THIS PRESENTATION INCLUDES:
INTRODUCTION
MAIN BLOOD SUPPLY BRANCHES TO PERIODONTIUM
BLOOD SUPPLY TO MAXILLARY TEETH AND PERIODONTIUM
BLOOD SUPPLY TO MANDIBULAR TEETH AND PERIODONTIUM
VENOUS DRAINAGE OF MAXILLARY AND MANDIBULAR TEETH AND PERIODONTIUM
BLOOD SUPPLY TO EACH COMPONENT OF PERIODONTIUM
CLINICAL SIGNIFICANCE OF BLOOD SUPPLYING THE PERIODONTIUM
CLINICAL CORELATIONS WITH GINGIVITIS AND PERIODONTITIS
CONCLUSION
REFERENCES
THIS PRESENTATION INCLUDES:
INTRODUCTION
MAIN BLOOD SUPPLY BRANCHES TO PERIODONTIUM
BLOOD SUPPLY TO MAXILLARY TEETH AND PERIODONTIUM
BLOOD SUPPLY TO MANDIBULAR TEETH AND PERIODONTIUM
VENOUS DRAINAGE OF MAXILLARY AND MANDIBULAR TEETH AND PERIODONTIUM
BLOOD SUPPLY TO EACH COMPONENT OF PERIODONTIUM
CLINICAL SIGNIFICANCE OF BLOOD SUPPLYING THE PERIODONTIUM
CLINICAL CORELATIONS WITH GINGIVITIS AND PERIODONTITIS
CONCLUSION
REFERENCES
Bone loss and patterns of bone destructionvidushiKhanna1
- introduction
- bone resorption
- factors causing bone destruction in periodontal disease
-- destruction by extension of gingival inflammation
--- histopathology
--- pathways of spread of inflammation
--- radius of action
--- periods of destruction
---- mechanism of destruction
-- bone destruction caused by TFO
-- bone destruction caused by systemic disorders
- factors determining bone morphology in periodontal disease
-- normal variation of alveolar bone
-- exostosis
-- butressing bone formation
-- food impaction
-- agressive periodontitis
- patterns of bone destruction
-- horizontal bone loss
-- vertical or angular defects
-- osseous craters
-- bulbous bone contours
-- reversed architecture
-- ledges
- furcation involvement
-- classification
-conclusion
INTRODUCTION
DEFINITION
TYPES OF TRAUMA FROM OCCLUSION
GLICKMAN CONCEPT
WAERHAUG CONCEPT
STAGES OF TISSUE RESPONSE TO INJURY
CLINICAL AND RADIOGRAPHIC FEATURES OF TFO
CLINICAL DIAGNOSIS OF TFO
TFO AND IMPLANTS
TREATMENT OF TFO
CONCLUSION
REFRENCES
Bone loss and patterns of bone destructionvidushiKhanna1
- introduction
- bone resorption
- factors causing bone destruction in periodontal disease
-- destruction by extension of gingival inflammation
--- histopathology
--- pathways of spread of inflammation
--- radius of action
--- periods of destruction
---- mechanism of destruction
-- bone destruction caused by TFO
-- bone destruction caused by systemic disorders
- factors determining bone morphology in periodontal disease
-- normal variation of alveolar bone
-- exostosis
-- butressing bone formation
-- food impaction
-- agressive periodontitis
- patterns of bone destruction
-- horizontal bone loss
-- vertical or angular defects
-- osseous craters
-- bulbous bone contours
-- reversed architecture
-- ledges
- furcation involvement
-- classification
-conclusion
INTRODUCTION
DEFINITION
TYPES OF TRAUMA FROM OCCLUSION
GLICKMAN CONCEPT
WAERHAUG CONCEPT
STAGES OF TISSUE RESPONSE TO INJURY
CLINICAL AND RADIOGRAPHIC FEATURES OF TFO
CLINICAL DIAGNOSIS OF TFO
TFO AND IMPLANTS
TREATMENT OF TFO
CONCLUSION
REFRENCES
this ppt depicts pattern of bone destruction. its a very good slide show showing the process of bone formation, bone destruction and their patterns in periodontal diseases.
BONE LOSS AND PATTERNS OF BONE DESTRUCTION ishu.pptxDr. Ishu SINGLA
Presentation on topic Bone Loss And Patterns of Bone Destruction.
This is for reading and knowledge purpose only. Text is taken from Standard books only.
This ppt gives information about alveolar bone . I am a post graduate student from the department of periodontics and implantology , I've tried to make the topic as easy as possible. Hope it is useful for the ug students.
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 .
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
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
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
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.
2. CONTENTS
Introduction
Development and Anatomy
Histologic features
Radiographic features
Pathologies involving loss of Alveolar bone
Alveolar bone & implants
Repair and regeneration
Conclusion
References
3. Introduction
The term periodontium describes tissues which:
1. Anchor the teeth to the bones of the jaws
2. Provide interdental linkage of the teeth within the dental arch
3. Facilitate epithelial lining of the oral cavity in the region of the erupted tooth.
The developmental, biological and functional unit of periodontium:
1. Gingiva
2. Root cementum
3. Periodontal ligament
4. Alveolar bone proper
4. Alveolar bone
Alveolar bone is defined as the parts of maxilla and mandible that form
and support the socket of teeth.
CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY- Jan Lindhe pg:34
Together with the root cementum and periodontal ligament, the alveolar
bone constitutes the attachment apparatus of the teeth.
Forms when tooth erupts to provide osseous attachment to the forming
PDL, disappears gradually after tooth is lost.
Develops and undergo remodeling with tooth formation, hence tooth-
dependent bony structures.
Size, shape, location and function of teeth determine their morphology.
6. Development
Formed during fetal growth by intramembranous ossification and consists of
a calcified matrix with osteocytes enclosed within spaces called lacunae.
During embryogenesis, the skeleton forms by either a direct or indirect
ossification process.
In the case of the mandible and the maxilla, mesenchymal progenitor cells
condensate and undergo direct differentiation into osteoblasts, a process
known as intramembranous osteogenesis.
Alveolar bone lost as a result of an injury, disease, or trauma undergoes a
repair process that is essentially a combination of endochondral and
intramembranous complementary osteogenic processes (Rabie et al., 1996;
Virolainen et al., 1995).
A similar process occurs in most of the bone-related implant site
development techniques, where osteoconduction, osteoinduction, and
osteogenesis are exploited.
7. Anatomy
Alveolar process consists of:
1. External plate of cortical bone
2. Inner socket wall- Alveolar bone proper
3. Cancellous trabeculae- Supporting alveolar bone
10. Trabeculae
2 main types
Type1:
The interdental and interradicular trabeculae are regular & horizontal in a
ladder like arrangement.
This type is seen most often in mandible.
Type 2:
Shows irregularly arranged, numerous, delicate interdental and
interradicular trabeculae.
This type is more common in maxilla.
12. Haversian system
Consists of the haversian canal and the Volkmann’s canal.
Haversian canal located in the center of the osteon.
Volkmann’s canal are the connecting vessels which connect the Haversian
canal.
They provides nutrition to the bone.
14. Histologic features
Three types of cells are distinguished:
1. Osteoblasts
2. Osteocytes
3. Osteoclasts
Osteoblasts:
Produce the organic matrix of bone are differentiated from pluripotent
follicle cells.
Comprise a mixed population of preodontoblasts with large nuclei and
fibroblast like cells with small nuclei
15. Osteocytes:
Arise from odontoblasts which becomes entrapped into bone.
Located in bony lacunae and are connected by long cell projections.
Immature osteocytes are smaller than osteoblasts, but have a similar
structure.
Mature osteocytes have a reduced set of organelles.
Osteoclasts:
Large, multinucleated giant cells, located on the surface pits of the
bone(Howship’s lacunae).
Arise by fusion of hematopoietic, mononuclear precursors of bone marrow.
Resorption of bone is facilitated by acidic phosphatases and other
hydrolytic enzymes.
16. Osteoblasts and osteoclasts
The combined process of bone formation and resorption by simultaneous
activity of osteoblasts and osteoclasts is called as coupling.
19. Intercellular matrix
Bone consists of 2/3rd inorganic matter and 1/3rd organic matrix.
Inorganic matter:
Calcium
Phosphate
Hydroxyl
Carbonate
Citrate
Trace amounts of sodium, magnesium and fluorine.
20. Organic matrix:
Type 1 collagen- 90%
Noncollagenous proteins such as :
• Osteocalcin
• Osteonectin
• Bone morphogenetic protein
• Phosphoproteins
• proteoglycans
21. Bone morphogenic protein
These are well studied group of growth factors belongs to the transforming
growth factor(TGF-β) subfamily, involved in the process of bone healing.
BMP induces the formation of both bone and cartilage by stimulating the
cellular events of mesenchymal progenitor cells.
However, only a subset of BMPs, most notably BMP 2,4,6,7,9 has
osteoinductive activity.
22. Guided bone regeneration
Guided Bone Regeneration (GBR) was originally developed by Hurley et al.
in 1959 and Boyne in 1964.
Barrier membranes are used, which are bio-inert materials that serve to
protect the blood clot and prevent soft tissue cells (epithelium and
connective tissue) from migrating into the bone defect, allowing
osteogenic cells to be established.
Barrier membranes could be either resorbable or non resorbable.
Osteoblasts derived from the periosteum and bone are selectively induced
on the osseous defect area, facilitating new bone formation.
23. GBR using a barrier membrane has become widely used for bone
regeneration of osseous dehiscences and fenestrations and for localized
ridge augmentation and immediate implant placement.
GBR in implant therapy is especially useful for fixture placement with dehis-
cence defects or fenestration defects.
In alveolar ridges with marked facial/buc- cal depressions or in knife-edge
alveolar crests, the position and direction of fix- ture placement is restricted.
Improvement of alveolar ridge morphology becomes possible, however,
with GBR.
24. Radiographic features
The interdental bone normally is outlined by a thin, radiopaque line
adjacent to the periodontal ligament (PDL) and at the alveolar crest,
referred to as the lamina dura.
Because the lamina dura represents the cortical bone lining the tooth
socket, the shape and position of the root and changes in the angulation
of the x-ray beam produce considerable variations in its appearance.
26. conditions involving loss of Alveolar
bone
The various causes of alveolar bone loss are:
I. Extension of gingival inflammation
II. Trauma from occlusion
III. Systemic factors
IV. Orthodontic treatment
V. Periodontitis
VI. Periodontal abscess
VII. Food impaction
VIII. Overhanging restoration
IX. Adjacent tooth extraction
X. Ill-fitting prosthesis
27. Extension of gingival inflammation
Most common cause of bone loss in periodontal disease is extension of
inflammation from marginal gingiva into supporting periodontal tissues.
Inflammatory invasion of bone surface and intial bone loss that follows mark
the transition from gingivitis to periodontitis.
the transition from gingivitis to periodontitis is associated with changes in
compostion of bacterial plaque.
In advanced stages number of motile organisms and spirochetes increases.
28. Mechanism of bone destruction
Factors involved are bacterial and host mediated
Bacterial plaque induces bone progenitor cells into osteoclasts
In aggressive periodontitis, bacterial micro colonies have been found
between collagen fibers and over the bone surface, suggesting a direct
effect.
Host factors released by inflammatory cells are capable of inducing bone
resorption.
These include host produce prostaglandins, IL-1a IL- β and TNF-a.
30. Extends along the collagen fiber bundles and follows the course of blood
vessels through loosely arranged tissues around them into the alveolar bone
Interproximally, inflammation spreads to the loose connective tissue around
the blood vessel channels that perforate the crest of the interdental
septum at the center of the crest, towards the side of the crest or at the
angle of the septum.
Also, inflammation may enter the bone through more than one channel.
Spread of inflammation from gingiva directly to PDL is less frequent.
31. Facially and lingually, inflammation from the gingiva spreads along the
outer periosteal surface of the bone and penetrates into the marrow
spaces through vessel channels in the outer cortex.
It courses from gingiva to the bone, inflammation destroys the gingival and
transeptal fibers, reducing them to disorganized granular fragments
interspersed among the inflammatory cells and edema.
32. Trauma from occlusion
Trauma from occlusion can produce bone destruction either in the absence or
presence of inflammation.
These changes are reversible in that they can be repaired if the offending
forces are removed.
However, persistent trauma from occlusion results in funnel shaped widening of
the crestal portion of the periodontal ligament, with resorption of the adjacent
bone.
These changes, cause the bony crest to have an angular shape.
It represent adaptation of the periodontal tissues aimed at cushioning
increased occlusal forces, but the modified bone shape may weaken tooth
support and cause tooth mobility.
When combined with inflammation, trauma from occlusion aggravates the
bone destruction caused by the inflammation and causes bizarre bone
patterns.
33. Trauma from occlusion
Occlusal force beyond physiological limits
Increased compression& tension of PDL
Increased osteoclasis
Necrosis of PDL and bone
Resorption of bone and tooth structure
35. Systemic factors
In recent years, interest has increased in the possible relationship between
periodontal bone loss and osteoporosis.
Osteoporosis is a physiologic condition of post menopausal women
resulting in loss of bone mineral content and structural bone changes.
Periodontal bone loss may also occur in generalized skeletal disturbances
by mechanism that may be totally unrelated to usual periodontal
problems.
36. Systemic factors
Diabetes mellitus:
A majority of well controlled studies show a higher prevalence and severity
of periodontal disease in diabetic patients than in nondiabetic patients
with similar local factors.
Findings include a greater loss of attachment, increased bleeding on
probing, and increased tooth mobility.
As with other systemic conditions, diabetes does not cause gingivitis or
periodontitis, but evidence indicates, it alters the response of periodontal
tissues to local factors, hastening bone loss & delays post surgical healing.
Alteration in collagen metabolism plays a significant role.
37. Hyperparathyroidism also known as osteitis fibrosa cystica or Von
Recklinghausen’s bone disease, exhibits loss of lamina dura and giant cell
tumors in the jaws.
Loss of lamina dura may also occur in Paget’s disease, fibrous dysplasia
and osteomalacia.
Reports have suggested that 25-50% of patients with hyperparathyroidism
have oral changes that includes malocclusion and tooth mobility.
Radiographic evidence of alveolar osteoporosis with closely meshed
trabeculae, widening of PDL space, absence of lamina dura.
38. Orthodontic treatment
Bone resorption occurs when there is increased orthodontic forces beyond
the physiological limits.
Rapid orthodontic movement leads to the insufficient Lag phase period
that tends to resorb the alveolar bone to which the force is directed.
It is more common in adult patients undergoing orthodontic treatment.
Whereas in other side, the single angular defect od interdental craters
could be eliminated by the orthodontic movement of the involved teeth.
39. Orthodontic relapse, apical root resorption, and crestal
alveolar bone levels-Wendy Sharpe et al
American Journal of Orthodontics and Dentofacial Orthopedics;Volume 91, Issue 3,
Pages 252–258, March 1987
This investigation examined the relationship of postorthodontic treatment relapse to crestal
alveolar bone support and root resorption.
The subjects in the relapse group had undergone longer periods of treatment and
exhibited significantly greater crestal alveolar bone level distances, indicating greater loss
of bone support than that observed in the non-relapse group.
The distances that teeth were translated seemed to affect the extent crestal bone loss
with smaller amounts of tooth translation seemingly more prone to demonstrate tissue loss.
40. Various Bone destructive patterns in
periodontal disease:
Horizontal bone loss
Vertical/Angular defects
Osseous craters
Bulbous bone contours
Reversed architecture
Ledges
Furcation involvement
41. Horizontal bone loss
When the bone loss occurs on a plane that is parallel to a line drawn from
the CEJ of a tooth to that of an adjacent tooth, it is called horizontal bone
loss.
It is one of the common pattern of bone loss in periodontal disease.
Significant feature of aggressive periodontitis.
The bone margin remains roughly perpendicular to the tooth surface.
43. Localized Aggressive Periodontitis
Localized Aggressive Periodontitis Localized aggressive (formerly “localized
juvenile”) periodontitis is characterized by the following:
1. 1. Initially, bone loss in the maxillary and mandibular incisor and/or first
molar areas, usually bilaterally, resulting in vertical, arc like destructive
patterns.
2. 2. As the disease progresses, loss of alveolar bone may become
generalized but remains less pronounced in the premolar areas.
45. Vertical bone loss
Vertical or angular defects occur in an oblique direction, leaving a
hollowed-out trough in the bone alongside the root.
The base of the defect is located apical to the surrounding bone.
Resorptive bone patterns may take a vertical or funnel form, resulting in
formation of infrabony defects.
Vertical bone loss usually consists of one or many infrabony pockets,
because the base of the pocket is usually located apical to the crest of the
surrounding bone.
Angular defects are classified on the basis of the number of osseous walls
47. Bone wall defects
Classified by Goldman and Cohen(1958)
One walled osseous defects where only one wall is present.
The one wall vertical defect is called as hemiseptum.
Two walled osseous defects where two walls are present.
Three walled osseous defects where three walls are present.
Interproximal vertical defects can often be detected radiographically,
whereas radicular surface vertical defects are not readily visible.
49. Interdental osseous craters
Interdental osseous craters are concavities in the crest of the alveolar septa
centered under the contact point of adjacent teeth.
As cancellous bone is more vascular and less dense than cortical bone it is
likely that, the central cancellous part of a broad alveolar septum will
resorb more rapidly than the lateral parts made up of cortical bone forming
interdental crater.
Following are the reasons for the high frequency of interdental craters:
a) The interdental area collects plaque and is difficult to clean.
b) The normal flat or even concave faciolingual shape of the interdental septum in
lower molars may favor crater formation.
c) Vascular patterns from the gingiva to the center of the crest may provide a
pathway for inflammation.
51. Bony exostosis
Bulbous bone contours are bony enlargements caused by exostoses,
adaptation to function, or buttressing bone formation which are found
frequently in the maxilla than in the mandible.
Exostosis is a localized harmless idiopathic thickening of bony tissue, whose
cause is unknown.
Depending on their location in the jaws, they are identified as torus
mandibularis (lingual mandibular plate) or torus palatinus (hard palate).
A peculiar condition consisting of bone exostosis has been reported to
occur in some patients after undergoing either a skin graft vestibuloplasty
or an autogenous free gingival graft.
A definitive female sex predilection is characteristic of this condition, which
usually presents in the canine- premolar area of the mandible or maxilla.
53. Reversed architecture & Ledges
Reversed architecture forms when the interdental septum resorbs more
rapidly than radicular bone.
Ledges are plateau-like bone margins caused by resorption of thickened
bony plates.
Furcation involvement refers to the invasion of the bifurcation and
trifurcation of multirooted teeth by periodontal disease.
56. Fenestration and dehiscence
Fenestrations are the isolated areas in which root is denuded of bone and
marginal bone is intact.
Dehiscences are the denuded areas that extend through the marginal bone.
Dehiscence and fenestration are both associated with extreme buccal or
lingual version of teeth.
It occurs in 20% of all teeth. The defects are very important clinically because
where they occur the root is covered only by the periosteum and overlying
gingiva.
58. Periodontal abscess
Periodontal abscesses are classified according to location as follows:
1. Abscess in the supporting periodontal tissues along the lateral aspect of
the root.
2. Abscess in the soft tissue wall of a deep periodontal pocket.
The former is related to bone resorption around the tooth due to its
progression in size.
60. Food impaction
Interdental bone defects often occur where proximal contact is abnormal
or absent.
Pressure and irritation from food impaction contribute to the inverted bone
architecture.
In some cases, the poor proximal relationship may result from a shift in tooth
position because of extensive bone destruction preceding food impaction.
In such patients, food impaction is a complicating factor rather than the
cause of the bone defect
62. Overhanging restoration
Overhanging restoration either in exaggerated crown margins or in class 2
restorations leads to angular bone loss.
It is most common in class 2 amalgam restorations with overhanging
margins.
Bone loss occurs due to impingement of the gingiva, followed by the
inflammatory process that leads to bone loss.
64. Adjacent tooth extraction
Normally, tooth extracted adjacent to a tooth will show significant bone
loss in the extraction site.
In case of extraction of a periodontally weakened tooth, adjacent tooth
will tend to show severe bone loss of interdental septa.
More common in delayed extraction of impacted 3rd molar.
Adjacent tooth tends to tilt towards the extracted site.
66. Ill-fitting prosthesis
Being one of the major factors for periodontal tissue destruction.
Most common in removable partial denture users.
Improper seating and design of the prosthesis could irritate the gingiva that
leads to the sequence of periodontal tissues inflammation.
Long term prosthesis users without periodic evaluation are attributed to this
consequence.
68. Alveolar bone in implants
Osseointegration is basically a union between bone and the implant
surface.
It is not an absolute phenomenon and can be measured as the proportion
of the total implant surface that is in contact with bone.
Greater levels of bone contact occur in cortical bone than in cancellous
bone, where marrow spaces are often adjacent to the implant surface.
Therefore, bone with well-formed cortices and dense trabeculation offer
the greatest potential for high degrees of bone to implant contact.
The degree of bone contact may increase with time.
69. Repair and regeneration
Remodelling is the major pathway of bony changes in shape, resistance to
force, repair of wounds.
The bone resorption with bone formation constitutes the remodelling
throughout the life.
Bone remodelling involves osteoblasts and osteoclasts which form and
resorb the mineralized connective tissue of the bone.
Regulation of bone remodelling involves harmones and local factors acting
in an autocrine and the paracrine manner.
Bone contains 99% of body`s calcium ions, Hence the major source for
calcium release when the calcium blood level decreases, which is
monitored by parathyroid gland.
70. Bone resorption
Decrease in blood calcium
Mediated by receptors on chief cells of parathyroid gland
Release parathyroid hormone(PTH)
Osteoblast stimulation to release il1and il6
Monocytes in bone area
Multinucleated osteoclasts
Resorbs bone
71. Remodelling
Alveolar bone is least stable of the periodontal tissues because of the
constant state of flux
Internal remodelling takes place by means of resorption and formation
regulated by local and systemic factors
Local factors include functional requirements on the tooth and age related
changes in the bone cells
Systemic factors are hormonal (PTH), calcitonin, vitamin D3
Remodelling affects its height contour and density and is manifestated in
the following:
1. Adjacent to PDL.
2. In relation to periosteum of facial and lingual plates.
3. Along endosteal surface of marrow spaces.
72. Conclusion
Alveolar bone is of utmost important for the healthy periodontium.
Thorough knowledge about pathologies involving alveolar bone enhances
basic methods in treating them.
Eliminating the bone loss is still being a challenge in treating periodontitis.
A better understanding of cell and molecular biology of developing and
regenerating alveolar bone offers appropriate idea in treating it for
regeneration.
73. References
Carranza’s clinical periodontology- 11th edition
Periodontology The essentials- H.P.MUELLER
Clinical periodontology and implant dentistry- Jan Lindhe(5th edition)
Chambers TJ: The cellular basis of bone resorption, Clin Orthop, p283, sep
1980.
Elliot JR, Bowers GM: Alveolar dehiscence and fenestration, periodontics
1:245, 1963
Goodson JM et al: the relationship between attachment level loss and
alveolar bone loss, J Clin periodontal 11:348, 1984.