Here saliva as a diagnostic biomarker has been explained via this powerpoint . extraction of saliva and diagnostic equipments and techniques are explained here by Dr Harshavardhan Patwal
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
This Presentation includes systematic compilation of the anatomy, physiology, biochemistry and pathology related to saliva and salivary glands. it also mentions about the role of saliva in dentistry. Any additions or mistakes are welcome!
Please do leave your comments and let me know if the presentations has helped you!
The presentation is available on request. Mail me at apurvathampi@gmail.com
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.
This paper was presented in the "SECOND INDIAN UNDERGRADUATE DENTAL CONVENTION-MOKSHAA'13" held on 6th & 7th April 2013 at Sri Venkateshwara Dental College & Hospital,Chennai.
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.
orthodontists & surgeons opinion on the role of third molars as a cause of de...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.for more details please visit
www.indiandentalacademy.com
Contents :
Classification of salivary glands
Mechanism of saliva secretion
Composition
Properties
Flow rate
Functions
Role in dental caries
Role in diagnostics
Clinical considerations (dentistry)
It is the surrounding environment of the teeth, which is one of the most important factors that can protect, process and predict the oral health of an individual. And the main thing that makes that environment is the SALIVA – one of the most important body fluid that is the nature’s miracle in your mouth, the primary defence system for the oral environment. The quality, quantity and composition depending, this miracle fluid helps us in maintaining our health in the following ways:
1. Keeping our mouth in a normal pH (acid-alkaline balance) - neutralizing acid challenges
2. Re-mineralization of teeth -delivering calcium, phosphate and fluoride to the tooth surface
3. Oxygenation and cleaning of oral tissues, flushing food and bacteria
4. Aid in speech and taste
5. Digest and swallow food
6. Anti-bacterial / Anti-viral / Anti-fungal
7. Diagnosis of diseases, hormones, pregnancy, drugs and alcohol testing
Definition
General properties
Composition
Function of saliva
Formation of saliva
Method for collecting saliva
Advantages
Limitations
Analysis of saliva done for the diagnosis of systemic disease
Definition:
by Stedmann’s & Lipincott medical dictionary.
A clear, tasteless, odourless, slightly acidic (pH 6.8) viscous fluid, consisting of the secretion from the parotid, sublingual, submandibular salivary glands and the mucous glands of the oral cavity.
General properties
Volume: 1000 to 1500 mL of saliva is secreted per day and, it is approximately about 1 ml/ minute.
Contribution by each major salivary gland is:
i. Parotid glands: 25%
ii. Submandibular glands: 70%
iii. Sublingual glands: 5%.
Reaction: Mixed saliva from all the glands is slightly acidic with pH of 6.35 to 6.85.
Specific gravity: It ranges between 1.002 and 1.012.
Tonicity: Saliva is hypotonSalivary flow
The average person produces approximately 0.5 L – 1.5 L per day
Unstimulated Flow (resting salivary flow―no external stimulus)
Typically 0.2 mL – 0.3 mL per minute
Stimulated Flow (response to a stimulus, usually taste, chewing, or medication [eg, at mealtime])
Typically 1.5 mL – 2 mL per minute
Similar to Saliva - A diagnostic marker ; Dr Harshavardhan Patwal (20)
Risk assessment is the determination of quantitative or qualitative estimate of risk related to a well-defined situation and a recognized threat (also called hazard). Quantitative risk assessment requires calculations of two components of risk (R): the magnitude of the potential loss (L), and the probability (p) that the loss will occur. An acceptable risk is a risk that is understood and tolerated usually because the cost or difficulty of implementing an effective countermeasure for the associated vulnerability exceeds the expectation of loss."Health risk assessment" includes variations, such as risk as the type and severity of response, with or without a probabilistic context.
Dental Implants have changed the face of dentistry over the last 25 years. What are dental implants? What is the history of dental implants? And how are they used to replace missing teeth? This section will give you an overview of the topic of dental implants, to be followed by more detail in additional sections.
As with most treatment procedures in dentistry today, dental implants not only involve scientific discovery, research and understanding, but also application in clinical practice. The practice of implant dentistry requires expertise in planning, surgery and tooth restoration; it is as much about art and experience as it is about science. This site will help provide you with the knowledge you need to make informed choices in consultation with your dental health professionals.
Dental Implants
Dental illustration by Dear Doctor
Let’s start from the beginning: A dental implant is actually a replacement for the root or roots of a tooth. Like tooth roots, dental implants are secured in the jawbone and are not visible once surgically placed. They are used to secure crowns (the parts of teeth seen in the mouth), bridgework or dentures by a variety of means. They are made of titanium, which is lightweight, strong and biocompatible, which means that it is not rejected by the body. Titanium and titanium alloys are the most widely used metals in both dental and other bone implants, such as orthopedic joint replacements. Dental implants have the highest success rate of any implanted surgical device.
Titanium’s special property of fusing to bone, called osseointegration (“osseo” – bone; “integration” – fusion or joining with), is the biological basis of dental implant success. That’s because when teeth are lost, the bone that supported those teeth is lost too. Placing dental implants stabilizes bone, preventing its loss. Along with replacing lost teeth, implants help maintain the jawbone’s shape and density. This means they also support the facial skeleton and, indirectly, the soft tissue structures — gum tissues, cheeks and lips. Dental implants help you eat, chew, smile, talk and look completely natural. This functionality imparts social, psychological and physical well-being.
There is no question that given the current state of the art in dentistry, that dental implants are pretty much the best way to replace teeth; they are stand alone tooth replacement systems that look and function just like natural teeth. They do not attach to adjacent teeth like a fixed bridge and don't have to be taken in and out like removable partial dentures.
A dental implant is a tooth root replacement made of titanium, which has the unique property of being osteophilic (osteo-bone, philic-loving) and actually fuses to bone. A crown, the part of the tooth that you see in your mouth, is attached to the implant. And the great thing about implants is they are not susceptible to decay or periodontal (gum) disease in the same way that teeth are.
Now here are a few important pointers, which hold for implants generally and are especially important in your case when replacing a front tooth for an imminent event . Dr Harshavardhan Patwal
Non surgical management of gingival recession- Dr Harshavardhan PatwalDr Harshavardhan Patwal
Treatment of gingival recession has become an important therapeutic issue due to the increasing number of cosmetic requests from patients. The dual goals of mucogingival treatment include complete root coverage, up to the cemento-enamel junction, and blending of tissue color between the treated area and non-treated adjacent tissues. Even though the connective tissue graft is commonly considered the “gold standard” for treatment of recession defects, it may not always be the best surgical option for every case. Dr Harshavardhan Patwal , Under non-experimental conditions, all root coverage procedures may be effective in terms of complete root coverage and excellent esthetics. Careful analyses of patient- and defect-related factors, however, are key considerations prior to selecting an appropriate surgical technique.
Occlusion, in a dental context, means simply the contact between teeth. More technically, it is the relationship between the maxillary (upper) and mandibular (lower) teeth when they approach each other, as occurs during chewing or at rest.
Malocclusion is the misalignment of teeth and jaws, or more simply, a "bad bite". Malocclusion can cause a number of health and dental problems.
Static occlusion refers to contact between teeth when the jaw is closed and stationary, while dynamic occlusion refers to occlusal contacts made when the jaw is moving. Dynamic occlusion is also termed as articulation. During chewing, there is no tooth contact between the teeth on the chewing side of the mouth.
Centric occlusion is the occlusion of opposing teeth when the mandible is in centric relation. Centric occlusion is the first tooth contact and may or may not coincide with maximum intercuspation. It is also referred to as a person's habitual bite, bite of convenience, or intercuspation position (ICP). Centric relation, not to be confused with centric occlusion, is a relationship between the maxilla and mandible. Dr Harshavardhan Patwal , Malocclusion is the result of the body trying to optimize its function in a dysfunctional environment. It can be associated with a number of problems, including crooked teeth, gum problems, the temporomandibular joint (TMJ), and jaw muscles. Teeth, fillings, and crowns may wear, break, or loosen, and teeth may be tender or ache. Receding gums can be exacerbated by a faulty bite. If the jaw is mispositioned, jaw muscles may have to work harder, which can lead to fatigue and or muscle spasms. This in turn can lead to headaches or migraines, eye or sinus pain, and pain in the neck, shoulder, or even back. Malocclusion can be a contributing factor to sleep disordered breathing which may include snoring, upper airway resistance syndrome, and / or sleep apnea (apnea means without breath). Untreated damaging malocclusion can lead to occlusal trauma.
Some of the treatments for different occlusal problems include protecting the teeth with dental splints (orthotics), tooth adjustments, replacement of teeth, medication (usually temporary), a diet of softer foods, TENS to relax tensed muscles, and relaxation therapy for stress-related clenching. Removable dental appliances may be used to alter the development of the jaws. Fixed appliances such as braces may be used to move the teeth in the jaws. Jaw surgery is also used to correct malocclusion.
Since the initial observations of oral bacteria within dental
plaque by van Leeuwenhoek using his primitive microscopes
in 1680, an event that is generally recognized as the
advent of oral microbiological investigation, oral microbiology
has gone through phases of “reductionism” and
“holism”. From the small beginnings of the Miller and
Black period, in which microbiologists followed Koch’s
postulates, took the reductionist approach to try to study
the complex oral microbial community by analyzing
individual species; to the modern era when oral researchers
embrace “holism” or “system thinking”, adopt new concepts
such as interspecies interaction, microbial community,
biofilms, poly-microbial diseases, oral microbiological knowledge
has burgeoned and our ability to identify the resident
organisms in dental plaque and decipher the interactions
between key components has rapidly increased, such
knowledge has greatly changed our view of the oral
microbial flora, provided invaluable insight into the
etiology of dental and periodontal diseases, opened the door
to new approaches and techniques for developing new
therapeutic and preventive tools for combating oral polymicrobial
diseases. Dr Harshavardhan Patwal
Like many other biological sciences, the study
of microbiology has gone through phases of
“reductionism” and “holism”. For a long time,
microbiologists took the reductionist approach to
study complex microbial communities by analyzing
individual bacterial species. The strategy was to
understand the whole by examining smaller components,
and has been the hallmark of much of the
industrial and scientific revolutions for the past
150 years. While reductionism has greatly advanced
microbiology, it was recognized that assembly of
smaller pieces cannot explain the whole! Modern
microbiologists are learning “system thinking” and
“holism.” From global gene regulation to “metagenomics”
to “biofilms”, microbiology is entering
an exciting new era with emphasis on revealing
and decoding the interactions of different elements
within a microbial community. The knowledge
obtained from “system thinking” is changing our
understanding of microbial physiology and our
ability to diagnose/treat microbial infections, and
will have great impact on oral microbiology as
well.
Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Oxidative stress from oxidative metabolism causes base damage, as well as strand breaks in DNA. Base damage is mostly indirect and caused by reactive oxygen species (ROS) generated, e.g. O2− (superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide).Further, some reactive oxidative species act as cellular messengers in redox signaling. Thus, oxidative stress can cause disruptions in normal mechanisms of cellular signaling. Dr Harshavardhan Patwal , Chemically, oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses, such as glutathione.The effects of oxidative stress depend upon the size of these changes, with a cell being able to overcome small perturbations and regain its original state. However, more severe oxidative stress can cause cell death and even moderate oxidation can trigger apoptosis, while more intense stresses may cause necrosis.
Production of reactive oxygen species is a particularly destructive aspect of oxidative* stress. Such species include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage.Most long-term effects are caused by damage to DNA
The periodontium is the specialized tissues that both surround and support the teeth, maintaining them in the maxillary and mandibular bones. The word comes from the Greek terms περί peri-, meaning "around" and -odont, meaning "tooth". Literally taken, it means that which is "around the tooth". Periodontics is the dental specialty that relates specifically to the care and maintenance of these tissues. It provides the support necessary to maintain teeth in function. It consists of four principal components, namely:
Gingiva
Periodontal ligament (PDL)
Cementum
Alveolar bone proper
Dr Harshavardhan Patwal explains the diffrent cell matrix interactions with emphasis on each components is distinct in location, architecture, and biochemical properties, which adapt during the life of the structure. For example, as teeth respond to forces or migrate medially, bone resorbs on the pressure side and is added on the tension side. Cementum similarly adapts to wear on the occlusal surfaces of the teeth by apical deposition. The periodontal ligament in itself is an area of high turnover that allows the tooth not only to be suspended in the alveolar bone but also to respond to the forces. Thus, although seemingly static and having functions of their own, all of these components function as a single unit .
Porphyromonas gingivalis belongs to the phylum Bacteroidetes and is a nonmotile, Gram-negative, rod-shaped, anaerobic, pathogenic bacterium. It forms black colonies on blood agar.
It is found in the oral cavity, where it is implicated in certain forms of periodontal disease, as well as in the upper gastrointestinal tract, the respiratory tract, and the colon. It has also been isolated from women with bacterial vaginosis. Collagen degradation observed in chronic periodontal disease results in part from the collagenase enzymes of this species. It has been shown in an in vitro study that P. gingivalis can invade human gingival fibroblasts and can survive in them in the presence of considerable concentrations of antibiotics.P. gingivalis also invades gingival epithelial cells in high numbers, in which cases both bacteria and epithelial cells survive for extended periods of time. High levels of specific antibodies can be detected in patients harboring P. gingivalis. Dr Harshavardhan Patwal , explains the various enzymes enzyme peptidyl-arginine deiminase, which is involved in citrullination.[4] Patients with rheumatoid arthritis have an increased incidence of periodontal disease, and antibodies against the bacterium are significantly more common in these patients.
P. gingivalis is divided into K-serotypes based upon capsular antigenicity of the various types.
Influence of systemic disorders on periodontal diseases is well established. However, of growing interest is the effect of periodontal diseases on numerous systemic diseases or conditions like cardiovascular disease, cerebrovascular disease, diabetes, pre-term low birth weight babies, preeclampsia, respiratory infections and others including osteoporosis, cancer, rheumatoid arthritis, erectile dysfunction, Alzheimer's disease, gastrointestinal disease, prostatitis, renal diseases, which has also been scientifically validated. This side of the oral-systemic link has been termed Periodontal Medicine and is potentially of great public health significance, as periodontal disease is largely preventable and in many instances readily treatable, hence, providing many new opportunities for preventing and improving prognosis of several systemic pathologic conditions. in this power point Dr Harshavardhan Patwal , highlights the importance of prevention and treatment of periodontal diseases as an essential part of preventive medicine to circumvent its deleterious effects on general health.
ggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) is a Gram-negative, facultative nonmotile, rod-shaped oral commensal often found in association with localized aggressive periodontitis, a severe infection of the periodontium, although it is also associated with nonoral infections. Its role in periodontitis was first discovered by Danish-born periodontist Jørgen Slots, a professor of dentistry and microbiology at the University of Southern California School of Dentistry.
'Bacterium actinomycetem comitans' was described by Klinger (1912) as coccobacillary bacteria isolated together with Actinomyces from actinomycotic lesions of man. It was reclassified as Actinobacillus actinomycetemcomitans by Topley & Wilson (1929) and as Haemophilus actinomycetemcomitans by Potts et al. (1985). The species has attracted attention because of its association with localized aggressive periodontitis. is explained here by Dr Harshavardhan Patwal
T-cells is explained with a emphasis with humoral and adaptive immunity . And the diffrent subsets of t cells are well explained by Dr Harshavardhan Patwal here .
explained here is bone loos and patterns of bone loos in alveolar bone to various insults . Dr Harshavardhan pawal also gives emphasis on rate on bone loss and radius of action .
contains descriptive and other studies on genetics and epigenetics and whole gene concepts from central dogma to future concepts . Dr Harshavardhan Patwal
this is a presentation on B lymphocytes and there role in humoral immune response . Dr Harshavardhan Patwal highlights on antibodies and B cell activation to name a few.
DISSERTATION on NEW DRUG DISCOVERY AND DEVELOPMENT STAGES OF DRUG DISCOVERYNEHA GUPTA
The process of drug discovery and development is a complex and multi-step endeavor aimed at bringing new pharmaceutical drugs to market. It begins with identifying and validating a biological target, such as a protein, gene, or RNA, that is associated with a disease. This step involves understanding the target's role in the disease and confirming that modulating it can have therapeutic effects. The next stage, hit identification, employs high-throughput screening (HTS) and other methods to find compounds that interact with the target. Computational techniques may also be used to identify potential hits from large compound libraries.
Following hit identification, the hits are optimized to improve their efficacy, selectivity, and pharmacokinetic properties, resulting in lead compounds. These leads undergo further refinement to enhance their potency, reduce toxicity, and improve drug-like characteristics, creating drug candidates suitable for preclinical testing. In the preclinical development phase, drug candidates are tested in vitro (in cell cultures) and in vivo (in animal models) to evaluate their safety, efficacy, pharmacokinetics, and pharmacodynamics. Toxicology studies are conducted to assess potential risks.
Before clinical trials can begin, an Investigational New Drug (IND) application must be submitted to regulatory authorities. This application includes data from preclinical studies and plans for clinical trials. Clinical development involves human trials in three phases: Phase I tests the drug's safety and dosage in a small group of healthy volunteers, Phase II assesses the drug's efficacy and side effects in a larger group of patients with the target disease, and Phase III confirms the drug's efficacy and monitors adverse reactions in a large population, often compared to existing treatments.
After successful clinical trials, a New Drug Application (NDA) is submitted to regulatory authorities for approval, including all data from preclinical and clinical studies, as well as proposed labeling and manufacturing information. Regulatory authorities then review the NDA to ensure the drug is safe, effective, and of high quality, potentially requiring additional studies. Finally, after a drug is approved and marketed, it undergoes post-marketing surveillance, which includes continuous monitoring for long-term safety and effectiveness, pharmacovigilance, and reporting of any adverse effects.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. • Saliva is “the aqua-vita” of the oral cavity.
• the principal protector of the soft and hard oral tissues.
Diminished secretion:
• oral tissues become susceptible to infection
• ability to masticate, swallow, speak and taste may be
disturbed.
3. Saliva is a clear, slightly acidic mucoserous exocrine secretion.
• Whole saliva:
“It is a complex mixture of fluids from major and minor salivary
glands and from gingival crevicular fluid, which contains oral
bacteria and food debris”. Edgar,1992.
4. Development of salivary glands
The three major sets of glands
• Parotid, submandibular,sublingual
• they originate in a uniform manner by oral ectodermal
epithelial buds invading the underlying mesenchyme
5. Classification
It is based on
• Size and location
• The histochemical nature of secretory products
On basis of size
Major salivary glands
Parotid gland
Submandibular gland
Sublingual gland
Minor salivary glands
Labial and buccal
glands
Glossopalatine glands
or lingual glands
10. 99% water
1% large organic and inorganic molecules.
Large organic
molecules
• protein,
• glycoproteins
• lipids
Small organic
molecules
• glucose
• urea
Electrolytes
• sodium,
• calcium,
• chloride
• phosphates
11. • Organic constituents:
– Protein
• Comprise approx. 200mg/100ml only 3% of the protein
conc. in plasma.
– Enzymes
– Immunoglobulins
– Antibacterialproteins
– Mucousglycoproteins
– Tracesof albumin,polypeptides andoligopeptides.
12. • Inorganic constituents:
– sodium, potassium, chloride and bicarbonate are the main
contributors to the osmolarity of saliva.
– Bicarbonate is also the principal buffer in saliva.
– Thiocyanate activates antibacterial effect of
sialoperoxidase.
– Fluoride content similar to plasma
13. The known stimulus may be
• Psychological (eg. Thinking of tamarind)
• Visual (eg. Seeing delicious food)
• Taste (tasting good food)
• Others (during vomiting)
Stimulated secretion of saliva is due to reflex (salivary reflex)
• Conditional
• Unconditional
Regulation of secretion
Spontaneous Stimulated
14. Factors influencing the composition of saliva
Flow Rate
• The accepted range of normal flow for unstimulated
saliva is anything above 0.1ml/min.
• For stimulated saliva flow rate is approx 0.2ml / min.
• As the flow rate increases, the concentration of proteins,
sodium, chloride and bicarbonate rises, while the levels of
phosphate and magnesium fall.
15. Flow rate in salivary glands according to individual
constituents
• total protein, amylase, sodium, bicarbonate
Substances whose concentration increases as the
flow rate increases:
• phosphate, urea, aminoacid, uric acid, serum, albumin
Substances whose concentration decreases with
the increase in flow rate:
• potassium, fluoride
Substances whose concentration does not change
with change in flow rate:
• Chlorine, calcium, protein bound carbohydrates
Substances whose concentration decreases at
first but increase as flow rate increases:
16. Differential
• In unstimulated whole saliva, the parotid gland contributes only about 10%
• stimulated whole saliva contains lower levels of calcium
Circadian rhythm
• The levels of calcium and phosphate ions are low in early morning.
Nature of stimulus
• salt stimulates higher protein content.
• sugar stimuli give rise to a high amylase content in saliva.
Diet
• Change in phosphate and urea conc. induced by dietary alterations
may be reflected in the saliva.
Duration of stimulus
17. Salivary function can be organized into
Mastication
and
deglutition
Taste
Facilitation
of speech
Buffering
action
Excretory
function
Starch
digestion
Maintenance
of the tooth
integrity
Antibacterial
factor
Pellicle and
plaque
formation.
18.
19. Buffering action
• bicarbonate , phosphate and amphoteric proteins: the salivary ph is
usually maintained alkaline.
• If the salivary ph falls from alkaline to acidic certain constituents of
saliva get precipitated -tartar - removing calcium from the tooth -
caries.
Mastication and deglutition
• This helps to convert food into a soft bolus which is coated with a
layer of mucous which acts as a lubricant and facilitates swallowing
(deglutition)
Taste
• has to be in solution.
• Saliva provides the water for this purpose and helps in the
appreciation of taste.
20. Starch digestion
• This is the only digestive function of saliva and is due to
ptyalin, which is a weak amylolytic enzyme
Boiled starch
Soluble starch
Erythrodextrin and maltose
Achrodextrin and maltose
Isomaltose and maltose
(Maltase converts maltose into glucose)
21. Facilitation of speech
• Saliva lubricates the oral cavity of proper activation of speech
Excretory function
• Helps in excreting certain heavy metals like lead and iodine
Maintenance of the tooth integrity
Saliva is supersaturated with calcium and phosphate ions that
provides minerals for
• post eruptive maturation.
• to counteract tooth dissolution by saliva (solubility product
principle)
• forms a film of glycoprotein on the teeth (the pellicle) that may
act as a diffusion barrier
22. Antibacterial factors: that influence bacteria.
Specific
Immunoglobulins
aggregate
specific bacteria
Non-specific
Lactoferrin
Lysozymes
Sialoperoxidase
Histidine
23. Role in oral disease
The role of saliva in oral disease is most apparent when
salivary flow is markedly reduced
• Pellicle and plaque deposition
• Plaque mineralisation to form calculus
• Dental caries
24. Pellicle and plaque deposition
• It is partly cellular, fundamentally bacterial, and partly
acellular, from bacterial, salivary and dietary sources.
It initiates plaque deposition by pellicle formation (or
cuticle) which occurs in stages
• Bathing of tooth surfaces by salivary fluid, which contains
numerous protein constituents
• Selective adsorption of certain negatively and positively
charged glycoproteins (electrostatic attraction of charged
molecules is a factor)
• Loss of solubility of the adsorbed proteins by surface
denaturation and acid precipitation
• Alteration of the glycoproteins by enzymes from bacteria and
the oral secretions
25. pellicle formation ( made up of salivary proteins and other macromolecules)
The amino-terminal segment of Proline-rich proteins adheres to the tooth,
leaving the carboxy-terminal region free to bind to the bacteria.
saliva continues to provide agglutinating substances to the intercellular matrix
and bacterial intercellular adhesion results.
Secondary colonization. Salivary proteins and carbohydrates serve as a substrate
for metabolic activity of the bacteria.
Salivary urea and ammonia have a profound effect on bacterial activity and
final plaque ph
26. Plaque mineralization and calculus formation
• Salivary calcium, phosphorus, magnesium, sodium, and
potassium become part of the gel like interstices of the plaque
and influence mineralization.
• Esterase, pyrophosphatase and possibly acid phosphatase may
play a role in plaque mineralization
• Persons who are heavy calculus formers have higher levels of
salivary glycoproteins than non-calculus formers.
27. Dental caries
Saliva can affect caries in five general ways
• To mechanically cleanse and thus lessen plaque accumulation
• To reduce enamel solubility by plaque modification through
calcium, phosphate and fluoride
• To buffer and neutralize the acids either produced by
cariogenic organisms or introduced directly through diet
• By direct anti bacterial activity
• By aggregation or clumping bacteria and reducing adherence
to tooth surface
28. SALIVA AS A DIAGNOSTIC TOOL
Analysis of saliva may be useful for the diagnosis of
• hereditary disorders
• autoimmune diseases
• malignant and endocrinal disorders
• assessment of therapeutic levels of drugs
• monitoring of illicit drug use
29. Collection of saliva
Aspects to be considered to collect saliva
Whether resting or stimulated saliva will be detected, and if
stimulated, how will it be stimulated?
The amount of saliva needed to complete the analysis
Pre-treatment of saliva before assaying and storage until assay.
If the patient may be taking medication or have a disease causing
dry mouth
Whether quantitative or qualitative assays will be seen on the
specimens
30. The main methods of whole saliva collection
Draining
Spitting
Suction
absorbent
methods
In it preweighed sponge is placed in the pt’s mouth for a set
amount of time. After collection the sponge is weighed again
and the volume of saliva is determined.
It requires the pt. to allow saliva to flow from the mouth into
a pre weighed test tube or graduated cylinder for a time
period.
Pt. allows the saliva to accumulate in the mouth and
then expectorates into a pre weighed graduated
cylinder usually every 60 sec for 2 to 5 min
It uses an saliva ejector to draw saliva from the mouth
into a test tube for defined time period.
31. Commercially available kits are
Sialometer, Salivette, Omnisal,
Orasure are used for collection
of saliva.
Paper indicator strips to
measure the pH of saliva.
Strip test to measure the
buffer capacity of saliva
Dip slide test for oral bacteria. Lab on chip Oral fluid nanosensor test
Testing of saliva
32.
33. Advantages
• Can be collected non invasively
• more accurate reflection of the active hormone in the body
specially steroid hormones
• can be collected with devices that will be stable at room
temperature for extended periods
• the health hazards associated with blood collection such as
cross contamination among patient do not apply to saliva
• secretory leucocyte protease inhibitor (SLPI) may be another
factor contributing to the safety of saliva as a diagnostic
specimen. SLPI expresses anti virus activity against free HIV-
1 and lymphocyte derived tumor cell lines.
34. Disadvantages
• Direct spitting into a tube or absorption in cotton balls
performs most saliva collections. samples not sterile and
subjected to bacterial degradation over time
• Interpretation of saliva assays is still difficult although
diurnal and monthly patterns generally parallel serum
values
• Polar hormones such as thyroxin and the peptide hormones
are subjected to variations by flow rate, so reliable levels
cannot be obtained in saliva
• Proficiency testing programmes are not yet available for
saliva, which makes validation of laboratory tests for
certified laboratories difficult.
35. Clinical problems in which saliva contributes to diagnosis.
• Digitalis toxicity.
• Stomatitis in cancer chemotherapy
• Immuno deficiency of secretory IgA
• Cigarette usages
• Dietary nitrates, nitrites and gastric cancer
• Ovulation time
36. Salivary assays in diagnosis
• Raised Na+,K+,Ca2+ and PO4
-levels
Sialadenitis
• Raised Na+,Ca2+,Mg2+ and Cl-levels
Radiation damage
• Raised Na+,Cl-and PO4
- in parotid gland saliva
• Raise total protein and 2-microglobulin levels in parotid
gland saliva
Sjogren’s syndrome
• Raised Na+,K+,Ca2+ and PO4
-levels.
• Raised total proteins ,amylase ,lysozyme in submandibular
gland saliva and glycoproteins in parotid gland saliva .
Cystic fibrosis
The findings of Mandel (1980) include the following
37. • Raised K+ levels
• Raised total protein and amylase in parotid gland saliva
Alcoholic cirrhosis
• Raised Ca2+ levels
• Raised total protein
Hyperparathyroidism
• Raised Ca2+ levels
• Raised total protein, IgA, IgG, IgM, and raised glucose levels
Diabetes mellitus
• Depressed HCO3
-levels
Chronic pancreatitis
• Possibly raised Na+ levels
Psychiatric illness (not other wise specified)
• Raised Na+ and K+levels
Digitalis intoxication
• Depressed amylase and lysozyme levels
Sarcoidosis
38. Drug monitoring
• Drug levels in saliva reflect the free non protein bound portion in
plasma
• therapeutic drug monitoring is most effectively used when the saliva
to plasma concentration ratio is constant
The determination of drugs in saliva depends on their
• concentration in the blood
• diffusion capacity
• liposolubility and molecular size.
Examples
anti convulsant drugs such as phenytoin, primidone, ethosuximide,
carbamazepine
theophylline monitoring for asthmatic children
salivary lithium in manic depressive patient
high correlation between ethanol concentrations in saliva and in serum.
39. Screening for antiviral and viral antigens
complete concordance between salivary and serum finding
for HIV positive people
the proportion of specific to total immunoglobulins is
similar in the saliva and serum of each individuals
40. Hormones monitoring
• the liposoluble hormones with lower molecular weights can be
detected reliably (Kaufman E, 2002).
• The steroid hormones assayed in saliva includes cortisol,
testosterone, 5α dihydro testosterone, 17 beta hydroxy
progesterone, progesterone, 17beta estradiol, sterol, estrone.
• estriol measurement during pregnancy for detecting fetal
growth retardation and the estriol progesterone ratios for
preterm labor.
• significant correlation between salivary and plasma insulin and
melatonin
• Higher salivary cortisol levels detected in severe periodontitis,
a high financial strain, and high emotion-focused
coping(Genco et al. 1998).
41. Application of salivary analysis of medicine
inorganic ions
• thiocyanate ion excellent indicator of smokers
• High levels of nitrate in the saliva associated with carcinoma
of the digestive tract
42. Saliva for periodontal diagnosis
• Probing depth
• Clinical attachment level
• Bleeding on probing (BOP)
• Plaque index (PI)
• Radiographic loss of alveolar bone (Polson & Goodson 1985)
• Monitoring of the microbial infection (Listgarten 1992)
• Analysis of the host response in GCF (Lamster 1997)
• Genetic analysis (Kornman 1997)
information primarily about disease severity, and are not useful
measures of disease activity.
43. Limitations of traditional methods
• Insufficient for determining site of active disease
• Insufficient for quantitative measurement of response to
therapy
• Insufficient for measuring susceptibility to future disease
progression.
• Time consuming
• Subject to measurement error
44. Why Saliva
• Contains biomarkers for unique physiological aspects of
periodontal/peri-implant disease.
• Quantitative changes in the biomarkers can identify patients
with enhanced disease susceptibility
• Identify sites with active disease.
• Identifying sites that will have active disease in future.
• Simple and non-invasive method of collection
45. Proposed markers for disease include
• proteins of host origin (i.e. enzymes, immunoglobulins)
• phenotypic markers (epithelial keratins)
• host cells, hormones (cortisol)
• bacteria and bacterial products
• volatile compounds and ions (Mandel 1991)
46. Markers affecting the dental biofilm
marker Relationship with periodontal disease periodontal disease
Specific Immunoglobins
IgA,IgM,IgG
Interfere in adherence and bacterial
metabolism, increased conc. in saliva of
periodontal patients
Chronic and Aggressive
Non specific Mucin Interfere with colonization of Aa Aggressive
Lysozyme Regulates biofilm accumulation Chronic
Lactoferrin Inhibits microbial growth, increased
correlation with Aa
Aggressive
Histatin Neutralizes LPs and enzymes known to
affect periodontium
Chronic and Aggressive
Peroxidase Interfere with biofilm accumulation,
increased correlation with periodontal
patients
Chronic
Systemic C reactive protein Increased conc found in serum and
saliva of periodontal patients
Chronic and Aggressive
47. Specific markers:
• Ig are important specific defense factors of saliva.
• the preponderant immunoglobulin found is IgA.
• Major and minor salivary glands contribute all of the secretory
IgA (sIgA) and lesser amounts of IgG and IgM.
48. sIgA
• forms specific immune defense mechanism in saliva
• parotid gland responsible for the majority of the IgA (Nair
1986).
• important in maintaining homeostasis in the oral cavity.
• control the oral micro biota by reducing the adherence of
bacterial cells to the oral mucosa and teeth (Morcotte and
Lovice.1998)
• two subclasses IgA1 and IgA2.
• sIgA levels, undetectable in newborns, increase progressively
and reach adult values in stimulated saliva by 2–4 years of age,
and in unstimulated saliva by 6–8 years of age (Burgio1980).
49. IgG
present in low concentration.
concentration increases during inflammation of the
periodontal tissues (Wilton,1989, Shapiro, 1979).
50. Immunoglobulin isotypes in saliva
• Basu (1976) increased IgG concentration in saliva and
decreased IgA concentration before periodontal therapy as
compared to post-treatment levels. Salivary levels of IgG and
IgA found to be higher in a group of NIDDM patients with
periodontitis.
• Guven (1982) positive correlation between the severity of
inflammation and IgA concentration.
• Sandholm (1984) Salivary IgA, IgG, and IgM levels were
higher in the JP patients
• Harding (1980) found decreased levels of IgA and IgG, but
elevated sIgA concentration, in saliva of the patients with
NUG.
51. Specific immunoglobulins in saliva
• Eggert (1987) saliva from treated periodontitis patients had
higher IgA and IgG for periodontal pathogens (P.g and T.d).
• Sandholm (1987) The level of salivary IgG antibody to A.a
was significantly elevated in 55% of the patients with
untreated JP and in 28% of the treated patients and 57% in AP.
• Schenk(1993)patients with a low mean number of bleeding
gingival units demonstrated significantly higher levels of
salivary IgA antibody reactive with S.mutans, A.a, and
Eubacterium.
52. Non specific markers:
Mucins
• glycoproteins produced by salivary glands
• mucins(MG1 and MG2)
• cytoprotection
• Lubrication
• protection against dehydration
• maintenance of viscoelasticity in secretions.
• The mucin MG2 affects the aggregation and adherence of
bacteria (A.a) and decreased conc of MG2 in saliva may
increase colonization with Aa.
53. Enzymes
Enzymes found in whole saliva originate from three
main sources:
(1) the actual salivary secretions per se
(2) the GCF, stemming from PMNs and tissue
degradation
(3) bacterial cells from dental biofilms and mucosal
surfaces. (Chauncey 1961).
Ingman et al. 1993 enzyme activity in whole saliva appears to
reflect the severity of periodontal disease
54. • salivary enzymes reported in increased conc in
periodontal disease are hyaluronidase, lipase, β-
glucuronidase and chondritin sulfatase, amino acid
decarboxylases, catalase, peroxidase and collagenase.
• proteolytic enzymes in the saliva contribute to the
initiation and progression of periodontal disease
• saliva contains antiproteases that inhibit cysteine
proteases such as cathepsins, antileucoproteases that
inhibit elastase and (TIMP) to inhibit the activity of
collagen – degrading enzyme
55. • Nakamura and Slots (1983) noted higher enzyme
activity in AP patients for alkaline phosphatase,
esterase, β-glucuronidase, β-glucosidase, and cysteine
aminopeptidases in JP.
• Gibert et al. relationship between attachment loss in
the periodontal group and a drop in ALP activity in
serum.
• Zambon et al. (1985) reduced salivary levels of
caprylate esteraselipase, leucine, valine and cysteine
aminopeptidases, trypsin, b-galactosidase, b
glucuronidase and b-glucosidase
decrease in proportions of subgingival black pigmented
bacteroides and motile organisms noted after treatment,
suggesting them as potential source.
56. Lysozyme
• hydrolytic enzyme cleaves the linkage between the glycopeptide (muramic
acid) – found in the cell wall of certain bacteria’s.
• cause lysis of bacterial cells by interacting with monovalent anions and
with proteases found in saliva. leads to destabilization of the cell membrane
as a result of the activation and degranulation of endogenous bacterial
autolysins.
• Lysozyme targets Veillonella species and A.a.
• It probably repels certain transient bacterial invaders of the mouth (Pullock
et al 1985)
Jalil et al. (1993) patients with low levels in saliva are more
susceptible to plaque accumulation which is considered as risk
factor for periodontal disease.
57. Lactoperioxidase
• Peroxidase activity is derived from 2 sources.
– Human lactoperoxidase (HS-LPO) is synthesized and
secreted by salivary glands.
– Myeloperoxidase (MPO) is found in PMN leucocytes &
migrate in to oral cavity by gingival crevice.
Salivary peroxide
• removes toxic hydrogen peroxide produced by oral
microorganisms and reduces acid production in the dental
biofilm, thereby decreasing plaque accumulation.
• Guven et al. (1996)higher activity in the diabetes patients,
serve as a marker for gingival inflammation
58. The lactoperoxidase-thiocynate system in saliva
catalyses the formation of bactericidal compounds e.g.
hypothiocyanate, by peroxidation of thiocyanate
bactericidal to certain strains of lactobacillus and streptococcus
prevents the accumulation of lysine and glutamic acid, both of
which are essential for bacterial growth.
Myeloperoxidase
• released by leukocytes and is bactericidal for Actinobacillus
• inhibits the attachment of Actinomyces to hydroxyapatite.
• Increased MPO activity was found in saliva of RPP and AP.
59. Histatin
• salivary protein with antimicrobial properties
• secreted from parotid and submandibular glands.
• neutralizes the LPS located in membrane of gram negative
bacteria.
• inhibitor of host and bacterial enzymes involved in the
destruction of the periodontium
• involved in the inhibition of release of histamine.
60. Other proteins
Cysteine proteinases
• proteolytic enzymes originated from pathogenic bacteria,
inflammatory cells, osteoclasts and fibroblasts.
• collagenolytic activity, which may cause tissue destruction.
(Cutler et al. 1995).
• Cystatins are physiological inhibitors of cysteine proteinases
• Henskens,1996 After periodontal treatment, total cystatin and
cystatin C concentration decreased to control levels.
• Evren, 2008 total saliva cystatin C levels were higher in health
61. Lactoferrin
•is a iron binding glycoprotein produced by salivary glands
•inhibits microbial growth by sequestering iron from the
environment thus depriving bacteria.
•strongly upregulated in mucosal secretions during gingival
inflammation and is detected at high conc. in saliva of patients
with periodontal disease.
•effective against Actinobacillus species (Arnold, 1980)
62. Platelet activating factor (PAF)
• a potent phospholipid mediator of inflammation
• Garito,1995 A significant positive correlation was observed
between the level of PAF in saliva and measures of periodontal
inflammation
63. Serine proteinases
Elastase
• Produced by PMN leukocytes.
• Elastase is held in inactive state within cell, by inhibitors
(α1proteinase inhibitor and α2 macroglobulin).
• Elastase is able to degrade proteoglycans and can also activate
latent collagenase
• Nieminen,1993 levels correlate with bleeding sites
• significantly higher in patients group from gingivitis to
periodontitis.
• Ingman,1993 higher in untreated AP patients.
64. Fibronectin
• is a glycoprotein, promotes selective adhesion and
colonization of certain bacterial species, while
inhibiting others.
• Gibbons et al. (1986) Higher proteolytic activity
observed in saliva collected immediately after
awakening, and the levels of enzyme activity
correlated with the state of cleanliness.
• Lamberts et al. (1989) salivary fibronectin levels
(used as an index of GCF flow into the oral cavity),
did not differ significantly between individuals with
or without periodontal disease.
65. Defensins
• These are antimicrobial peptides which are induced in
epithelial tissues upon inflammation.
• These peptides are part of the innate immune system, have
broad spectrum antibacterial and antifungal activity.
Calprotectin
• Main source of salivary calprotectin are GCF and oral surface
epithelium.
• Salivary calprotectin levels are raised in patients with oral
candidiasis.
66. Epidermal growth factor (EGF)
• involved in oral wound healing and stimulates epithelial cells.
• Oxford(1998) found a transient increase in salivary EGF levels
in response to periodontal surgery.
Vascular endothelial growth factor (VEGF)
a multifunctional angiogenic cytokine important in inflammation
and wound healing.
Taichman 1998 Higher levels of VEGF were detected in whole
saliva from periodontitis patients
67. Epithelial keratins
• Epithelial cells from the lining of the oral cavity found in
saliva
• McLaughlin (1996) higher conc of keratin in GCF at sites
exhibiting gingivitis and periodontitis
• not observed in saliva.
68. Inflammatory cells
• leukocytes in saliva varies from person to person, and vary for
an individual during the course of the day.
• Klinkhammer (1968) standardized collection and counting of
leukocytes in saliva
• developed the orogranulocytic migratory rate (OMR). The
OMR was found to be correlated with gingival index
• Raeste(1978) the OMR reflects the presence of oral
inflammation
69. Salivary ions
Calcium(Ca)
• A high concentration of salivary Ca was correlated with good
dental health
• no relationship detected with periodontal bone loss as
measured from radiographs (Sewon & Makela 1990).
• Sewon et al. 1990 salivary Ca, and the saliva Ca to phosphate
ratio were higher in periodontitis- affected subjects
70. Volatiles
• Salivary volatiles suggested as possible diagnostic markers
and contributory factors in periodontal disease.
• primarily hydrogen sulfide and methylmercaptan(Rosenberg &
McCulloch 1992).
• pyridine and picolines were found only in subjects with
moderate to severe periodontitis (Kostelc et al. 1980).
71. Vitamins
thiamine, riboflavin, niacin, pyridoxine, pantothenic acid, biotin,
folic acid and vitamin C and B12, and vitamin K
Coagulation factors
coagulation factors VIII, IX, X, plasma thromboplastin
antecedent (PTA) and the Hageman factors
hasten blood coagulation and protect the wounds from bacterial
invasion.
72. Bacteria
• De Jong,1984 serve as a growth medium for oral Streptococus
species and A. viscous.
• Bowden ,1997 number of bacterial cells for a in unstimulated
saliva may show active growth in plaque.
Oral microbial rinse test (Oratest)
• described by Rosenberg,1989
• for estimating oral microbial levels.
• provides a reliable estimate of gingival inflammation
73. • Asikainen,1991 A.a when recovered from subgingival sites
was also found in 69.9% and 35.9% of the samples of
stimulated and unstimulated saliva.
• Umeda,1998 bacterial detection in whole saliva had a
sensitivity of 42.6% for A. a, 68.4% for T.f, 97.8% for P. g, and
88.7% for P. i. The specificity of bacterial detection for these
microorganisms in saliva was 88.5%, 71.2%, 77.9% and
77.1%.
• Von Troil-Linden,1995 salivary levels of the periodontal
pathogens reflected the periodontal status.
• Christoph A,2009 Elevated salivary MMP-8 and T. denticola
biofilm levels in periodontal disease
74. Systemic markers related to periodontal infection
C-reactive protein
• released during the acute phase of an inflammatory
response
• produced by liver and stimulated by circulating cytokines
such as TNFa,IL1
• may reach saliva via gcf or salivary glands.
• High levels associated with chronic and aggressive
periodontal diseases
• measurable from saliva using lab on chip method.
75. Markers of periodontal soft tissue inflammation
• During the initiation of an inflammatory response
PGE2,IL1β,IL6,TNFa are released from the cells of junctional
epithelium and from ct fibroblasts, macrophages and pmn
leckocytes.
• Subsequently enzymes such as MMP8,9,13 are produced by
pmn and osteoclasts leading to degradation of ct collagen and
alveolar bone.
• Bradon,2008 increase in TNF in periodontitis
76. Markers of alveolar bone loss
MMP
Host proteinases responsible for both tissue degradation and
remodeling.
MMP-8 most prevalent in diseased tissues and gcf
found in elevated level in saliva from patients with periodontal
disease
elevated in peri-implant sulcular fluid in peri-imlantitis lesions.
Integrated Microfluidic Platform for Oral Diagnostics
(IMPOD) mean MMP-8 concentration in the saliva of the
periodontally healthy individuals was 10-fold less than that of
the periodontally diseased patients Herr AE,2007
77. MMP-9,is produced by neutrophils and degrades collagen, intercellular
ground substance.
2 fold increase found in patients with progressive attachment loss.
Makela et al. (1994) higher concentration of MMP-9 in whole saliva
of periodontitis patients
MMP-13 has been implicated in peri-implantitis
found in elevated level corresponding to the vertical bone loss around
loosening dental implants.
Hayakawa et al. (1994) reported lower conc of TIMP-1 in whole
saliva of patients with periodontal disease with higher collagenase
activity
Increased TIMP-1 and decreased collagenase activity observed after
initial therapy
78. Uitto et al. (1990)
Collagenase originated from PMNs entering the oral cavity
through the gingival sulcus.
activity was in higher and active form in the periodontitis
patients.
Very little collagenase activity detected in saliva of edentulous
subjects.
79. Pyridinoline Cross-Linked Carboxyterminal Telopeptide
of Type I Collagen (ICTP)
• to detect bone resorption in periodontitis and
periimplantitis
• Palys et al. strongly correlated with whole subject levels
of several periodontal pathogens including T.f, P. g, P. i,
and T. d.
• Golub et al. 70% reduction in GCF ICTP levels after
treatment.
80. Osteonectin
polypeptide that binds strongly to hydroxyapatite and other
extracellular matrix proteins including collagens.
has been implicated in the early phases of tissue mineralization.
Osteopontin
• highly concentrated at sites where osteoclasts are attached to
the underlying mineral surface
• conc increased proportionally with the progression of disease
81. CONCLUSION
The knowledge of normal salivary composition, flow and
function is extremely important on a daily basis when treating
the patients.
Recognition should be given to saliva for the many contribution it
makes to the preservation and maintenance of oral and
systemic health
Saliva as a diagnostic specimen can give not only the same
information as serum testing but also additional or new
information that cannot be obtained from serum.
82. • The device performs rapid microfluidic chip-based
immunoassays (<3–10 min) with low sample volume
requirements (10 μL) and appreciable sensitivity (nM–
pM). Our microfluidic method facilitates hands-free
saliva analysis by integrating sample pretreatment
(filtering, enrichment, mixing) with electrophoretic
immunoassays to quickly measure analyte
concentrations in minimally pretreated saliva samples.
The microfluidic chip has been integrated with
miniaturized electronics, optical elements, such as
diode lasers, fluid-handling components, and data
acquisition software to develop a portable, self-
contained device.