish a definitive diagnosis via
histopathologic and immunologic findings.
The goal of treatment should focus on eradication of the lesions
prior to any periodontal therapy, following a conservative
approach.
These diseases may not be limited to the oral cavity, and it is
crucial that appropriate consultations are made to ensure
optimal patient care. The Periodontist has a unique opportunity
to make the diagnosis and then refer the patient to a medical
specialist for treatment.
Thus a thorough understanding of these conditions is necessary
so as to provide complete care to our patients .
100
94. REFEREN
CES
101
• Newman Takei, Klokkevold Carranza. Desquamative Gingivitis.
Carranza’s Clinical Periodontology. 12th ed.
• Oles, R.D. Chronic desquamative gingivitis. J Periodont 38:485
Nov-Dec 1967.
• R. J. Nisengardt and R. S. Rogers. The Treatment of Desquamative
Gingival Lesions. J Periodontol. 1987 Mar;58(3):167-72
• NA Robinson,D Wray. Desquamative gingivitis: A sign of
mucocutaneous disorders – a review. Australian Dental Journal
2003;48:4.
• Gizem KARAGÖZ, Kıvanç BEKTAŞ-KAYHAN, Meral ÜNÜR.
DESQUAMATIVE GINGIVITIS: A REVIEW. Istanbul Univ Fac Dent
2016;50(2):54-60.
95. • Garrod et al. Desmosome structure, composition and function.
Biochimica et Biophysica Acta 1778 (2008) 572–587.
• KV Arun. Molecular biology of periodontium. 1st Ed. 2010.
• Mihai et al. Immunopathology and molecular diagnosis of
autoimmune bullous diseases. J. Cell. Mol. Med. Vol 11, No. 3, 2007
pp. 462-481
• S. Sangeetha et al. The molecular aspects of oral mucocutaneous
diseases: A review. International Journal of Genetics and Molecular
Biology Vol. 3(10), pp. 141-148, November 2011
• Floris van Minden. Use of female sex hormone in the treatment of
chronic desquamative gingivitis. J Am Dent Assoc. 1946 Oct;33:1294-7
• Yih WY, Richardson L, Kratochvil FJ, Avera SP, Zieper MB. Expression of
estrogen receptors in desquamative gingivitis. J Periodontol. 2000
Mar;71(3):482-7.
96. • L Lo Russo et al. Effect of desquamative gingivitis on periodontal
status: a pilot study. Oral Diseases (2010) 16, 102–107.
• Mehdi Vatankhah et al. Treatment of Desquamative Gingivitis with Free
Gingival Graft: A Case Report. Dent Res Dent Clin Dent Prospect 2010;
4(1):33-36.
• Okuda K, Momose M, Murata M, Saito Y, lnoie M, Shinohara C, Wolff
LF, Yoshie H. Treatment of chronic desquamative gingivitis using
tissue-engineered human cultured gingival epithelial sheets: a case
report. Int J Periodontics Restorative Dent. 2004 Apr;24(2):119-25.
• Yilmaz HG, Kusakci-Seker B, Bayindir H, Tözüm TF. Low-Level Laser
Therapy in the Treatment of Mucous Membrane Pemphigoid: A
Promising Procedure. J Periodontol. 2010 Aug;81(8):1226-30.
99. Management of patients who are on long term steroid
therapy?
• Administration of prophylactic steroids in pts on steroid therapy is a common
practice.
• However, Shapiro et al, found that pt.s using 5-20mg/day steroids maintain
some adrenal reserves after immediate termination of steroids.
• Higher dosesuppress adrenal glands when used for more than 2-3
weeks, but its ability to respond to stress may return quickly after
termination of steroid therapy.
• Hopkins et al: recovery of HPA axis following exposure to exogenous GCs
requires 6-12 months.
• For pt. who are currently on steroid therapy:
no supplements needed, if their usual dose is taken within 2 hr prior to
surgery.
• Supplements are needed:
For pts undergoing lengthy, major surgical procedure,
Expected to have significant blood loss
Who have extremely low adrenal function
For these individuals, physician consultation and steroid supplementation
is indicated.
Periodontal Tx of medically compromised patients.
Editor's Notes
Gingivosis, as described by Schour and Massler, was apparently a gingival manifestation of chronic and acute nutritional deficiency in children.
Most of cases of dg are seen in association with MMP, followed by olp pv & le
According to different case series, MMP is responsible for ;35% to 48% of cases of DG. OLP and
PV account for 24% to 45% and 3% to 15%19,23 of
cases, respectively
Before going into the etiopthogenesis im going to discuss briefly about the epithelial biology which is relevant to the disease.
A basic knowledge about the epithelial biology is necessary in order to understand the pathogenesis of dg.
Among theses des, hemids and their structural proteins ply an important role in the pathogenesis of dg
Desmosomes contains proteins like desmogleins and desmocollins. Desmogleins are glycoproteins of the cadherin-supergene family which
link to cytokeratins via desmoplakins and plakoglobin. Cadherins are a family of calcium-dependent cell to cell
adhesion molecules that play important role in the formation and maintenance of complex tissue integrity.
They are composed of an extracellular domain involved in calcium dependent binding to adjacent cells, a
transmembrane and an intracellular domain that binds to catenins and thence to actin (Masayuki, 2010). There are
four desmoglein isoforms, designated as Dsg1–4. Expression of desmoglein 1 and 3 is restricted to
stratified squamous epithelia. Dsg 1 and 3 are both expressed in skin but in oral epithelium only the 130 KDA
molecule Dsg 3 is preferentially expressed. The intraepithelial expression patterns of Dsg 1 and 3 in skin and
mucous membranes differ. In the skin, Dsg 1 is expressed throughout the epidermis, but more intensely in
the superficial layers, while Dsg 3 is expressed in the lower portion of the epidermis, primarily in the basal and
parabasal layers.
The autoab formed against these ag will bind to them either intercellulary or at th ep.-ct interface resulting in the formation of Ag-ab complexes
Activates complement, attracts immune cells etc.. Finally cause acantholysis/dissolution of ep-basal lamina junc. Leading to an inra or sub ep clefts
Glickman and Smulow have described three forms of desquamative gingivitis viz mild, moderate, and severe.
Pathogenesis:
Current data suggest that OLP is a T cell-mediated
autoimmune disease in which auto-cytotoxic CD8+
T cells trigger apoptosis of oral epithelial cells.
However, the precise cause of OLP is unknown.
The two major antigenic determinants of bullous pemphigoid are:
230-kD protein plaque known as BP1
180-Kd collagen-like transmembrane protein BP2.
epidermal and mucous membrane blisters occur when the
cell-to-cell adhesion structures are damaged by the action of circulating
autoantibodies and by the in vivo binding of these autoantibodies
to the pemphigus vulgaris antigens, which are cell-surface
glycoproteins that are present in keratinocytes.
(Fine JD. Et al N Engl J Med 1995.Korman NJ. Et al Dermatol Clin 1990 Eversole LR. Et al Oral Surg Oral Med Oral Pathol 1994 Calvanico NJ et al J Autoimmun 1991)
60% of patients with pemphigus vulgaris, the
oral lesions are the first sign of the disease
Combination of Sulfones and Dapsone.
Small amounts of Prednisone (10-30mg/day) can be
added.
Alternatively, tetracycline (2g/day) combined with
nicotinamide (1-5g/day) have shown promising results.
An increase in the incidence of skin and oral manifestations of hypersensitivity to drugs has been noted since the advent of sulfonamides, barbiturates, and various antibiotics
A thorough clinical history is mandatory to begin the assessment of desquamative gingivitis.
Data regarding the symptomatology associated with this condition as well as its historical aspects (i.e., when the lesion started, whether it has worsened, if there is a habit that exacerbates the condition) provide the foundation for a thorough examination.
Information regarding previous therapy to alleviate the condition should also be documented.
HPA axis suppression resulting in reduced cortisol response may cause an impaired stress response and an inadequate host defence against infections, which remains a cause of morbidity and death.
a 25 yr old female pt diagnosed with erosive lp presenting dg was tx with fgg and corticosteroids
Although recurrence of the lesions was observed following both treatment modalities, free gingival graft despite being an aggressive therapy, proved more effective and with fewer side effects compared with topical or systemic steroid therapy, and seems to be a promising treatment modality with the benefit of more stable results, among others.
A 60 f with dg Is treated with hcges
Cells are harvested from tissue obtained from retromolar pad
Degree of suppression is dependent on drugs used, dose, duration of administration, time elapsed since steroid therapy was terminated & route of admins.