7- periodontal classification

What did the 1999 Armitage classification lead to?

Difficulties in establishing a clear diagnosis

Put preventative and therapeutic measures into practice

What are the 3 entities for classification of gingivitis and what is it based on?

Periodontal and gingival health

Gingivitis- dental biofilm induced

• Biofilm alone

• Systemic or local risk factors

• Drug influenced gingival enlargement

Gingival diseases- non dental biofilm induced

based on history of periodontal disease, clinical attachment level

What characteristics does biofilm induced gingivitis have? (Biofilm alone)

Confined to gingiva

Plaque main etiological factor

Inflammation changes colour, shape, texture, bleeding on stimulation, elevated sulcular temp

No bone loss, stable clinical attachment

Reversible

What are 6 systemic or local risk factors of gingivitis?

Smoking

Hyperglycemia- diabetes

Nutritional factors

Pharmacological agents

Sex steroid hormones

Haematological conditions

How does smoking cause gingivitis?

Microvascular vasoconstriction and fibrosis masks clinical signs like bleeding despite underlying pathology

How can nutritional factors cause gingivitis and how will the gingiva look?

Ascorbic acid (vitamin c) deficiency can exacerbate gingiva response to plaque

Gingiva looks bulbous, spongy, hemorrhagic, swollen, erythematous gingival lesions

How can pharmacological agents cause gingivitis?

Oral contraceptives cause higher incidence of gingival enlargement, inflammation- but reversible

Other drugs affect salivary flow, endocrine function

How do sex steroid hormones cause gingivitis?

Puberty- increases gingivitis

Menstrual cycle- minor gingivitis during ovulation, exudate increase- reversible

Pregnancy- in 2nd or 3rd trimester, gingivitis, pyogenic granuloma

How do hematological conditions cause gingivitis?

Leukemia associated gingivitis- oral manifestations are acute

Cervical adenopathy

Petechia

Gingival enlargement

Mucous ulcers

What are example of drugs involved in drug induced gingival enlargement, characteristics and treatment?

Anticonvulsant- e.g Dilantin- 50% incidence

Immunosuppressant- cyclosporin- 25-30%

Ca2+ channels blocking agents- hypertensive drugs- nifedipine, verapmil, diltiazem- 15-20%

Higher prevalence in children, onset within 1st 3 months, stippling of gingiva, starts in anterior interproximal then expands

Control etiological factors, do full mouth gingivectomy- may need annually

What are 7 types of gingival diseases- non dental biofilm induced?

Genetic/developmental disorders- hereditary gingival fibromatosis

Specific infections

Inflammatory and immune conditions

Reactive processes

Neoplasms

Endocrine, nutritional and metabolic diseases

Traumatic lesions

Gingival pigmentation

What are the different type of origins for specific infections which cause gingival lesions?

Bacterial- neiserra gonorrhoeae, treponema pallidum, mycobacterium tuberculosis, streptococcal gingivitis

Viral- coxsackie, herpes, varicella zoster, molluscum contagiosum, HPV

Fungal- Candidiasis, histoplasmosis- granulomatous

What is herpes simplex virus type 1 responsible for?

Primary Herpetic gingivostomatitis- primary infection- painful ulcers, edema, stomatitis, high fever, malaise, vesicles rupture causing crusty lips

Need palliative treatment

Recurrent oral herpes- virus reactivates in 20-40%

What are the different types of inflammatory and immune conditions?

Hypersensitivity- conatct allergy of dental materials, toothpaste, mouthwash, foods presentation of type 4 sensitivity

Plasma cell gingivitis- velvet erythematous gingiva, dense infiltrate of plasma cells in lamina propia

Erythema multiforme- produces froth which rupture and leave ulcers, swollen crusty lips

What are the types of neoplasms associated with gingival diseases?

Premalignant- leukoplakia, erythroplakia

Malignant- oscc, leukemia, lymphoma (Hodgkin, non Hodgkin)

What are examples of endocrine/nutritional/metabolism diseases?

Vitamin deficiencies-

Fat soluble vitamins- a, d, e

Water soluble- complex band vitamin c

What are the 3 entities for classifying periodontitis?

Necrotising periodontal diseases

Periodontitis

Periodontitis as a manifestation of systemic disease

What is the difference between necrotising gingivitis and necrotising periodontitis?

NG- pain, ulcers, inflamed, erythema, halitosis, decapitated interdental papilla

Sometimes with fever, cervical lymphadenopathy- indicates severity

Gray white pseudomembranous lesions- fibrin, bacteria, wbc, epithelial cell remains

NP- diff stage of same disease, loss of attachment, necrosis of gingival tissues, pdl, alveolar bone

Common in immunosuppressed and malnourished

What is necrotising stomatitis?

Evolution of NG and NP

Affects beyond mucogingival junction- tongue, Buccal mucosa or palate

Erosions, ulcers, necrosis of bone

How can systemic diseases that affect the periodontum be grouped?

Genetic disorders affecting immune response or ct

Metabolic and endocrine disorders

Inflammatory conditions

How is periodontitis divided into stages and grades?

Stage 1- initial

2- moderate

3- severe with potential for tooth loss

4- severe with potential for loss of dentition

Extent and distribution- localised, generalised, molar incisor distribution

Grade A- slow progression- lots of plaque proportionally to bone loss

B- moderate- plaque amount proportional to bone loss

C- rapid- little plaque proportionally to bone loss

What is a periodontal abscess and how can it arise?

Localised accumulation of pus within gingival wall of periodontal pocket

Easily detectable clinical symptoms

Pulp necrosis, periodontal infections, trauma, surgery, foreign body, pericoronitis

What is an endoperiodontal lesion?

Clinical conditions involving both pulp and periodontal tissues

Chronic or acute

Associated with recent traumatic or iatrogenic event

Signs- deep pocket close to apex, negative pulp vitality response

What is an occlusal trauma and the 2 types?

Occlusal forces cause injury- tissue changes in attachment apparatus

Primary- to a tooth with normal periodontal support, no attachment or bone loss, excessive occlusal forces

Secondary- to a tooth with reduced periodontal support