Periodontics, Gingiva and Oral Health

• These notes cover the periodontium in health and disease, periodontal and endodontic infections, basic virology, mycology, dental therapeutics, caries, plaque and gingivitis.

Three Types of Gingiva

• Marginal gingiva is located right above the apical part of the tooth, forming the gingival margin but not directly attached to the underlying bone.
• Attached gingiva is located further towards the lip and away from the teeth, firmly bound to the underlying alveolar bone and cementum, providing support and stability.
• Interdental gingiva is located between two teeth, preventing food impaction and underlying structure damage.

Gingiva Composition

• Gingiva consists of epithelial and connective tissue.
• Epithelial tissue comprises stratified squamous epithelium, acting as a protective barrier against mechanical forces and bacteria.

Three Types of Epithelial Tissue

• Oral epithelium covers the outer surface of the gingiva and is keratinized.
• Sulcular epithelium lines the gingival sulcus and is non-keratinized.
• Junctional epithelium attaches to the tooth surface, forming a seal against bacteria.

Connective Tissue

• Connective tissue includes lamina propria, collagen fibers, fibroblasts, blood vessels, and immune cells.
• Epithelium contains keratinocytes, melanocytes, Langerhans, and Merkel cells.
• Fully developed epithelium takes around 20 days to form.
• Melanocytes, involved in melanin production, are located in the basal and spinosum layers of the gingival epithelium.
• Dendritic and Langerhans cells are phagocytic, antigen-presenting cells located among keratinocytes that fight bacteria.
• Merkel cells have nerve endings for tactile receptors involved with sensory mechanisms of light touch and pressure.
• Connective tissue includes dentogingival, dentocrestal, and crestogingival fibers.
• Attachment fibers of periodontal ligaments can be found in the alveolo gingival, inter-radicular, oblique, and apical attachment areas.
• Collagen helps maintain the structure of gingival tissue; its early destruction leads to changes in tissue morphology.

Gingiva Clinical Characteristics Include

• Contour
• Dimensions
• Color
• Surface texture

Gingival Color

• Keratinized tissues appear paler because thicker epithelial layers reduce the visibility of underlying blood vessels.
• Non-keratinized gingiva appears softer, more delicate, and darker due to increased visibility of blood vessels.
• Vascularization affects gingival color; increased vascularity results in a redder appearance, while lower vascularity results in a lighter pink color.
• Pigmentation, mainly from melanin produced by melanocytes in the gingival epithelium, influences gingival color.
• Epithelial thickness affects gingival appearance; thicker epithelium appears lighter, while thinner epithelium appears darker.

Additional Notes on Gingiva

• Alveolar mucosa is rich in elastic fibers, allowing easy movement.
• Alveolar mucosa has thin epithelium, minimal keratinization, and loose connective tissue with elastic fibers.
• Keratinized mucosa has thick epithelium, keratinization, dense connective tissue, and is collagen-rich.
• Attached gingiva is pink, firm, bound to bone, resilient, and has a rough texture with stippling.
• Teeth with the least amount of keratinized tissue are most prone to recession.
• Incisors and molars have more gingiva than canines and premolars. Zenith positioning, the most apical point of the gingival marginal scallop, serves as a reference for implant, crown, and orthodontic positioning
• Maintaining interdental papilla, the gum tissue that fills the space between teeth, is hard to reconstruct and should be preserved.
• Clinical characteristics of gingiva include vertical and horizontal dimensions.
• Biological width is the measurement of junctional epithelium and connective tissue attachments to the root surface of a tooth; respecting this attachment apparatus is crucial to prevent inflammation.

Periodontal Infection and Inflammation Notes

• Gingiva covers the alveolar process and surrounds the cervical portion of teeth.
• It's vital to prevent the buildup of biofilm, rather than trying to achieve zero bacteria.
• The immune system is the main defense against diseases in the mouth and includes Innate and Adaptive responses

Innate vs Adaptive Response

• Innate response is the first line of defense, present from birth, antigen non-specific, and lacks immunologic memory, including saliva, crevicular fluid, physical barriers (epithelium), and cells like neutrophils and macrophages.
• Adaptive response is antigen-specific, with immunologic memory and involves T lymphocytes, antigen-presenting cells, B lymphocytes, and plasma cells.
• Saliva provides mechanical cleaning, acid buffering, and inhibits bacterial growth.
• Saliva contains lysozymes, hydrolytic enzymes, lactoperoxidase, myeloperoxidase, antiproteases, and secretory IgA to help protect against bacteria.
• Crevicular fluid, an inflammatory exudate from serum, contains cytokines, antibodies, cells, and enzymes, with increased flow during inflammation.
• Epithelium acts as a physical barrier
• Intercellular unions maintain the integrity of the oral epithelium through tight junctions and desmosomes.
• Langerhans cells detect and respond to foreign invaders.
• Peptides (B-defensins) are antimicrobial peptides secreted by epithelial cells, protecting the oral mucosa.
• Periodontal disease results from a combination of a susceptible host, pathogens, reduction of beneficial species, and a favorable environment.
• The amount and types of bacteria change when brushing is neglected.
• Bacteria can be found on pellicle (biofilm) within a few hours, with primary colonization mostly by gram-positive bacteria like streptococcus.
• The number and species of bacteria change dramatically over time; a lot develops in 21 days.

Infectious Diseases and Pathogenesis

• Infectious disease occurs when a pathogenic organism causes signs and symptoms of an inflammatory response or organ dysfunction.
• Pathogenesis phases include initial (increased neutrophils), early, established, and advanced stages.
• Periodontal destruction can be direct (enzymes, endotoxins, cell inhibitors) or indirect (inflammatory/immunologic response).
• Inflammation is the reaction of vascularized tissues to local aggression.
• Acute inflammation has a sudden onset, short duration, and involves leukocyte migration to the injury site.
• An early lesion worsens the initial lesion with increased clavicular fluid and additional loss of gingival collagen.
• Increased vascular permeability occurs in inflammation through histamine and complement serum components C3a and C5a.
• Serum complement proteins involves phagocyte recruitment, pathogen ingestion, and vascular changes.
• Inflammation can be acute, long-standing, or a proliferative response with chronic inflammatory cells.
• Established lesion represents the progression of an early lesion, leading to an increase in plasma cells and additional loss of gingival collagen and connective tissue.

Gingivitis

• Gingivitis is associated with biofilm signs and symptoms.
• Edema
• Erythema
• Bleeding on probing
• Probing attachment level = 0
• Probing depths can be <3mm or >3mm
• Gingivitis treatment involves oral health instructions without calculus and scaling is needed with calculus.
• Periodontal disease is a series of destructive infections affecting multiple sites, leading to the loss of supporting periodontal tissues.
• Advanced lesion occurs when the lesion reaches alveolar bone and the periodontal ligament resulting in Periodontal pocket formation.
• Increase in the number of plasma cells.
• Attachment loss has occurred.
• Treponema denticola is a gram-negative anaerobe with a helical shape, associated with chronic periodontitis and periodontal disease recurrence.
• Porphyromonas gingivalis is a gram-negative anaerobe that produces black pigment, with increased prevalence in periodontal lesions and decreased presence in healthy sites.
• Tannerella forsythia is a gram-negative anaerobe that increases periodontal lesions, pocket depth, and recurrent disease.
• Aggregatibacter actinomycetemcomitans is a gram-negative, facultative anaerobe that increases periodontal lesions, active lesions, and serum antibodies, while decreasing healthy sites.

Oral conditions

• Leukocyte adhesion deficiency is present in periodontitis.
• Subgingival microbiome dysbiosis increases the risk of periodontal breakdown.
• Ecological plaque hypothesis is that a change in key environmental factors triggers a change in the balance of resident microflora and may predispose a site to disease.
• IgM and IgG play roles as part of the body's immune response against pathogens.
• Coupling is the process by which bone-resorbing cells are followed by bone-forming cells during bone remodeling.
• Periodontitis involves inflammatory infiltrate close to alveolar bone w/ bone destruction greater than bone formation and uncoupling in bone remodeling; net bone loss.
• Bone loss can occur rapidly.
• Inflammation can resolve itself.
• Macrophages can be inflammatory or resolving.
• Key to control biofilm and maintain periodontal health.

Endodontic Infections

• Inflammation is the cellular and vascular response to tissue injury.
• Infection is the invasion and proliferation of pathogenic microorganisms.
• Calcified areas appear white on X-rays, while non-calcified areas appear dark; a dark area around the root tip may indicate resorption.
• Inflammation can occur without infection.
• Bacteria, like Pseudoramibacter Treponema, Dialister prevotella, Porphyromonas, and Fusobacterium, can produce proteolytic enzymes, organic acids, and endotoxins, causing inflammation in the pulp and periapical areas.
• Inflammation is caused by wounds, damaged tissue, hypersensitive reactions, and chronic diseases.
• The purpose of inflammation is to release chemical mediators to repair damaged tissue.
• Cardinal manifestations of swelling, color change, pain, heat, and fever, are all signs of inflammation
• Injury leads to the release of chemical mediators and causes several changes inside the body
• Changes in vascular flow
• Structural changes in microvasculature (vascular leakage)
• Migration of PMN’s into site of injury by chemotaxis
• Vasodilation and increased blood flow which are brought about by mediators, like prostaglandins and nitric oxide, that relax the vascular smooth muscle and also lead to changes in vascular permeability
• Venule events result in:
• Blood flow slowdown
• Margination
• Transmigration
• Exudate Increases
• Increase of fighting cells
• Discoloration and pain

Mediators of Pain

• Histamine, serotonin, bradykinin (Kinin cascade), prostaglandins (Arachidonic acid cascade) are pain mediators.
• Histamine, stored in mast cells and basophils, causes pain, endothelial cell contraction, and increased permeability.
• Serotonin sensitizes nerve cells involved in pain.
• The kinin cascade, through factor 12, lowers the threshold of nerves to cause pain.
• NSAIDs block the arachidonic acid cascade, lessening pain and inflammation.
• Main pain-generating mediators include histamine, serotonin, bradykinin, and prostaglandins.
• Cracked teeth, caries, or trauma allow pathogens to enter the dental pulp.

Bacteria in Root canals

• S. mutans, lactobacilli, treponema, prevotella are common bacterias in root canals
• Invasion of pathogens into dental pulp and root canal cause results in the release of mediators which result in tissue necrosis and destruction
• Bacteria is a culprit for destruction of pulp
• Bacterial endotoxin kills macrophage and causes osteoclast activation
• Corticosteroids reduce oral inflammation associated with autoimmune diseases, either topically like Triamcinolone and clobetasol propionate or systematically
• NSAIDs such as Aspirin and Ibuprofen lead to gastrointestinal problems, renal, and hepatic impairment as well as hemorrhage
• Arachidonic acid is metabolized into prostaglandins, leukotrienes, and other arachidonic acid metabolites which lead to alveolar bone loss
• NSAIDs inhibit the formation of prostaglandins by blocking the cyclo-oxygenase pathway of arachidonic acid metabolism

Systemic Conditions

• Systemic administration of medications can help, but are not recommended for the long term due to possible side effects
• Activated osteoclasts use both and digesting enzymes to aid bone ECM production
• Tissue injury can lead to inflammation and can cause swelling and pain
• Infections can result in bacteria entering tooth pulp or tissues, leading to necrosis

Antibiotics And Indications

• Systemic antibiotics are indicated only for the systemic spread of infection
• Fever, malaise, and lymphadenopathy are all signs to use systemic antibiotics
• Penicillin and amoxicillin are first line antibiotics and should be given, especially amoxicillin
• Adult dose is 500 mg three times a day for 3 days until the patient is reviewed
• Amoxicillin: Loading dose of 1.0 gram followed by a maintenance dose of 500 mg/TID for 3 days
• Azithromycin: Loading dose of 1.0 gram on day 1, followed by 500 mg once a day for 2 additional days.
• Clindamycin: Loading dose of 600 mg on day 1, followed by 300 mg four times a day for 3 days.
• Avoid tetracyclines as drug resistance has increased.
• Some antibiotics such as Metronidazole can have synergistic effects if taken in combination with amoxicillin

Systemic Antibiotics

• Systemic antibiotics provide advantages and disadvantages for use in systemic conditions
• Metronidazole is specifically active against anaerobic bacteria is a Systemic Periodontal Antibiotic Therapy
• Antibiotics are not always required for gingivitis and can be treated with plaque removal and antiseptics
• Infective endocarditis is a bacterial infection of the endocardial surface of the heart and requires premedication by some people
• Amoxicillin is generally the antibiotic given at 2g 30-60 min before a procedure

Dental Prescriptions

• It is not appropriate to prescribe schedule 1 and schedule 2 drugs in the dental setting
• A 0.12% solution of chlorhexidine is recommended for rinsing for 30 seconds
• Prescriptions can be dispensed licensed health physicians and nurses
• Inscriptions should include:
• Drug name
• Quantity
• Dosage

Basic Virology Concepts

• Viruses are diverse acellular parasitic pathogens that are obligate intracellular parasites that contain RNA and DNA
• Viruses have different shapes, sizes, genomes, and replication/expression strategies.

Viral Strategies Include

• Attachment
• Uncoating
• Expression
• Replication
• Assembly
• Release
• The size of of the virus is realtively small compared to cells and organelles

Viral structure consists of

• Genome
• Capsid
• Nucleocapsid
• Spikes
• Matrix
• Envelope
• Non-structural proteins
• Regulatory proteins
• Enveloped viruses are more sensitive to heat, drying, detergents, and lipid solvents as is compared to non-enveloped viruses.
• Non-enveloped viruses can survive in environments for a longer time.
• Baltimore classification for viruses – viruses need to converge to make mRNA

Viral life cycle

• Attachment/entry of virus into host requires receptors and coreceptors
• Uncoating releases the viral genome
• Expression produces mRNA and viral proteins
• Replication makes genomes and components
• Assembly makes viral progeny
• Release releases viral progeny
• DNA viruses replicate in the nucleus and RNA viruses replicate in cytoplasm which use RNA polymerase

Virology

• Diversity in RNA virus genome is misincorporation of nucleotides
• Antigenic shift creates influenza viruses with slightly modified antigens to counteract the body's natural processes
• Early immune responses, fever, inflammation and interferons are all the body's defense against viruses
• Cell-mediated immunity directed first and then antibodies activated later.
• Nucleic sensing pathways, immune evasion, viral subversion of cytokine signalling lead to immune evasion
• Outcomes from virus-cell interactions consist of : -abortive infection
  • productive infection
  • Latency
  • Transformation
• Viruses are isolated through filters and grown in animals, eggs and cell cultures
• Viral detection involves assays and effects
  • hemagglutination assay detects red blood cells in detection
  • Cytopathic effect are observations by induced changes of cells
  • Immunofluorescence antibodies are used to detect

Treatments

• Tests

  • ELISA detects viral antigens
  • PCR amplifies DNA/RNA to diagnose

• Vaccines

  • Live Attenuated
  • Inactivated
  • Subunit
  • mRNA
  • Vector-based

• Antiretroviral therapy blocks

  • Fusion -Reverse transcriptase -Integrase
  • Protease

Neuro

• Neurotropic viruses include

  • Blood-brain
  • Blood-Meningeal
  • Blood-cerebrospinal

• Viral encephalitis/meningitis mostly affect newborns/young children; elderly, immunocompromised

• Common conditions

  • Encephalitis
  • Meningitis

• Arbovirus, Enterovirus and HSV are common causes

  • Non-polio enteroviruses, Herpes simplex virus and Poliovirus are all subtypes

• Viral is diagnosed through spinal fluid

• Hematogenous and Axonal transport are entry methods

Prions

• Prions - proteinaceous infectious agent
• Prion diseases - change in shape of cellular protein and they are long lasting, short and resistant
• Prions are broken up by Spontaneous, Genetic and Acquired
  • vCJD and iCJD are two types, with vCJD decreasing from cattle -vCJD and iCJD types are more commin in different ares
• Prions are caused by a mutant protein
• Prions are resistant to activation, and requires unique methods to inactive
• Prions don't cause inflammatory responses or antibody production genetic testing cannot be spontaneous cases

Phamracology (Antiviral)

• Attachment drugs attach to nucleic acid synthesize
  • Oseltamivir, Peramivir and Zanamivir
  • Baloxavir - GI upset
• Acyclovir/Valacyclovir topical is Inhibitors of DNA polymerase -Ganciclovir/Valganciclovir inhibits DNA polymerase

Mycology

• Fungi are non plant like eukaryotes that are found to be saprobes- organisms that feed on dead or decaying organic matter o Mycoses, which caused more systemic issues

• There aree two types:

  • Molds: large mass
  • Yeast: single cell

• Yeast versus Bacterial Colonies - Reproduce only asexually by budding

• Dimorphism- the conditions which they are located dictate type

• Candida albicans- is yeast at room temperature but pseudohyphae at warm

Reproduction

• Hyphae- the subunits or the structural element of fungi(secrete enzymes for external digestion) -Septate- subunit is distinct -Non-septate- one unit -Pseudohyphae- not rigid walls and budding constrictions Asexual Reproduction- -Sporangiospores- released spore -Conidiophores- bud off and have no supportive vessel -Arthrospores- Fragmentation -Chlamydospores- within the hyphae with thick walls

Reproduction

• Sexual Reproduction-
• Zygomycota- the opposite types fuse
• Ascomycota- fuse and Nuclei moves to a zygote

Yeast

• Yeast vs Bacterial Colonies -Reproduce only asexually by budding

Sources of Infection

    -Geophilic- soil
    -Zoophilic- animals
    -Anthropophilic- humans

Immunity

     -Phagocyte immunity vs Humoral Immunity

Diagnosis

     -Histological Stain
        - Macroscopic features
         -Morphological color

Medication

    -Allyamines (Inhibit ergosterol synthesis; Terbinafine) 
    -Azole Drugs(Imidazoles) 
    -Polyenes (Nystatin/Amphotericin B)
    -Cell Division Inhibitors(Griseoflavin)

Types of Mycosis II

    -Superficial- Keratinized layer: outermost layer
    -Mucocutaneous- mucous membrane gl/urogenital
    -Subcutaneous- Traumatic entry(granulomas like mass)
    -Systemic- Histoplasmosis or blastomycosis
    -Opportunistic

Trichophyton- T stands for three so its the hair, nails plus skin - Hair versus Microsporum

Skin infections

    - Invasions come from dermophytes and attack karatined surfaces, with an inflammatory response

Tinea Infections-

    -Corporis-smooth and bare
    -Tinea Cruris- hot groin

Tinea Conditions

     - Tinea pedis(Athlete's foot)- skin on toes starts to separate
    -Tinea Captis- hair shaft penetration
    -Tinea Versicolor (Pityriasis)  furful on epidermis

Mycosis (subcutaneous)

Sporotrichosis (Rose Gardener’s Disease)-

• Infects people involved in plants

Opportunistic Mycoses

    -Pulmonary(inhale) or zoonotic(infection)
    -From cats

Mycetoma- bacteria or actino(lumpy jaw); enters area with decay from spores

3 and infections is what?

Endemic vs opportunistic vs systematic

Types of Infection

-Opportunistic
    -Cryptococcosis
         -Aspergillosis
    -PJP

    -Candidas
    -Mucomycosis 

• Fungus is high system vs immunity is very important

Candidias

• Very very high infection worldwide -High for antibiotics
• Has great transformation rate and is very good for skin -Hyphae resists phagocytosis
• Testing requires skin samples like scrapping and Dextrose agar is needed

Diseases

Pneumocystis Pneumonia -Is fungal- -Comes airborne

    -Needs cellular and structural check: a S liver stain is used

• Aspergillis -Exposure from spores

    -Testing requires tests
  

• Mucormycosis- only uncontrolled with uncontrolled

Fungal Infection Testing?

            -Through the help of radiology or histo examinations

34/35

Anti fungals is the main way to kill fungal

Contemporary microbiology

• Mix w carbs
• Before 1990's - Closed versus open testing systems
• Specific plaque are related to specific bacteria - Streptococcus is important to tooth issues
• Mutans causes root carrots
• Bacteria like candida is very pathofire

Caries

Low for teeth - Strep mutans are very acidic - Disturbance of the acidity can destroy/attack teeth - Argene to cutraline with the enzyme A.D is a byproduct - Micro is related - Mutans had been to long - Cariagen is a threat • Caries is now thought to be caused by a microbial dysbiosis in response to an ecological stress, resulting in Ο Altered microbial community composition and function Ο Imbalanced metabolic activity