The document discusses the pathogenesis and histopathology of periodontal pockets. It begins by defining a periodontal pocket and describing different classifications. It then discusses the normal gingival sulcus and junctional epithelium. The key points are:
- Pocket formation is initiated by the breakdown of cellular continuity and detachment of junctional epithelium from the tooth surface. Microbes and their products like gingipains are thought to directly disrupt epithelial cell junctions.
- Histologically, pockets are lined by proliferating pocket epithelium that is detached from the tooth and shows increased permeability and leukocyte infiltration compared to healthy junctional epithelium.
- As pockets progress, the residual junctional epithelium reduces
Here's all that you need to know about dental calculus.
With proper references and all the recent advances, along with the detailed facts and description.
Each and every statement is provided with an accurate reference and all the things to know are very well summarised in one place.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
Here's all that you need to know about dental calculus.
With proper references and all the recent advances, along with the detailed facts and description.
Each and every statement is provided with an accurate reference and all the things to know are very well summarised in one place.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
Bevels and flares are very important components of resin restoration procedure. This presentation focuses on bevels and flares in restorative procedure.
This presentation describes the gingival recession, its classifications and theories of pathogenesis and different etiological factors in its progression.
Cavosurface margins in various restorations /certified fixed orthodontic cou...Indian dental academy
Welcome to Indian Dental Academy
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Bevels and flares are very important components of resin restoration procedure. This presentation focuses on bevels and flares in restorative procedure.
This presentation describes the gingival recession, its classifications and theories of pathogenesis and different etiological factors in its progression.
Cavosurface margins in various restorations /certified fixed orthodontic cou...Indian dental academy
Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Similar to The periodontal pocket: pathogenesis, histopathology and consequences DIETER D. BOSSHARDT (20)
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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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.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. barrier in the form of a keratinized cell layer, may,
however, allow microorganisms and their products
to invade the junctional epithelium. Normally, the
junctional epithelium masters this difficult task as a
result of its very sophisticated structural and func-
tional properties that provide potent antimicrobial
mechanisms (6, 44). In this defense system, the
junctional epithelium provides a structural frame-
work through which mainly neutrophilic granulo-
cytes migrate to reach the sulcus bottom. These
transmigrating neutrophils provide the first line of
defense around teeth.
The nature of the dento–gingival junction is very
heterogeneous and consists of: (i) cell attachment to
the tooth surface via hemidesmosomes and basal
lamina; (ii) cell-to-cell attachment within the junc-
tional epithelium, primarily via desmosomes (macu-
lae adherentes); and (iii) attachment to the
surrounding gingival connective tissue via a base-
ment membrane (6, 44). Knowledge of this complex
dento–gingival junction is key to understanding the
initiation of pocket formation. Epithelial cell attach-
ment to the tooth surface is first established by ame-
loblasts and later maintained by the innermost cells
A B
Fig. 1. Light micrographs illustrating
early gingival pocket formation
around a porcine tooth. The rectan-
gle in A is enlarged in B. (A) Subgin-
gival calculus with biofilm is present
on the enamel. (B) Note the inflamed
gingival connective tissue adjacent
to the pocket epithelium (PE).
A B
Fig. 2. Light micrographs illustrating
a suprabony (A) and an intrabony
(B) periodontal pocket from dog
teeth. Subgingival calculus and sub-
and supragingival biofilm are seen
in both pockets. PE, pocket epithe-
lium. (Fig. 2B from Bosshardt &
Lang. Dental Calculus. In: Clinical
Periodontology and Implant Den-
tistry. J Lindhe, NP Lang, eds. Wiley
Blackwell. 2015.)
Bosshardt
2
3. of the junctional epithelium (6). The epithelial attach-
ment mechanism is considered to be of high strength.
Of equal importance are the cell-to-cell contacts con-
necting neighboring epithelial cells. In fact, intact
cell-to-cell connectivity is an absolute requirement
for the correct functioning of cells, tissues and entire
organisms (9). Cell-to-cell adherence and communi-
cation between cells is mediated by the so-called
intercellular junction complexes consisting of desmo-
somes, adherens junctions, tight junctions and gap
junctions. Compared with other types of epithelia,
junctional epithelial cells are interconnected by a few
desmosmes only and occasional gap junctions (44).
The low number of desmosomes and wide intercellu-
lar spaces enable sulcular fluid and inflammatory and
immune cells to transmigrate through the junctional
epithelium. The importance of proper functioning of
intercellular junctions can be demonstrated in a wide
spectrum of inherited, infectious and autoimmune
diseases. Direct or indirect disruption of desmosomes
results in one group of diseases by virtue of their great
importance in maintaining tissue integrity. Among
these pathologies are cardiomyopathy, epidermal and
mucosal blistering, palmoplantar keratoderma,
woolly hair, keratosis, epidermolysis bullosa, ectoder-
mal dysplasia and alopecia (9). On the other hand,
microorganisms and inflammatory stimuli are known
to increase transepithelial permeability by inducing
disassembly of epithelial junctions, as seen in inflam-
matory bowel disease (24). Crohn’s disease, one
major type of bowel disease, falls into the class of
autoimmune diseases and is associated with peri-
odontitis (8, 20, 52).
As the conversion of junctional epithelium to
pocket epithelium is regarded as a hallmark in the
development of periodontitis, the potential factors
contributing to the initiation of pocket formation
need to be critically analyzed. Microorganisms are
the primary etiologic cause of periodontal disease
and there is good evidence that pocket formation is
related to bacterial colonization of the subgingival
tooth surface. Nevertheless, there is a lack of experi-
ments evaluating the mechanisms of pocket forma-
tion. Previous discussions on the initiation of pocket
development centered around whether: (i) the
epithelial cells first recede and later, as a consequence
of this, biofilm can migrate apically; or (ii) bacterial
products force the epithelial cells to migrate apically.
Degenerative changes, such as loss of cellular conti-
nuity and detachment from the tooth, are first
observed in the coronal-most portion of the junc-
tional epithelium (i.e. at the sulcus bottom) (22, 36,
41, 44, 48). Whether detachment of junctional
epithelial cells from the tooth surface or destruction
of cell junctional complexes is more important for
pocket development remains unclear. However, the
important question is why does loss of cellular conti-
nuity, and thus loss of structural integrity, occur at all
at this site? Are host-derived factors associated with
inflammation (such as cytokines) the primary cause
or do microbial products directly trigger destruction
of the junctional epithelium and thereby destabilize
the structure–function relationship?
Several possibilities have been proposed to explain
intra-epithelial cleavage in the junctional epithelium.
With increasing degree of inflammation, an increase
in both migration of polymorphonuclear neutrophils
and passage of gingival crevicular fluid through the
intercellular spaces occurs (1, 2, 27–29). A moderate
distension of intercellular spaces is not considered to
compromise the structural and functional integrity of
the junctional epithelium (44). An increased number
of leukocytes is, however, considered as a contribut-
ing factor that eventually leads to focal disintegration
of the junctional epithelium (44). This is in line with
the concept that the host itself is the driving force
behind decomposition of the junctional epithelium.
Apart from this view, direct influence of bacteria on
the breakdown of the coronal portion of the junc-
tional epithelium has to be taken into consideration.
Indeed, it has been hypothesized that pocket forma-
tion results from the subgingival spread of bacteria
under impaired defense conditions (41). In this con-
text, the cysteine proteinases, referred to as gingi-
pains (namely virulence factors produced by
Porphyromonas gingivalis, a species of bacterium
implicated as a major etiological agent of chronic
periodontitis), have been the focus of intense
research (7, 23, 35). As a result, a new effect of gingi-
pains was discovered. Gingipains specifically prote-
olytically degrade components of cell-to-cell
junctional complexes in epithelial cells (10, 25, 26, 32,
45, 53). In addition, gingipains also cleave intercellu-
lar adhesion molecule-1 on oral epithelial cells, which
consequently leads to disruption of the interaction
between polymorphonuclear neutrophils and epithe-
lial cells, a sort of immune evasion by P. gingivalis
(47). Intercellular adhesion molecule-1, also known as
CD54, a member of the immunoglobulin superfamily
of recognition molecules, mediates cell-to-cell inter-
actions in inflammatory reactions by functioning as a
ligand for the b2 integrins present on leukocytes and
thus has an important function in the control of
leukocyte migration to inflammatory sites (11, 12, 16,
49, 50). Thus, specific degradation of cell junctional
complexes and disturbance of the intercellular
Periodontal pocket formation
3
4. adhesion molecule-1-dependent adhesion of poly-
morphonuclear neutrophils to epithelial cells through
gingipains point to the importance of these virulence
factors in the breakdown of the junctional epithe-
lium, which eventually leads to pocket development.
In an apical direction, the pocket epithelium remains
contiguous with a junctional epithelium of reduced
height (41). To maintain an epithelial attachment, the
residual junctional epithelium proliferates further
apically, as the pocket deepens. What the conse-
quences of this pathological situation are is probably
best demonstrated histopathologically.
Histopathology
Histopathologically, a pocket is ‘a pathologically
altered gingival sulcus, lined to a variable extent with
pocket epithelium’ (54). Furthermore, the pocket
epithelium, which lines the pocket wall facing peri-
odontal tissues, is defined as ‘unattached epithelial
lining of the pocket, which extends from the sulcular
epithelium to the junctional epithelium. It is charac-
terized by marked proliferation of retial ridges around
inflamed connective tissue papillae and by a ten-
dency to micro-ulceration’ (54).
Much of our knowledge on the histopathologic
appearance of gingival and periodontal pockets is
derived from observations made in animals, mainly
dogs, with ligature-induced periodontal diseases (38,
39, 42) or neutropenia (3, 40) and from ‘broken-
mouth’ periodontitis in sheep (13, 15). Studies
describing the histopathology of gingival and peri-
odontal lesions in humans were mainly focused on
the host response to microbial challenge (4, 14, 17, 31,
34, 56, 57).
At first view, the junctional epithelium (Fig. 3A)
and pocket epithelium (Figs 3B and 4) have some fea-
tures in common, such as formation of a barrier
against microorganisms and their products, passage
of gingival fluid and leukocytes (in particular neu-
trophilic granulocytes) and concomitant infiltration
with mononuclear leukocytes (39). On closer inspec-
tion, however, the pocket situation demonstrates
characteristic features distinctly different from the
healthy conditions in a gingival sulcus environment
(Figs 3–5). The major differences can be summarized
as follows:
definite detachment of junctional epithelium from
the tooth surface and conversion into pocket
epithelium, leading to formation of an intra-
epithelial cleft.
proliferation of epithelial ridges into the inflamed
soft connective tissue with very thin regions
between these ridges.
focal micro-ulcerations of the epithelial ridges and
at the free surface of the pocket epithelium.
increased permeability of the pocket epithelium.
high infiltration, particularly of the epithelial
ridges, with lymphocytes, including T- and B-cells
and plasma cells.
increased migration of neutrophilic granulocytes
through the pocket epithelium.
change in direction of the exudate from apico-cor-
onal to horizontal (i.e. toward the tooth root sur-
face).
seamless transition from pocket epithelium to
junctional epithelium at the pocket fundus.
significant reduction in height of the residual
junctional epithelium.
The condition of the soft connective tissue may
depend on the severity and duration of the disease.
Figure 4 shows a very active phase of destruction in
which all fibroblasts and collagen fibers around the
epithelial ridges are lost and replaced with inflamma-
tory and immune cells. More peripheral, residual col-
lagen fibers and fibroblasts demarcate the highly
infiltrated (former) connective tissue area from
healthy tissue. The morphology of the pocket can
vary greatly because extension of the pocket occurs
A B
Fig. 3. Light micrographs demon-
strating (A) junctional epithelium
(JE) and (B) pocket epithelium (PE).
The JE adheres on the enamel sur-
face (ES, enamel space), while the PE
is separated from the biofilm (BF)-
covered tooth surface by the pocket
space (PS).
Bosshardt
4
5. not only by apical deepening but also by widening in
a horizontal direction, which leads to undermining
pockets.
Pockets also occur in conditions of disease around
dental implants (Fig. 6). In recent reviews, it was con-
cluded that peri-implant mucositis and peri-implanti-
tis lesions do not differ fundamentally from gingivitis
and periodontitis lesions, respectively, from the per-
spectives of etiology, pathogenesis, risk assessment,
diagnosis and therapy (21, 30). However, there appear
to be histopathological differences in the host
response to infections around implants and teeth in
the sense that persistent biofilm may elicit a more
pronounced inflammatory response in mucosal tis-
sue around implants than around teeth (5, 21). Struc-
tural changes (in vascularity and the fibroblast-to-
collagen ratio) and, consequently, functional dispari-
ties may account for this difference. It is noteworthy
that the presence of excess cement at the abutment–
crown interface provides an ideal substrate for plaque
and calculus deposition and retention (Fig. 6) and is
associated with peri-implant disease (55). Overhang
at such sites may impede calculus and biofilm
removal. It has been shown that clinical and endo-
scopic signs of peri-implant disease are absent in the
majority of cases after excess cement removal (55).
Consequences
The defense mechanisms in a healthy periodontal sit-
uation are generally sufficient to control the constant
microbiological challenge through a normally func-
tioning junctional epithelium and a concentrated
powerful mass of inflammatory and immune cells
and macromolecules transmigrating through this
epithelium. In contrast, the destruction of the struc-
tural integrity of the junctional epithelium, which
includes disruption of cell-to-cell contacts and
detachment from the tooth surface, consequently
leading to pocket formation, disequilibrates this deli-
cate defense system. Deepening of the pocket and
apical, but also horizontal, expansion of the biofilm
puts this system to a grueling test. There is no more
A
C D
B
Fig. 4. Light micrographs showing
acute inflammation of a human
tooth affected by periodontitis. The
rectangles in A are enlarged in B, C
and D. (A) The area of the inflamed
connective tissue (ICT) is quite large
and demarcated by residual collagen
fibers (CF) seen in the lower left
right. The pocket epithelium (PE)
has proliferated deeply into the ICT.
(B) Higher magnification of the bor-
der region between ICT and intact
connective tissue. (C) The surface of
the PE facing the pocket space is
very thin. (D) Occasionally, the PE is
ulcerated and the adjacent ICT is
heavily infiltrated.
Periodontal pocket formation
5
6. this powerful concentration of defense cells and
macromolecules that are discharged at the sulcus
bottom and that face a relatively small biofilm surface
in the gingival sulcus. In a pocket situation, the
defense cells and the macromolecules are directly
discharged into the periodontal pocket and the
majority of epithelial cells directly face the biofilm.
The thinning of the epithelium and its ulceration
increase the chance for invasion of microorganisms
and their products into the soft connective tissue and
A B
C D
Fig. 5. Transmission electron micro-
graphs showing higher magnifica-
tions of the tissue biopsy seen in
Fig. 4. (A) The pocket epithelial cells
(EC) are poorly connected to one
another in the epithelial ridges and
leukocytes are seen within and adja-
cent to the pocket epithelium. (B)
Other regions show better cell con-
nectivity within the pocket epithe-
lium. Total disappearance of
collagen fibers and fibroblasts is evi-
dent in the inflamed (former) con-
nective tissue. (C) Various leukocytes
are present in the inflamed former
connective tissue. (D) Towards the
margin of the inflamed region, colla-
gen fibers (CF) are present.
A B
Fig. 6. Peri-implant mucositis with-
out (A) and with (B) the presence of
excess cement at the abutment–
crown interface. The excess cement
provides an ideal substrate for pla-
que and calculus deposition and
retention. Detachment of the epithe-
lium indicates peri-implant pocket
formation. The detachment of the
apical-most portion of the epithe-
lium, however, may be an artifact
caused by histological processing.
PE, pocket epithelium. (Fig. 6B from
Bosshardt Lang. Dental Calculus.
In: Clinical Periodontology and
Implant Dentistry. J Lindhe, NP
Lang, eds. Wiley Blackwell. 2015.).
Bosshardt
6
7. aggravates the situation. Depending on the severity
and duration of disease, a vicious circle may develop
in the pocket environment, which is difficult or
impossible to break without therapeutic intervention.
References
1. Attstr€om R. Presence of leukocytes in crevices of healthy
and chronically inflamed gingivae. J Periodontal Res 1970:
5: 42–47.
2. Attstr€om R, Egelberg J. Emigration of blood neutrophils and
monocytes into the gingival crevices. J Periodontal Res
1970: 5: 48–55.
3. Attstr€om R, Schroeder HE. Effect of experimental neutrope-
nia on initial gingivitis in dogs. Scand J Dent Res 1979: 87:
7–23.
4. Berglundh T, Liljenberg B, Lindhe J. Some effect of peri-
odontal therapy on local and systemic immunological
parameters. J Clin Periodontol 1999: 26: 91–98.
5. Berglundh T, Zitzmann NU, Donati M. Are peri-implantitis
lesions different from periodontitis lesions? J Clin Periodon-
tol 2011: 38(Supp. 11): 188–202.
6. Bosshardt DD, Lang NP. The junctional epithelium: from
health to disease. J Dent Res 2005: 84: 9–20.
7. Bostanci N, Belibasakis GN. Porphyromonas gingivalis: an
invasive and evasive opportunistic oral pathogen. FEMS
Microbiol Lett 2012: 333: 1–9.
8. Brito F, Zaltman C, Carvalho AT, Fischer RG, Persson R,
Gustafsson A, Figueredo CM. Subgingival microflora in
inflammatory bowel disease patients with untreated peri-
odontitis. Eur J Gastroenterol Hepatol 2013: 25: 239–245.
9. Brooke MA, Nitoiu D, Kelsell DP. Cell-cell connectivity:
desmosomes and disease. J Pathol 2012: 226: 158–171.
10. Chen T, Nakayama K, Belliveau L, Duncan MJ. Porphy-
romonas gingivalis gingipains and adhesion to epithelial
cells. Infect Immun 2001: 69: 3048–3056.
11. Crawford JM, Hopp B. Junctional epithelium expresses the
intercellular adhesion molecule ICAM-1. J Periodontal Res
1990: 25: 254–256.
12. Crawford JM. Distribution of ICAM-1, LFA-3 and HLA-Dr in
healthy and diseased gingival tissue. J Periodontal Res 1992:
27: 291–298.
13. Cutress TW, Schroeder HE. Histopathology of periodontitis
(“broken-mouth”) in sheep: a further consideration. Res Vet
Sci 1982: 33: 64–69.
14. Donati M, Liljenberg B, Zitzmann NU, Berglundh T. B-1a
cells and plasma cells in periodontitis lesions. J Periodontal
Res 2009: 44: 683–688.
15. Frisken KW, Tagg JR, Laws AJ, Orr MB. Black-pigmented
Bacteroides associated with broken-mouth periodontitis in
sheep. J Periodontal Res 1987: 22: 156–159.
16. Gao Z, Mackenzie IC. Patterns of phenotypic expression of
human junctional, gingival and reduced enamel epithelia
in vivo and in vitro. Epithelial Cell Biol 1992: 1: 156–167.
17. Gemmell E, Walsh JL, Savage NW, Seymour GJ. Adhesion
molecule expression in chronic inflammatory periodontal
disease tissue. J Periodontal Res 1994: 29: 46–53.
18. Glickman I, Smulow JB. Periodontal disease: clinical, radio-
graphic, and histopathologic features. Philadelphia, London,
Toronto: W.B. Saunders Company, 1974.
19. Grant D, Stern I, Listgarten M. Periodontics. St. Louis, MO:
The C.V. Mosby Company, 1988.
20. Habashneh RA, Khader YS, Alhumouz MK, Jadallah K, Yji-
louni Y. The association between inflammatory bowel dis-
ease and periodontitis among Jordanians: a case-control
study. J Periodontal Res 2012: 47: 293–298.
21. Heitz-Mayfield LJ, Lang NP. Comparative biology of chronic
and aggressive periodontitis vs. peri-implantitis. Periodon-
tol 2000 2010: 53: 167–181.
22. Hillmann G, Vipismakul V, Donath K. Die Entstehung
plaquebedingter Gingivataschen im Tiermodell. Eine histol-
ogische Studie an unentkalkten D€unnschliffen. Dtsch
Zahn€arztl Z 1990: 45: 264–266.
23. Imamura T. The role of gingipains in the pathogenesis of
periodontal disease. J Periodontol 2003: 74: 111–118.
24. Ivanov AI, Parkos CA, Nusrat A. Cytoskeletal regulation of
epithelial barrier function during inflammation. Am J
Pathol 2010: 177: 512–524.
25. Katz J, Sambandam V, Wu JH, Michalek SM, Balkovetz DF.
Characterization of Porphyromonas gingivalis-induced
degradation of epithelial cell junctional complexes. Infect
Immun 2000: 68: 1441–1449.
26. Katz J, Yang QB, Zhang P, Potempa J, Travis J, Michalek SM,
Balkovetz DF. Hydrolysis of epithelial junctional proteins
by Porphyromonas gingivalis gingipains. Infect Immun
2002: 70: 2512–2518.
27. Klinkhamer JM. Quantitative evaluation of gingivitis and
periodontal disease. I. The orogranulocytic migratory rate.
Periodontics 1968: 6: 207–211.
28. Klinkhamer JM, Zimmerman S. The function and reliability
of the orogranulocytic migratory rate as a measure of oral
health. J Dent Res 1969: 48: 709–715.
29. Kowashi Y, Jaccard F, Cimasoni G. Sulcular polymorphonu-
clear leukocytes and gingival exudate during experimental
gingivitis in man. J Periodontal Res 1980: 15: 151–158.
30. Lang NP, Bosshardt DD, Lulic M. Do mucositis lesions
around implants differ from gingivitis lesions around teeth?
J Clin Periodontol 2011: 38(Suppl. 11): 182–187.
31. Lindhe J, Liljenberg B, Listgarten M. Some microbiological
and histopathological features of periodontal disease in
man. J Periodontol 1980: 51: 264–269.
32. Nakagawa I, Inaba H, Yamamura T, Kato T, Kawai S,
Ooshima T, Amano A. Invasion of epithelial cells and prote-
olysis of cellular focal adhesion components by distinct
types of Porphyromonas gingivalis gingipain fimbriae. Infect
Immun 2006: 74: 3773–3782.
33. Nibali L. Development of the gingival sulcus at the time
of tooth eruption and the influence of genetic factors.
Periodontol 2000 2016: In press.
34. Page RC, Schroeder HE. Pathogenesis of inflammatory peri-
odontal disease. A summary of current work. Lab Invest
1976: 34: 235–249.
35. Potempa J, Banbula A, Travis J. Role of bacterial proteinases
in matrix destruction and modulation of host responses.
Periodontol 2000 2000: 24: 153–263.
36. Schluger S, Youdelis RA, Page RC, eds. Periodontal disease.
Philadelphia, PA: Lea and Febiger, 1977.
37. Schroeder HE. Ultrastructure of the junctional epithelium
of the human gingiva. Helv Odontol Acta 1969: 13: 65–83.
38. Schroeder HE, Lindhe J. Conversion of stable established
gingivitis in the dog into destructive periodontitis. Arch Oral
Biol 1975: 20: 775–782.
Periodontal pocket formation
7
8. 39. Schroeder HE. Histopathology of the gingival sulcus. In:
Lehner T, editor. The Borderland between caries and peri-
odontal disease. London and New York: Academic Press,
1977: 43–78.
40. Schroeder HE, Attstr€om R. Effect of mechanical plaque
control on development of subgingival plaque and initial
gingivitis in neutropenic dogs. Scand J Dent Res 1979: 87:
279–287.
41. Schroeder HE, Attstr€om R. Pocket formation: an hypothesis.
In: Lehner T, Cimasoni G, editors. The borderland between
caries and periodontal disease II. London: Academic Press,
New York, NY: Grune Stratton; 1980: 99–123.
42. Schroeder HE, Lindhe J. Conditions and pathological fea-
tures of rapidly destructive, experimental periodontitis in
dogs. J Periodontol 1980: 51: 6–19.
43. Schroeder HE. The junctional epithelium: origin, structure
and significance. A review. Acta Med Dent Helv 1996: 1:
155–167.
44. Schroeder HE, Listgarten MA. The gingival tissues: the
architecture of periodontal protection. Periodontol 2000
1997: 13: 91–120.
45. Sheets SM, Potempa J, Travis J, Casiano CA, Fletcher HM.
Gingipains from Porphyromonas gingivalis W83 induce cell
adhesion molecule cleavage and apoptosis in endothelial
cells. Infect Immun 2005: 73: 1543–1552.
46. Stahl SS. Marginal lesion. In: Goldman HM, Gohen DW,
editors. Periodontal therapy. Saint Louis, MO: The C.V.
Mosby Company, 1968: 110–166.
47. Tada H, Sugawara S, Nemoto E, Imamura T, Potempa J,
Travis J, Shimauchi H, Takada H. Proteolysis of ICAM-1 on
human oral epithelial cells by gingipains. J Dent Res 2003:
82: 796–801.
48. Takata T, Donath K. The mechanism of pocket formation. A
light microscopic study on undecalcified human material. J
Periodontol 1988: 59: 215–221.
49. Tonetti MS. Molecular factors associated with compart-
mentalization of gingival immune responses and transep-
ithelial neutrophil migration. J Periodontal Res 1997: 32:
104–109.
50. Tonetti MS, Imboden MA, Lang NP. Neutrophil migration
into the gingival sulcus is associated with transepithelial
gradients of interleukin-8 and ICAM-1. J Periodontol 1998:
69: 1139–1147.
51. Trackman PC, Kantarci A. Molecular and clinical aspects of
drug-induced gingival overgrowth. J Dent Res 2015: 94:
540–546.
52. Vavricka SR, Manser CN, Hediger S, V€ogelin M, Scharl M,
Biedermann L, Rogler S, Seibold F, Sanderink R, Attin T,
Schoepfer A, Fried M, Rogler G, Frei P. Periodontitis and
gingivitis in inflammatory bowel disease: a case-control
study. Inflamm Bowel Dis 2013: 19: 2768–2777.
53. Wang PL, Shinohora M, Murakawa N, Endo M, Sakata S,
Okamura M, Ohura K. Effect of cysteine protease of Porphy-
romonas gingivalis on adhesion molecules in gingival
epithelial cells. Jpn J Pharmacol 1999: 80: 75–79.
54. WHO: Epidemiology, etiology, and prevention of periodon-
tal diseases. Technical Report Series No. 621, 1978.
55. Wilson TG Jr. The positive relationship between excess
cement and peri-implant disease: a prospective clinical
endoscopic study. J Periodontol 2009: 80: 1388–1392.
56. Yamazaki K, Nakajima T, Aoyagi T, Hara K. Immunohisto-
logical analysis of memory T lymphocytes and activated B
lymphocytes in tissues with periodontal disease. J Periodon-
tal Res 1993: 28: 324–334.
57. Zitzmann NU, Berglundh T, Lindhe J. Inflammatory lesions
in the gingiva following resective/non-resective periodontal
therapy. J Clin Periodontol 2005: 32: 139–146.
Bosshardt
8