Perio exam sumary

BOP >10% is an early sign of inflammation, suggesting inflammatory lesions of the epithelium and connective tissue, but is not a good predictor of attachment loss.

Remove the allergen.

Estrogens stimulate collagen metabolism, promote angiogenesis, and decrease keratinization of gingival epithelium.

Progesterone increases vascularity, permeability, and the oedematous inflammatory response of the gingiva.

Anti-virals and nutrition support.

Part of masticatory mucosa; in health: coral pink, firm, scalloped outline; FGM sits coronal to CEJ; from free gingival margin to mucogingival line; col fills interdental space; types: free or attached.

Contraceptives can lead to increased gingival inflammation and exudate.

An autoimmune condition that can be systemic, chronic, or subacute, affecting the kidney, heart, mucosa, and skin, with oral mucosa ulceration and malar rash.

Subgingival margins are more irritating to periodontal tissues and are more plaque-retentive, increasing the risk of periodontal disease.

1. Construction: Channels create a primitive circulatory system, organisms organized by function. 2) Teamwork: Maintain homeostasis, exchange nutrition, inner organisms provide nutrition, outer organisms offer protection. 3) Communication: Quorum sensing and gene exchange increase pathogenicity and resistance.

Consistency: edematous + fibrotic; Texture: ulcerated JE, rete pegs, smooth + shiny in chronic inflammation; Colour: red, red/blue, pale, grey, metallic pigmentation; Recession: can occur due to trauma or repeated pathological inflammation; Contour: Stillman's clefts, McCall festoons, enlargement.

Smoking alters PMN chemotaxis, phagocytosis, and oxidative burst, increases the extent and severity of periodontal destruction, and decreases antibodies (IgG and IgA).

Treatment involves drainage and irrigation, antibiotics if systemic signs are present, and possibly removal of tissue or tooth.

1. Inflammatory (gingivitis); 2) Drug induced; 3) Associated with systemic conditions; 4) Neoplastic; 5) Idiopathic.

Absence of BOP is a good negative predictor of attachment loss.

Blister formation/peeling when pressure is applied.

Risk factors include smoking, plaque, socioeconomic status (SES), genetics, and overall inflammatory burden.

Presence of inflammation (bleeding).

Discomfort, itching, stinging, erosion, ulceration, vesicles.

Keratinised stratified squamous epithelium consisting of a basal layer, spinosum or prickle cell layer, granular layer, and keratinised layer.

A bullous and macular mucocutaneous disease primarily affecting young adults, characterized by target lesions and hemorrhagic crusting of the vermilion border.

Endogenous factors like iron, bilirubin, melanin; Addison's disease leads to pigmented (melanin); Iron can cause blue/grey discoloration.

Treatment includes drainage by incision, scaling, analgesics, and warm saline rinses, with no antibiotics unless systemic signs are present.

Hormonal variations during puberty can increase gingival inflammation, leading to papillary and interdental bleeding, and a higher prevalence of P. intermedia.

PDL has less fibroblasts; Cementum deposition; Dense CT.

Dysphagia, fever, malaise, submandibular adenopathy, oral erosion ulcers.

Information includes presenting complaint, social history (smoking, work/stress, recreational drugs), past dental history, oral hygiene habits, examination findings, periodontal analysis (plaque, BOP, PD, local retentive factors), diagnosis, and prognosis.

1. Inflammatory lesion that extends apically + laterally; 2) Resorption of alveolar bone; 3) Apical migration of the junctional epithelium.

Overhangs retain plaque and prevent effective cleaning, leading to inflammation and periodontal disease.

Cementum is a specialized mineralized tissue covering the root, characterized by a connective tissue-epithelium interface, hemidesmosomes, and two layers: lamina lucida (most superficial) and lamina densa (underlying). It contains collagen (60%), vessels and nerves (35%), and fibroblasts (5%).

Phagocytosis, acting as antigen-presenting cells (APC), and producing immune mediators. They are recruited to the area and activated by binding to LPS, phagocytosing dying cells, modulating inflammation, and secreting inflammatory mediators.

It has two layers: basal and suprabasal, is triangular in shape with the base towards the coronal, and attaches the gingiva to the tooth.

The principal fibers in the PDL include Sharpey's fibers, which consist of groups such as alveolar crest, apical, horizontal, and oblique fibers, with ends embedded in the alveolar bone and cementum.

Orthodontic factors include crowding, malalignment, and the presence of brackets and wires that limit the ability to clean and retain plaque.

Complications include adverse pregnancy outcomes, increased risk of pre-term birth, transient bacteraemia that may reach placental tissue, and increased risk of fetal death.

The primary cause is plaque.

During menstruation, there is an increase in gingivitis, changes in progesterone levels, increased GCF exudate, inflammation, and tooth mobility.

1. Direct: Release of H2S, NH3, fatty acids, indole (virulence factors), LPS, fimbriae, proteases, leukotoxins. 2) Indirect: Induction of host response via prostaglandins (PGE2), cytokines (IL-1, TNF-a), and MMPs.

Treatment includes systemic corticosteroids.

Increased progesterone levels lead to increased capillary permeability, more exudate, stimulation of prostaglandin synthesis, and decreased keratinization of the epithelium.

The epithelium in contact with the tooth, developing as ameloblasts become reduced in height to form reduced enamel epithelium, which is replaced by junctional epithelium.

They bind to fibroblasts and stimulate further production of inflammatory mediators.

Dentogingival fibers are connective tissue fibers located between the junction of the tooth and gingiva, including types such as dentogingival, alveolo-gingival, interpapillary, transgingival, circular, dentoperiosteal, trans-septal, periostogingival, intercircular, and intergingival.

Red color due to increased number and size of blood vessels, decreased thickness and keratinization of epithelium, margin at or below CEJ, and BOP >10%.

Fibrotic gingiva is characterized by rolled margins.

Modifying factors can alter microbiota, susceptibility, and clinical presentation of periodontal disease.

Reticular, atrophic, erosive, and bullous types.

Main risk factors include diabetes, smoking, medications, hormones, HIV, stress, and autoimmune conditions.

Main cell in the EARLY stages (PMNs); Kill bacteria intracellularly via phagocytosis and extracellularly via release of destructive enzymes & free radicals.

Transformed into plasma cells; Produce specific antibodies; In presence of complement, they cause enhanced PMN bacterial killing.

Smoking leads to increased severity of pocket depths, attachment loss, increased plaque and calculus, and a higher risk of tooth loss and furcation involvement.

Causes include HSV, Mycoplasma, and drug reactions.

Melanocytes (pigment synthesising), Langerhans (defense cells), Merkel’s (sensory), and inflammatory cells (defense).

The periodontium is reduced for reasons not related to periodontitis, with BOP >10%.

Conditions include Lichen Planus, Cicatrial Pemphegoid, Lupus, Pemphigus vulgaris.

1. Gradual attachment loss: Slow, continuous, progressive. 2) Rapid attachment loss: Random burst, asynchronous.

Absence of inflammation.

Masticatory mucosa, Specialized mucosa, Lining mucosa.

A pregnancy granuloma is a pedunculated fibrogranulomatous lesion due to estradiol, affecting anterior papillae and maxillary teeth.

1. Ask about tobacco use; 2) Advise smokers to quit; 3) Assess readiness to quit; 4) Assist in quitting, set a date (using nicotine replacement therapy, varenicline, or bupropion); 5) Arrange follow-up visits or referral.

1. Pristine gingiva 2) Initial lesion (clinically healthy) 3) Early lesion (early gingivitis) 4) Established lesion (established gingivitis) 5) Advanced lesion (periodontitis).

1. Microbial challenge: Antigens + LPS trigger host response. 2) Host immune-inflammatory response: Production of antibodies and PMNs, releasing cytokines, prostaglandins, and MMPs. 3) Bone & tissue metabolism: Tissue degradation in response to inflammatory mediators. 4) Signs of disease.

Histological findings include ulceration, epithelial atrophy, and perivascular inflammation.

Lines the gingival sulcus, is multi-layered, parakeratinised, has rete pegs, and provides defense against microorganisms.

Factors include open interproximal contacts, uneven marginal ridges, cervical enamel projections, and bifurcation ridges.

Absence of BOP, absence of erythema and oedema, absence of symptoms (pain), absence of attachment loss, and crestal bone 1-1.5mm from CEJ.

Increase in size of the gingiva via hypertrophy, hyperplasia or fibrosis (defective cell proliferation, impaired immune response).

Mouth-urticarial reaction, Angioedema, Erythema multiforme, Contact allergy, Burning, itching, stinging.

Distributes & resorbs masticatory forces; Lamina dura – compact bone surrounding the PDL; Volkman’s canals – communication between Haversian canals; Osteon – unit of bone containing concentric lamellae, surrounding Haversian canal, osteocytes in lacunae, and canaliculi between the lacunae.

HSV-1.

Occurs within 2-4 days, triggered by inflammation. Bacterial products/toxins cross JE, stimulating epithelium + CT to produce inflammatory mediators. Blood vessels dilate and become more permeable, allowing defence cells to travel towards chemotactic stimuli.

An autoimmune bullous disorder characterized by mucous membrane blisters and potential fatality due to damage to cell-cell adhesion.

Free gingiva is coral pink, firm with a rounded margin and extends to the free gingival groove; attached gingiva extends from the free gingival groove to the mucogingival junction and is more parakeratinised.

In smoking patients, gingivitis shows less inflammation and fewer clinical signs of inflammation such as bleeding on probing (BOP) and edema.

The types of fibers in the PDL include oxytalan, collagen, reticulin, and elastin.

Smoking increases levels of bacteria, introduces more bacterial species, especially at incisor regions, and increases colonization of shallow pockets.

Health: Coral pink; Gingivitis: Red; Contour: Scalloped + knife edge in health, rolled with bullous papillae in gingivitis; Texture: Stippling + firm in health, oedematous + no stippling in gingivitis; Margin: Above CEJ in health, below CEJ in gingivitis.

Grade 1 – no enlargement; Grade 2 – enlargement confined to interdental papilla; Grade 3 – enlargement of papilla + margin; Grade 4 – covers ¾ crown.

Intense erythema, desquamation, ulceration of free + attached gingiva, with mild burning intense pain.

Smoker: >100 cigarettes and currently smoke; Non-smoker: <100 cigarettes; Former smoker: >100 cigarettes and don’t smoke for at least 5 years.

Healthy gingiva → Early gingivitis → Established gingivitis (stable vs unstable).

Protective factors include genetics and the innate immune response.

The main changes included the classification for gingival health, the removal of aggressive periodontitis, and the addition of periodontal abscesses and endo-perio lesions.

Main cytokines include PGE2, TNF-a, IL-1. They inhibit osteoblasts, stimulate osteoclasts for bone resorption, increase production of MMPs, and disrupt the balance of the connective tissue matrix.

No treatment or topical antivirals.

Changes associated with the presence of micro-organisms, release of collagenase, protease, sulphatise, hyaluronidase, endotoxins, potential damage to epithelium + CT, activation of monocytes/macrophages, and release of vasoactive substances.

Glycosaminoglycans incorporate water and electrolytes, regulating fluid diffusion and flow within the periodontal ligament.

An abscess occurring in healthy gingiva or gingivitis patients without attachment loss, always associated with a foreign body impacted in the gingiva.

An abscess that occurs in pericoronal tissue, often associated with partially erupted third molars and trismus.

Smokers show decreased response to non-surgical treatment, less reduction in pocket depth, and less gain in clinical attachment level. Surgical outcomes also show less reduction in pocket depth and an increased risk of peri-implantitis/failure.

Alveolar bone, Alveolar bone proper, PDL, Junctional Epithelium, Gingiva, Root cementum.

1. Infiltration of connective tissue by large amounts of defence cells; 2) Destruction of normal anatomy; 3) No apical migration of JE (only in periodontium).

Enamel pearls, especially at furcations, make debridement harder and are prone to plaque accumulation.

Attachment loss, apical migration of JE, loss of collagen + CT.

Dilation + engorgement of capillaries, thinning sulcular epithelium more prone to BV rupture, affected by medications, pregnancy, haemorrhagic disorders.

The defense cells in the PDL include mast cells, lymphocytes, macrophages, plasma cells, and neutrophils.

Physiological changes include peripheral vasoconstriction and decreased subgingival temperature.

Restorative factors include overhangs, subgingival margins, and poorly contoured restorations that retain plaque and prevent effective cleaning.

A risk factor changes susceptibility to periodontal disease, while a pre-disposing factor increases the probability of disease occurrence, usually locally.

Dysbiosis is the disruption to the normal microbiome that disrupts the symbiotic relationships between host and organisms.

PSR stands for Periodontal Screening and Recording. The codes are: 0 - no BOP; 1 - BOP no pocket; 2 - BOP + calculus + overhang; 3 - Pocket 4-5mm; 4 - Pocket >6mm.

Cemental tears are fractured cementum that can lead to plaque accumulation and pocketing, worsening periodontal health.

The PDL is a soft, rich vascular and cellular connective tissue that surrounds the roots of teeth, joining alveolar bone to cementum. Its functions include force distribution and mobility.

The blood supply to the PDL comes from superperiosteal vessels, PDL vessels, and alveolar bone vessels. The supply to teeth includes the superior/inferior alveolar artery, dental artery, intraseptal artery, and rami perforantis. The supply to gingiva includes sublingual, mental, buccal, facial, greater palatine, infraorbital, and posterior superior dental arteries.

Mechanisms include vascular system activation, inflammation, immune system activation, and interference with tissue healing.

The main components of connective tissue in the PDL include collagen (60%), vessels and nerves (35%), and fibroblasts (5%). It has two layers: papillary and dense.

Smoking increases blood pressure, heart rate, and respiratory rate, decreases skin temperature via peripheral vasoconstriction, and decreases immunity.

Inflammatory lesions from the interaction between dental plaque and host immune response, contained within the gingiva, and most commonly chronic, slow onset, and painless.

1. Acellular extrinsic – coronal + midroot; 2) Cellular mixed stratified – apical 1/3 + furcation; 3) Cellular intrinsic – in resorption lacunae in apex.

Mechanical, thermal, chemical, and pharmacological injuries.

Root anatomy features like palato-gingival grooves, root trunk length, and concavities can complicate cleaning and increase the risk of periodontal issues.