periodontal ligament

1. SEMINAR
ON
PERIODONTAL LIGAMENT
Dr.ANUBHUTI MOHANIA

2. REFERENCES
 Orban’s,oral histology & embryology,twelth edition
 A.R.Tencate,textbook of oral histology,fifth edition.
 B.K.B.Berkovitz,G.R.Holland,B.J.Moxham,textbook of oral
anatomy,histology & embryology,third edition.
 James.K.Avery,textbook of essentials of oral histology &
embryology-a clinical approach.
 P.K.Garant,textbook of oral cells & tissues.
 Atlas of oral histology by Akramjuaim
 Carranza 9th and 10th edition

3.  Periodontal Manifestationsin Systemic Sclerosis - A Review
 Tensile behaviour of the periodontal ligament,W. J. Ralph,Journal of
Periodontal Research Volume 17, Issue 4, pages 423–426, August 1982)
 Journal of dental biomechanics
 Stem Cell Research & Therapy 2011, 2:33
doi:10.1186/scrt74Published:28 July 2011
 Osteogenic differentiation of human periodontal ligament stem cells
expressing lentiviral NEL-like protein 1
(Authors: Cai-Yun Chen, Ya-Jing Liu, Sheng-Gen Shi, Fa-Ming Chen,
Chuan Cai, Bing Li, Jing Wang, Liang Shi, Yan Li, Zhong-Yu Liu, Zhong-
Ying Niu
Published online on: Wednesday, July 4, 2012 )

4. CONTENTS
• INTRODUCTION
• DEVELOPMENT
• CELLS
• EXTRACELLULAR SUBSTANCE
• BLOOD SUPPLY
• NERVE SUPPLY
• FUNCTIONS OF PDL
• AGE CHANGES IN PDL
• CLINICAL CONSIDERATIONS

5. DEFINITION
Periodontal ligament is a
highly vascular and cellular
connective tissue that
surrounds the root of the
tooth and connects it to the
inner wall of the alveolar
bone.

6. INTRODUCTION
• Periodontal ligament is an integral part of periodontium.
• The periodontium (cementum,periodontal ligament & alveolar bone &
dentogingival junction) is an attachment apparatus of the teeth.
6

7.  The periodontal ligament is a soft,
fibrous specialized connective tissue
 The periodontal ligament extends
coronally up to the most apical part
of lamina propria of gingiva.
 The collagen fibers are attached to
the cementum and alveolar bone, the
ligament provides soft tissue
continuity between the mineralized
connective tissues of periodontium.
7

8. STRUCTURE
The shape of the periodontal ligament is like an “HOUR GLASS”, and is
narrowest in the mid root level.(fulcrum of physiologic movement in
this region).
• The average width of the periodontal ligament ranges from 0.15 – 0.38
mm.
• Thickness measures .21mm in young adult,.18mm in mature adult & .15mm
in older adult.
• Decrease in thickness with age.

9. • Functional movement of tooth helps in maintaining thickness of
PDL.
• Thick in teeth exposed to excessive functional load & thin in non
functional & embedded teeth.
• The periodontal spaces of permanent teeth-narrower than
deciduous teeth.

10. THICKNESS OF PDL OF 154 TEETH FROM 14 HUMAN JAWS
AVERAGE AT
ALVEOLAR
CREST(mm)
AVERAGE AT
MID ROOT(mm)
AVERAGE AT
APEX(mm)
AVERAGE
FOR ENTIRE
TOOTH(mm)
AGES 11-16(83 TEETH
FROM 4 JAWS)
0.23 0.17 0.24 0.21
AGES 32-50(36 TEETH
FROM 5 JAWS)
0.20 0.14 0.19 0.18
AGES 51-67(35 TEETH
FROM 5 JAWS)
0.17 0.12 0.16 0.15
TABLE SHOWS THAT WIDTH OF PDL DECREASES WITH AGE & IT IS WIDER AT CREST & APEX THAN
AT MIDROOT

11. COMPARISON OF PERIODONTAL LIGAMENT IN DIFFERENT
LOCATIONS AROUND THE SAME TOOTH(SUBJECT 11 YEARS
OF AGE)
MESIAL (mm) DISTAL (mm) LABIAL(mm) LINGUAL(mm)
UPPER RIGHT CENTRAL
INCISOR,MESIAL & LABIAL DRIFT
0.12 0.24 0.12 0.22
UPPER LEFT CENTRAL
INCISOR,NO DRIFT
0.21 0.19 0.24 0.24
UPPER RIGHT LATERAL
INCISOR,AND LABIAL DRIFT
0.27 0.17 0.11 0.15
THE TABLE SHOWS THE VARIATION IN WIDTH OF THE MESIAL,DISTAL,LABIAL AND LINGUAL SIDES
OF SAME TOOTH

12. •The average value for the ultimate tensile strength of the ligament
was found to be 2.4 N/mm2.(Tensile behaviour of the periodontal
ligament,W. J. Ralph,Journal of Periodontal Research Volume 17,
Issue 4, pages 423–426, August 1982)
•Elastic modulus value of 5OMPa.
PHYSICAL PROPERTIES

13. •The mechanical strength of the PDL was found similar to skin, which comprises a
three-dimensional mesh of collagen fibres.
• Cortical bone and tooth dentin contain large amounts of collagens are mineralised-
mechanical strengths are 10- to 40-fold greater than that of the PDL.
•Artificial materials such as glass fibre and steel show strengths 200- to 600-fold
greater than those of the PDL.
•Mechanical strength is measured as the load needed to fracture a specimen, which
causes breaks in the covalent linkages of the collagen molecular chains and slippages
between the unit molecular chains .

14. • Ligament appears as periodontal
space of .4 to 1.5 mm on
radiograph.
• Radiolucent area between
radiopaque lamina dura of
alveolar bone proper &
cementum.

15. DEVELOPMENT
• Development of periodontal ligament begins with root formation,
prior to tooth eruption.
• Continuous proliferation of internal & external enamel epithelium
forms cervical loop of tooth bud.
• This sheath of epithelial cells grows apically in the form of
HERTWIGS EPITHELIAL ROOT SHEATH between dental
papilla & dental follicle.

16. • Sheath forms a circumferential
structure encompassing dental
papilla separating it from dental
follicle.
• Dental follicle cells between
alveolar bone & epithelial root
sheath –composed of two
subpopulations
 Mesenchymal cells of dental
follicle proper
 Perifollicular
mesenchyme(bounded by dental
follicle proper & developing bone)
are stellate shaped ,small &
randomly oriented.
bone
Perifollicular
mesenchyme
Dental
epithelium
Dental
follicle
Dental
papilla

17. • As root formation continues-cells in perifollicular area –gain
polarity,cellular volume & increase in synthetic activity.
• Actively synthesise & deposit collagen fibrils & glycoproteins in
developing periodontal ligament.
• Developing PDL & mature PDL contain undifferentiated stem
cells that retain the potential to differentiate into
OSTEOBLASTS,CEMENTOBLASTS & FIBROBLASTS.
• Stem cells occupy perivascular sites in PDL & in adjacent
endosteal spaces.

18. • 2 lineages of PDL fibroblasts-
 A common C.T fibroblast
 Osteoblast-like fibroblast- gives rise to
bone cells & cementum.
• The nascent fiber bundles (fringe fibers)
are tightly packed by action of
cementoblasts during initial development of
acellular extrinsic fiber cementum,at
newly formed root dentin.similar fringe
fiber bundles originate along bone surface.
• During tooth eruption ,as PDL matures,the
fringe fibers merge across width of
ligament to form principal fiber bundles.

19. • With continued development of root,major collagen bundles
(principal fibers) are established as continuous structures
embedded as sharpey’s fibers in bone & cementum.

20. DEVELOPMENT OF THE PRINCIPAL FIBRES
• Immediately before tooth eruption & sometime thereafter,active
fibroblasts adjacent to cementum of coronal third of root appear
to become aligned in an oblique direction to long axis of tooth.
• Soon,thereafter the first collagen fiber bundles of the ligament
become discernible.
• These are the precursors of the ALVEOLAR CREST FIBER
BUNDLE GROUP.
• Upon eruption of tooth in oral cavity only alveolar crest fibres of
PDL are discernible histologically.

21. • Further apically ,organised fiber
groups are not seen.
THE GROUP OF ALVEOLAR CREST FIBERS,FIRST FORMING IN A,
ARE INITIALLY OBLIQUE B,
THEN HORIZONTAL C,
AND THEN OBLIQUE AGAIN D.
A B C D

22. • By the time first occlusal contact of tooth with its
antagonist –principal fibres around coronal third of root-
horizontal group are almost completely developed.
• The oblique fibres in the middle third of the root are
still being formed.
• As eruption continues & definite occlusion is established
there is a progressive apical maturation of oblique fiber
bundles.
• With the formation of apical fiber group the definitive
periodontal ligament architecture is established.
• Type VI & TYPE XII appears after tooth has erupted.

23. The mature periodontal
ligament can be subdivided
into three regions:
a) A bone-related region, rich in
cells and blood vessels,
b) A cementum-related region
characterized by dense well-
ordered collagen bundles, and
c) A middle zone containing fewer
cells and thinner collagen
fibrils
Histological section showing the
periodontal ligament (PDL), dentin
(D), cementum (C) and alveolar
bone (AB)
D PDL AB
C

24. COMPOSITION
PDL consists of:
70% vol. of PDL-dense CT,cells & fibers.
30%-loose CT-blood vessels,lymphatics,nerves.
a) Cellular elements
b) Extracellular substance
i) fibers
ii) ground substance

25. CELLULAR COMPOSITION
The cells of periodontal ligament are categorized as:
1.Synthetic Cells
a) Osteoblasts
b) Fibroblasts
c) Cementoblasts
2.Resorptive Cells
a) Osteoclasts
b) Cementoclasts
c) Fibroblasts
3.Progenitor Cells
4.Epithelial Cell rests of malassez
5.Connective Tissue cells
a) Mast cells
b) Macrophages
25

26. FIBROBLAST
• Fibroblasts are most abundant cells in
periodontal ligament.
• Have neural crest origin.
• A subpopulation of osteoblast like
fibroblasts –rich in alkaline phosphatase -
Capacity to give rise to bone cells &
cementoblasts.
• Also responsible for production of acellular
extrinsic fiber cementum in mature PDL.
• PDL fibroblasts –maintain normal width of
PDL by preventing encroachment of bone &
cementum into PDL space.

28. • Progenitor fibroblasts are smaller ,less polarised and contain
less RER & fewer golgi saccules.
• Cytoplasmic polarity is evident-nucleus located in narrow
end,golgi complex faces broad end of cell.
• Macula adherens & gap junction between cell processes of
neighbouring fibroblasts.
• PDL fibroblasts –active, elongated, contain large amount of RER
& well developed golgi complexes indicative of high rate of
protein synthesis, well polarised cytoplasm with extensive areas
of contact to collagen fibers.

30. GOLGI COMPLEX OF FIBROBLAST
• Contains several golgi stacks composed of cisternae & terminal
saccules.
• Each golgi stack contains 5 cisternae(2µm in length),terminating
at each end in an expanded saccule.
• Immature cisternae at cis surface of golgi –slightly dilated &
devoid of stainable content.,saccules of these cisternae contain
fine loosely arranged filaments.Coated vesicles(condensing
vacuoles) are seen in these saccules.

31. • Cisternae of trans surface –
contains dense material.
• Associated saccules contain
rodlike structure with globular
terminal elements resembling
segment long spacing collagen
aggregates.
• These saccules are released to
form presecretory granules that
associate to microtubules

32. • Autoradiographic studies - of incorporation & secretion of tritiated
amino acids such as proline & glycine & biochemical studies-have
confirmed high rate of protein secretion in PDL.
Proline is incorporated in collagen polypeptides in RER of PDL fibroblasts within
min of exit from bloodstream.
At 10 min newly synthesised procollagen molecules are present inside golgi
vesicles & by 20 min are ready for secretion within secretory granules
associated with microtubules.
In less than 30 min newly synthesised collagen fibrils are present in immediate
vicinity of fibroblasts.
At 1 hour newly secreted collagen fibrils are heavily labeled with tritiated
proline.

33. • An intact microtubular network is required for movement of collagen
secretion granules from trans golgi network to secretory pole of cell.
• During transmigration secretory pole of PDL fibroblast is also its
leading edge.
• PDL fibroblasts contain well defined actin filament bundles in cortical
cytoplasm.

34. FIBROBLAST-TO-MATRIX ADHESION AND TRACTION
• Fibroblasts attach to the substratum of the extracellular
matrix via surface receptors for collagen and fibronectin.
• In the formation of these adherent contacts, the cell
membrane integrin α5β1 attaches to the arginine-glycine-
aspartic acid sequence of fibronectin.(glycoprotein in
ground substance).

35. • Integrin receptor attaches to the peripheral cytoplasmic protein,
talin, which in turn interacts with a protein called vinculin(undergoes
conformational changes).
• vinculin binds to actin microfilaments in the cytoplasm, thereby
completing a molecular ‘‘bridge’’ between the cell’s contractile
apparatus and fibronectin in the extracellular matrix.
• The molecular linkage extends from the cytoplasmic contractile
apparatus to an extracellular collagen fiber network, establishing a
mechanism for exerting traction on the collagen fibers.
• Tension in the extracellular matrix is transmitted to fibroblast
integrin receptors, leading to signaling events that alter the activity
of the cell.

36. • FIBROBLAST LIGAMENT TRACTION THEORY-This theory states
that PDL is rich in fibroblasts that contain contractile tissue.The
contraction of these periodontal fibers (mainly the oblique group of
fibers) results in axial movement of the tooth.
• The force initiated by fibroblast is transmitted to extracellular
compartment via fibronexuses & to collagen fiber bundles aligned in
appropriate inclination,bring about tooth movement.
• Fibroblasts exhibit motility & contractility-actin cytoskeleton of
fibroblasts allows them to move through ground substance.
• Fibroblasts form specialised focal contact called fibronexus- dense
plaque on cytoplasmic side of cell membrane.

38. The periodontal collagen contraction hypothesis
• This hypothesis, was developed by Thomas 1965, it
involves a Tractional force being developed with in the
PDL.
• First criterion-
The proposed system must be capable of producing a
force under physiological conditions which is sufficient to
move a tooth.
There is yet no evidence that under physiological
conditions collagen can contract.
• 2nd criterion-
• Experimentally induced changes to the system should
cause predictable changes in eruption.

39. • Gould(1968) and Barnes(1972) have shown that ascorbic acid plays
an important role in the formation of collagen. In scorbutic animals-
• The synthesis of collagen is depressed
• Collagen degradation
• Little or no new collagen formation in wounds and this deficiency
may account for a loss of tensile strength.
• retarded the eruption rate.

40. • 3rd criterion-
• The system requires characteristics that enable it to sustain
eruptive movements over long periods of time.
• Firstly, in order to sustain eruptive movements over long periods,
periodontal collagen would have to exhibits high turnover rates.
• Secondly, its necessary to provide some specialized remodeling
mechanism with in PDL in order to allow contraction of periodontal
collagen to be sustained while maintaining new tooth position
resulting from previous contractions.
• It was thought that the intermediate fibre plexus might provide
such a remodeling mechanism.

41. • 4th criterion-
• The biochemical characteristic of the system should be
consistent with the production of an eruptive force.
• Thomas (1965,1976) has suggested a variety of biochemical
mechanisms for the contraction of collagen, including-
 A decrease in entropy during electrostatic attraction of
disordered tropocollagen macromolecules and alignment along
lines of stress.
 A linear polymerization producing a decrease in length of
macromolecules.
 A shrinkage associated with dehydration.
 A system analogous to the sliding of actomysin filaments.
 An interfibrillar repulsion produced by the interaction of
adjacent electrical double layers.
 The formation of intermolecular crosslinks

42. • 5th criterion-
• The morphological features associated with the system should be
consistent with the production of an eruptive force.
• The evidence against the notation that periodontal collagen
contraction is responsible for generating eruptive force is so strong
that the hypothesis appears to be disproved.

43. FUNCTIONS OF FIBROBLASTS
• Collagen synthesis & secretion occurs across entire width of
PDL.
• Fibroblast involved in formation & removal of collagen.
• Striated collagen fibrils –observed in vesicles of fibroblasts.
• Localisation of acid phosphatase in same vesicles –fibroblasts
are involved in lysosomal digestion of collagen fibrils.
• Lysosomal cysteine proteinases (cathepsins B,L& N) of lysosomal
granules –rapid degradation of internalised collagen fibrils.

44. • Cell surface MMP’s & integrin collagen receptors localised in
phagocytic clefts –regulate fibril internalisation.
• Plasma membrane alkaline phosphatase –promote collagen
phagocytosis-through its ability to bind collagen.
• The extracellular pathway –involving collagenase –large scale
indiscriminate removal of collagen fibrils-as in inflammation.
• In physiologic remodelling –controlled enzymatic attack required-
intracellular phagocytic pathway is used.

46. • Native type I and type III collagen fibrils-major in PDL-
degraded by
Fibroblast –type collagenase-MMP-1
During inflammation by neutrophil type collagenase-MMP-8
• Expression of MMP-1 & MMP-3(STROMELYSINS-attacks
proteoglycans,elastin,fibronectin,laminin & other collagen types)
– stimulated by IL-1β & decreased by TGF- β.
• MMP-1 penetrates triple helix of type I & cleaves it in 2
halves.,segments further degrade by gelatinases A & B (MMP-2
& MMP-9).
Extracellular activation of MMPs
Plasminogen plasmin (serine proteinase).
Plasminogen activator

47. FIBROBLASTS RESPONSE TO GROWTH FACTORS
• platelet- derived growth factor-BB and insulin-like growth factor-1
have potent chemotactic & mitogenic effects.
• PDGF-BB & TGF-β (main source s are macrophages & platelets) ,
stimulate collagen synthesis.
• TGF- β , stabilises collagen matrices by decreasing synthesis &
secretion MMPs by fibroblast.
• Above is potentiated by increasing plasminogen activator inhibitor 1
secretion which decreases conversion of plasminogen to plasmin.

48. • Epidermal growth factor & its receptors –maintain PDL
fibroblast phenotype.
• Differentiation of cementoblasts & osteoblasts –downregulation
of receptor for epidermal growth factor.

49. OSTEOBLASTS
 Bone forming cells.
 The osteoblasts covering the periodontal
surface of alveolar bone constitute a
modified endosteum and not a periosteum. A
periosteum comprises at least two distinct
layers:
1. Inner – CELLULAR LAYER/CAMBIUM
LAYER
2. Outer – FIBROUS LAYER
 A cellular, but not an outer fibrous layer is
present on the periodontal surface of
alveolar bone. (surface of bone lining dental
socket is interior surface of bone).
B, alveolar bone
O, osteoid layer
OB, osteoblasts
OC, former osteoblast
about to become an
osteocyte

50. • Osteoblasts secrete the type I collagen as well non-collagenous
matrix of bone.
• Osteoblasts differentiate from progenitor cells of the
connective tissue at site of bone formation.
• As the osteoblasts secrete the organic matrix of bone, it is at
first devoid of mineral salts and is called osteoid tissue and
after mineraliztion of osteoblasts, they become embedded in it
and form osteocytes and are important in deposition of bone.

51. • Surface of bone-covered by osteoblasts & occassional
osteoclasts.
• Collagen fibres of PDL penetrate alveolar bone & intervene
between cells.
• Cuboidal in shape,prominent round nucleus at basal end of cell.
• RER,mitochondria & vesicles abundant in active cell.
• Appear basophilic due to abundant RER.
• Golgi localised & extensive- indicated by pale juxtanuclear area.
• Microfilaments –prominent beneath cell membrane at secreting
surface.
• Cells contact each other through desmosomes & tight jnction.

52. CEMENTOBLASTS
• Line the surface of cementum.
• Not regularly arranged as
osteoblasts.
• Cuboidal with large vesicular
nucleus,one or more nucleoli &
abundant cytoplasm.
• Organelles for protein synthesis &
secretion present.
• Have abundant mitochondria &
less RER than PDL fibroblasts.
Periodontal ligament cells near cementum
surface.
Legends:
BV, blood vessels
C, cementum
CB, cementoblasts
M, epithelial cell rests of Malassez

53. • Cells actively depositing cellular cementum-abundant
basophilic cytoplasm & cytoplasmic processes.
• Cells depositing acellular cementum do not have prominent
cytoplasmic process.
• Cementum is constantly being formed as new principal
fibers are embedded along root surface.
• Cemental resorption may also occur for reasons as occlusal
relationship changes or tooth movement –new
cementoblasts become active in repair of resorbed
cementum.

54. RESORPTIVE CELLS
OSTEOCLASTS
• Resorb bone-large & multinucleated.
• Cells may appear to occupy bays in
bone(howship’s lacunae)
• Cytoplasm has numerous mitochondria
& lysosomes,abundant golgi saccules &
free ribosomes but little RER.
• The surface of an osteoclasts which is
in contact with bone has a ruffled
border from which hydrolytic enzymes
are secreted.
• The ruffled border is separated from
rest of plasma membrane by zone of
specialised membrane that is closely
applied to bone,underlying cytoplasm
devoid of organelles –called clear zone.
54

55. • The area of bone sealed off by ruffled border is exposed to highly
acidic PH (active pumping of protons by osteoclast into this
environment).
• Resorption occurs in two stages:
• The mineral is removed at bone margins and then exposed organic
matrix disintegrates. The osteoclasts demineralise the inorganic part as
well as disintegrates the organic matrix. Osteoclasts are rich in acid
phosphatase, which is contained in lysosomes.

56. MECHANISM OF BONE RESORPTION
migration of osteoclast by chemotaxis
attachment of the osteoclast's plasmalemma to the
underlying bone
release hydrogen ions (H2O + CO2 → HCO3- + H+)
through the ruffled border acidifying and dissolving the
mineralized bone matrix

57. CEMENTOCLASTS
• Ocassionally found in normal
functioning PDL.
• Cementum not remodeled as
alveolar bone & PDL but
undergoes continual deposition
• Resortion of cementum –
certain circumstances.
57
Fig. 1 - Area of cement covered by periodontal
ligament (HE 157X).
Fig . 2 – Little resorption of cement tissue. Note
the presence of cementoclast near the area
(arrow). (HE 157X)
Fig. 3 – Areas of cement resorption, covered by
periodontal ligament (HE 157X).

58. PROGENITOR CELLS
• Progenitor cells are the undifferentiated mesenchymal cells,
have capacity to undergo mitotic division and replace
differentiated cells dying at the end of their life span.
• When cell division occurs, one of the daughter cells
differentiate into functional type of connective tissue cells.
The other remaining cells retain their capacity to divide.
• These progenitor cells in PDL –highest conc. adjacent to bld.
Vessels & enter PDL thg. penetrations from adjacent endosteal
spaces.
• Small size,responsiveness to stimulating factors & slow cycle
time.
• Progenitor cells have small,close-faced nucleus & little
cytoplasm.,less RER & golgi saccules.
58

59. • In repair-migration of new fibroblasts to site –facilitated by
fibrin & fibronectin.
• Cells of osteoblast subtype-high alkaline phosphatase.
• It is not known whether a single progenitor cell give rise to
daughter cells that differentiate into fibroblasts, osteoblasts &
cementoblast or whether separate progenitors exist for
different cell types

60. ORIGIN OF PERIODONTAL STEM CELLS
• Periodontal ligament-formed by cells of dental follicle.
• Cells derived from ectomesenchyme.
• Stem cell marker STRO-1 found in bone marrow stromal cells-also
expressed by human Periodontal stem cells.
• Periodontal ligament stem cells also have common expression of
perivascular cell marker CD146 with bone marrow stromal cells.
• Proportion of these cells-coexpress α smooth muscle actin and /or
pericyte associated antigen 3G5.
• Above points to-perivascular origin.

61. • Many mature mineralised tissue markers-alkaline phosphatase,type
I collagen,osteonectin,osteopontin,osteocalcin & bone sialoprotein
are expressed.
• Have potential to express variety of antigens associated with
endothelium-cd106,perivascular tissue (α muscle actin,CD146,3G5) &
soft CT proteins type I & type III collagens.
• Studies imply-PDL cells represent unique population of postnatal
stem cells distinct from bone marrow derived mesenchymal stem
cells.
• Within total fibroblastic colony forming unit population-there is
mixture of stromal progenitor cells at various stages of
development –maintained by minor population of
multipotential,mesenchymal stem cells with capacity for cell
renewal.

62. RELATIONSHIP BETWEEN CELLS
• Cells form three dimensional network.
• Adjacent cells in contact through their processes.
• Contacts-marked by modification of structure of plasma
membrane.

63. Electron micrograph,Gap junctions b/w fibroblastic processes
&desmosomal junction b/w fibroblast

64. EPITHELIAL RESTS OF MALASSEZ
• The PDL contains epithelial cells
found close to cementum.
• First described by Malassez
in1884 ,are remnants of epithelium
of Hertwigs epithelial root sheath.
• At time of cementum formation –
continuous layer of epithelium
covering surface of newly formed
dentin breaks into lacelike strands.
• They lie about 25µm from
cementum .
• In cross section –appear cluster
like-cluster arrangement appears
like a duct with cells separated
from surrounding CT by basal
lamina.
(1) The HERS, (2) epithelial rests of
Malassez, (3) dental follicle, (4)
cementoblasts, (5) periodontal
ligament, (6) alveolar cells, (7) bone,
(8) odontoblasts

65. Epithelial Cell Rests of Malassez

66. • Distinguished from fibroblasts-close
packing of cuboidal cells & deepy
stained prominent nucleus.
• Cytoplasm scanty,organelles reflect
lack of protein synthesis.
• Attach to & spread rapidly on
fibronectin ,vitronectin & type I
collagen in ECM.
• Less numerous in older individuals &
more in children.
• Upto second decade-most common
in apical region,later mainly located
cervically in gingiva above alveolar
crest.
• Cells may proliferate to form cysts &
tumors or may undergo calcification
to become cementicles.
Tooth at bottom, bone near top.
the line of epithelial root sheath cells (rests of
Malassez) in the perioodontal ligament
and a few osteoclasts beside the bone.

67. DEFENSE CELLS
• Includes macrophages,mast cells & eosinophils.
MAST CELLS
• Round or oval cell of dia 12-15 µm
• Often associated with blood vessels.
• Characterised by numerous cytoplasmic granules-obscure
small,round nucleus.
• Granules are dense,membrane bound vesicles approx 0.5 - 1µm.
• Cell stimulated-it degranulates.
• Granules contain heparin & histamine.

68. • These are defense cells
located in periodontal
ligament
• They play a major role in
various inflammatory
conditions & are responsible
for defense against
microorganism
LEUCOCYTES

69. • MACROPHAGES
• Predominantly located adjacent to blood vessels.
• Derived from monocytes.
• These cells have a horse-shoe shaped or kidney shaped
nucleus with peripheral chromatin and cytoplasm contain
phagocytosed material
• Phagocytosis,secrete growth factors –regulate proliferation of
adjacent fibroblasts.
• Synthesise interferons,prostaglandins & factors that enhance
growth of fibroblasts & endothelial cells.

70. EXTRACELLULAR SUBSTANCE
FIBERS GROUND SUBSTANCE

71. EXTRACELLULAR SUBSTANCE
• FIBRES
• GROUND SUBSTANCE
71
•COLLAGEN
•ELASTIC-OXYTALAN
•RETICULAR
•SECONDARY
•INDIFFERENT FIBER PLEXUS
•GLYCOSAMINOGLCANS
•PROTEOGLYCANS
•GLYCOPROTEINS

72. FIBERS
• The CT fibers are mainly collagenous,may be
small amounts of OXYTALAN & RETICULIN
FIBERS.
• The collagen fibril diameters of the human
periodontal ligament are relatively small, with
mean diameters of the order 45-55 mm
(Berkovitz et al.2) which is much less when
compared to other connective tissues, e.g.
Tendon fibril diameters may reach up to 250
mm.
• The small diameter of the fibrils in the
periodontal ligament could be the result of
either the high rate of collagen turnover or the
absence of mature collagen fibrils (Berkovitz et
al.2).

73. Diameter of fiber bundle
• Close to cementum- 3 – 10 µm
• Close to alveolar bone- 10 – 20 µm
• Remaining are – 1 – 4 µm

74. COLLAGEN
• Protein composed of different amino acids-
GLYCINE,PROLINE,HYDROXYLYSINE &
HYDROXYPROLINE.
• Collagen is gathered to form bundles approx 5µm
in dia
• Bundles termed PRINCIPAL FIBERS.
• Within each collagen bundle –subunits collagen
fibrils.
• These fibrils –formed by packing individual
tropocollagen molecules.
• Collagen fibrils have transverse striations(due to
overlapping arrangement of tropocollagen
molecules) with periodicity of 64nm.
• Small dia of fibrils –due to high rate of collagen
turnover or absence of mature collagen fibrils.

75. BIOSYNTHESIS
Tropocollagen
molecules Microfibriles Fibrils
Principal Fibers
or large bundles Fibers

76. • Main types of collagen in PDL are TYPE I(more than 70%) &
TYPE III
• TYPE I
-uniformly distributed in PDL.
-contains two identical α1 chains & chemically different α2
chain.
-low in hydroxylysine & glycosylated hydroxylysine.

77. • TYPE III
-accounts for about 20% of collagen fibres.
-consists of three identical α1 chains.
-high in hydroxyproline,low in hydroxylysine & contains cysteine.
• Type III collagen is covalently linked to type I collagen
throughout tissue.
• Type III –found at periphery of sharpey’s fibers attachment at
alveolar bone.

78. • Small amounts of type V & VI collagens & traces of type IV &
VII .
• Type V(increases in periodontal inflammatory disease) coats cell
surfaces & other types of collagen.
• TypeVI maintains integrity & elasticity of extracellular matrix.
• Type IV & VII –associated with epithelial cell rests & blood
vessels.
• Type IV does not form fibrils .structural role –maintaining
integrity of PDL by anchoring elastic system to vasculature.
• Type XII –when ligament is fully functional.

79. STRUCTURE OF COLLAGEN I & III
• Collagens form predominant protein of periodontal tissues.
• Type I-80%
• Type III-15%
• Undergo polymerisation to form collagen fibrils.

80. TYPE I
• Made of three polypeptide chains (α chains)
assembled in a left handed tripple helix.
• Nascent polypeptide α chains synthesised in
RER consists of 5 domains-NH2 & COOH
terminal propeptides ,N & C-telopeptides,&
larger α helical middle segments.
• α helical segment of type I collagen contains
1014 amino acid residuesof
• 338 glycine-X-Y triplets.
• Proline often in X position.
• Hydroxyproline in Y position.
• Regular occurrence of glycine at every third
position permits polypeptide chain to fold & to
hydrogen bond with adjacent α chains to form
triple helix.

81. • Type I two α chains, α1 –similar in amino acid sequence & third is
different, α2.
• Disulfide bonds b/w carboxylate ends stabilises helix.
• Helical shape of collagen –protects its peptide bonds from
attack by proteolytic enzymes other than matrix
metalloproteinases.

83. • Lateral alignment with 67 nm overlap or quarter stagger of adjacent
collagen molecules gives rise to typical striated appearance of mature
fibrils-creates holes in fibrils-sites for biomineralisation &enzymes can
gain access to inner regions of fibrils.
• Type III collagen molecule contains only one class of α chains,
α1(present in small argyrophilic fibrils,reticular fibers)

84. COLLAGEN CRIMPING
• Collagenous tissues exhibits a
quantifiable periodicity of
structure of variable scale,
ranging from submicroscopic
to anatomical.
• The waveform that describes
this periodicity referred to as
“crimp.”
• Crimping is a regular banding
of dark lines across a
collagenous bundle observed in
polarized microscope.
The PDL in health and disease, Barry K B Berkovitz, 2nd Edition

85. • It may be sharp zig-zag
arrangement of collagen
fibrils or microanatomical
organization of collagenous
sheets and bundles.

86. • Principal fiber group is ALVEOLODENTAL
LIGAMENT-consists of 5 fiber groups.
 Alveolar crest
 Horizontal
 Oblique
 Apical
 Interradicular

87. ALVEOLAR CREST GROUP
• Extend obliquely from the cementum just beneath the
junctional epithelium to alveolar crest.
• Fibers also run from the cementum over the alveolar crest
and to fibrous layer of periosteum covering alveolar bone.
• Resist tilting,intrusive,extrusive & rotational forces.
87

88.  ALVEOLAR CREST GROUP
Alveolar crest

89. HORIZONTAL GROUP
• Horizontal fibers extend at right
angles to long axis of tooth from
the cementum to alveolar bone.
• Found immediately apical to
alveolar crest fiber group.
• Pass from their cemental
attachment directly across PDL
space to become inserted in
alveolar process as sharpey’s
fibers.
• Limited mostly to coronal one
fourth of PDL space .
• Resist horizontal & tipping forces.

90. • HORIZONTAL GROUP
Horizontal

91. OBLIQUE GROUP
• Oblique fibers, the largest group in periodontal ligament.
• Occupy nearly two third of ligament.
• extend from cementum in a coronal direction obliquely to bone.
• They bear the brunt of vertical(& intrusive forces) masticatory
stresses and transfer them into tension on the alveolar bone.

92. • OBLIQUE GROUP
Oblique

93. APICAL GROUP
• From cementum at root tip,radiate through periodontal space to
become anchored into fundus of bony socket.
• Resist forces of luxation,prevent tooth tipping & protect
delicate blood & lymph vessels & nerves transversing PDL space
at root apex.
• Not seen on incompletely formed roots.

94. • APICAL GROUP
Apical

95. INTERRADICULAR
• Inserted into cementum from crest of interradicular septum in
multirooted teeth.
• Resist tooth tipping,torquing & luxation.
• Lost if age related gingival recession proceeds to extent to
furcation exposure.
• Total loss of it occurs in chronic inflammatory periodontal
disease.
95

96. • INTERRADICULAR GROUP
Interradicular

97. TRANSEPTAL GROUP
• These fibers extend interproximally over alveolar bone crest
and are embedded in the cementum of adjacent teeth.
• They are reconstructed even after the destruction of
alveolar bone resulting from periodontal disease.
• These fibers may be considered as belonging to the gingiva
because they do not have osseous attachment.
97

98. • TRANSEPTAL GROUP
Transeptal
group

99. SHARPEY’S FIBERS
• Known so, after the name of person who
first described it –WILLIAM SHARPEY.
• Collagen fibers embedded into cementum
on one side of PD space & into alveolar
bone on the other.
• Are more numerous but smaller at their
attachment into cementum than alveolar
bone.
• TRANSALVEOLAR FIBERS-few sharpey’s
fibers pass uninterrutedly through the
bone of alveolar process to continue as
principal fibers of adjacent PDL.
• Transalveolar fibers may serve as a
mechanism to connect adjacent teeth.

100. INTERMEDIATE PLEXUS
• Earlier believed-principal fibers followed wavy course from
cementum to bone & are joined in mid region of periodontal
space-zone of distinct appearance-INTERMEDIATE PLEXUS.
• Considered an area of high metabolic activity-in which splicing &
unsplicing of fibers may occur.
• Research demonstrated
-once cemental fibers meet & fuse with osseous fibers no such
plexus remains.
-entire PDL is metabolically active not just intermediate zone.
-With tooth movement areas of highest activity are fiber terminals
near cementum & bone,not in the middle.

101. ELASTIC FIBERS
• 3 types of elastic fibers-histochemically & ultrastructurally
different.
 Elastic fibers
 Elaunin fibers
 Oxytalan fibers
• Elaunin & oxytalan fibers –immature elastic fibers.
• Mature elastic fibers-consist of microfibrillar component
surrounding an amorphous core of elastin protein.
• Elastin protein contains high percentage of glycine,proline &
hydrophobic residues with little hydroxyproline & no
hydroxylysine.

102. • Found in walls of afferent blood vessels –constitute elastic
laminae of larger arterioles & of arteries of larger caliber.
• Elaunin fibers –seen as bundles of microfibrils embedded
in relatively small amount of amorphous elastin,found
within fibers of gingival ligament.
• Elastic meshwork –in PDL-composed of many elastin
lamellae with peripheral oxytalan fibers & elaunin fibers.

103. • Oxytalan fibers
• Not susceptible to acid hydrolysis.
• Approx 0.5-2.5 µm dia & appear to have
elastin &type IV collagen.
• Different orientation from collagen
fibers.
• Instead of running from bone to tooth-
run in axial direction-one end embedded
in cementum or bone & other often in
wall of blood vessel.
• Support blood vessels of pdl.

104. RETICULAR FIBERS
• Fine immature fibers with
argyrophilic staining properties
and are related to basement
membrane of blood vessels &
epithelial cells which lie within PDL.
• Composed of type III collagen.
• Reticular fibers crosslink to form
a fine meshwork (reticulum). which
acts a supporting mesh in soft
tissues such as liver, bone marrow
etc.
• Many of these types of collagen
have been combined with
carbohydrate. Thus, they react
with silver stains and with periodic
acid-Schiff reagent

105. SECONDARY FIBERS
• Located between & among principal fibers .
• Relatively non directional & randomly oriented.
• represent newly formed collagenous elements not incorporated
in principal fiber bundles.

106. INDIFFERENT FIBER PLEXUS
• Small collagen fibers associated with large principal collagen
fibers.
• Run in all directions-forming plexus.

107. GROUND SUBSTANCE
Comprises of
GLYCOSAMINOGLYCANS
PROTEOGLYCANS
GLYCOPROTEINS

108. GLYCOSAMINOGLYCANS & PROTEOGLYCANS
• Glycosaminoglycans are polymers of repeating disaccharides
of hexosamine & carboxylate or sulfate ester .
• Glycosaminoglycan chains link covalently with core proteins
to form PROTEOGLYCANS.

109. GROUND SUBSTANCE
• Amorphous background material that binds tissues and fluids
• Similar to most connective tissue ground substance
• Dermatan sulfate is the major glycosaminoglycan
• 70% water; critical for withstanding forces
• When function is increased PDL is increased in size and fiber
thickens
• Bone trabeculae also increase in number and thickness.
• However, in reduction of function, PDL narrows and fiber
bundles decreases in number and thickness (this reduction in
PDL is primarily due to increased cementum deposition)

110. GLYCOSAMINOGLYCANS
HYALURONIC ACID-
• A large glycos amino glycan present in most connective tissue
• Found abundantly in embryonic tissues & cartilage
• Forms a viscous hydrated gel with its bound water
• In cartilage hyaluronic acid forms a large aggregate with 50 to
100 molecule of proteoglycan monomer, aggrecan

111. • This aggregated proteoglycan along with its bound water
provides resistance to cartilage to compressive forces
• Hyaluronic acid is a major component of the extra cellular
matrix of periodontal ligament (PDL) contributing to the
structural and functional integrity.
• Hyaluronic acids contribute to the buffering effect of the PDL
during chewing, and they are also important in inflammation and
wound healing.
• Because of its anti inflammatory & anti edematous properties it
is used in gel form for T/t of plaque induced gingivitis3

112. PROTEOGLYCANS
FIBROMODULIN-
• Fibromodulin (FMOD) is the most abundant member of the
leucine-rich repeat protein family, first described as a 59
kDa collagen binding protein
• Fibromodulin involves the process regulating the
orientation of collagen fibers.

113. • This protein contains keratan sulfate with four potential
substitution sites, all present in the leucine rich region.
• FMOD is known to interact with both types I and II collagens
• Decorin & fibromodulin bind to collagen & probably function in
regulating growth, diameter or both of collagen fibrils. In contrast,
the more distinct relative decorin (DCN) binds to a different site
• Binding of FMOD to type XII collagen has also been reported
• Fibromodulin is one of the small PGs in the PDL-matrix and may
fulfill construction and maintenance functions in this tissue.4

114. NONCOLLAGENOUSPROTEINS/
GLYCOPROTEINS
• Adhesion molecules like fibronectin,tenascin & vitronectin.
• Fibronectin wide distribution in PDL.
• Tenascin-concentrated at surface of mineralised cementum &
bone.
• Vitronectin-attachment factor associated with elastic fibers of
loose CT-found thgout PDL including cells lining cementum &
bone surfaces.also participates in regulation of blood
coagulation,plasminogen activation & fibrinolysis.

115. GLYCOPROTEIN-
FIBRONECTIN-
• Its structure consists of 2 identical disulphide linked
polypeptide chain & binds to cell at 1 site & collagen, heparin &
fibrin at other
• Cells preferentially adhere to fibronectin which may be involved
in cell migration & orientation

116. • Has a considerable biosignificance in PDL in view of high rate of
turn over
• Immuno chemical techniques have revealed that fibronectin is
uniformly distributed throughout the PDL both during eruption &
in fully erupted teeth
• Fibronectin has been expressed strongly along attachment sites
of PDL collagen fibers to cementum but not to alveolar bone
• Involved in blood coagulation, wound healing & chemotaxis

117. GLYCOPROTEIN-
LAMININ-
• Laminin is the major non-collagenous component of the basal lamina
• It has 4 arms that can bind to four other molecules.
• The 3 shorter arms are particularly good at binding to other laminin
molecules, which is what makes it so great at forming sheets.
• The long arm is capable of binding to cells, which helps anchor the
actual organs to the membrane.

118. • Laminins are secreted and incorporated into cell-associated
extra cellular matrices.
• Laminin is vital to making sure overall body structures hold
together.
• Laminin-like molecule produced by periodontal ligament
fibroblasts (PLFs) induces gingival epithelial cell chemotaxis.

119. GLYCOPROTEIN-
TENASCIN-
• Another glycoprotein tenascin has been identified in PDL & is
characteristic of immature connective tissue
• It is a protein with 6 arms extending from a central core
• They are abundant in the extra cellular matrix of developing
vertebrate embryos and they reappear around healing wounds
and in the stroma of some tumors.

120. • Expression of tenascin is only maintained during wound healing &
in bone marrow & periodontal tissues
• Unlike fibronectin it is not uniformly localized throughout PDL
but is conc. adjacent to alveolar bone & cementum
• Found between less densely packed fibers of PDL

122. BLOOD SUPPLY
• Its main blood supply is from
superior & inferior alveolar
arteries.
• These arteries pursue an
intraosteal course & give off
alveolar branches that ascend
within the bone as inter
alveolar branches

123. • Numerous branches arise from inter alveolar vessels to run
horizontally & penetrate the alveolar bone & enter PDL space
• They are more abundant in PDL of posterior teeth than in
anterior teeth & in greater number in mandibular than in
maxillary teeth

124. Reaches the periodontal ligament from 3 sources-
• Apical vessels- supply the apical region of the
periodontal ligament before enter the dental pulp.
• Penetrating vessels from the alveolar bone and,
• Anastomosing vessels from the gingiva.
• Transalveolar vessels that perforate the lamina dura and
enter the ligament.
• The interseptal vessels continue to vascularize the
gingiva; these gingival vessels in turn anastomose with
the periodontal ligament vessels of the cervical region.

125. • The vessels with in the PDL are contained in interstitial
spaces of loose C.T b/w the principal fibers and are
connected in a netlike plexus that runs longitudinally and
closer to the bone than the cementum.
• Blood supply increases from incisors to molars.
• Greatest – gingival 3rd of single rooted teeth
• Less – apical 3rd
• Least – middle (is equal in the apical and middle 3rd of
multirooted teeth)
• Greater on the mesial and distal surfaces than on the
facial and lingual .

126. Venous drainage
• Venules receive the blood through the abundant
capillary network;
• Also arteriovenous anastomoses bypass the
capillaries.
• These are more frequent in apical and interradicular
regions.

127. NERVES
• Usually associated with blood
vessels, pass through foramina in
the alveolar bone, including the
apical foramen, to enter the PDL.
• The nerve supply originates from
the inferior or the superior
alveolar nerves.
• The fibers enter from the apical
region and lateral socket walls.

128. • The apical region contains
more nerve endings (except
Upper Incisors)
• Nerve bundles pass into the
PDL from periapical area &
through channels from the
alveolar bone that follow the
course of blood vessels.

129. • 4 types of neural
transmission are-
• Free endings- tree like
configration, carry pain
sensation.
• Ruffini-like
mechanoreceptors-
located in apical area.
• Coiled meissner;s
corpuscles
mechanoreceptor-
located in the mid-root
regions.
• Spindle like pressure and
vibration ending- located
in the apex and
surrounded by fibrous
capsule.

130. CEMENTICLES
• Cementicles are small calcified bodies present in the periodontal
ligament.
• They may form into large calcified bodies and fuse within
cementum or remain free.
• These are found in old age.
• The degenerated epithelial cells form a nidus for calcification.
130

131. FUNCTIONS OF PDL
Physical
Formative and remodeling
Nutritive
Regulation of PDL width
Sensory

132. • PHYSICAL
• Provision of a soft tissue “casing” to protect the vessel and nerve
from injury by mechanical forces.
• Transmission of occlusal forces to the bone.
• Attachment of the teeth to the bone.
• Maintains the gingiva in proper relationship with teeth.
• Resistance to the impact of occlusal forces.
( shock absorption )

133. Two theories pertaining to the mechanism of
tooth support:
Tensional theory
Viscoelastic theory
Resistance to impact of occlusal forces
(shock absorption)

134. TENSIONAL THEORY
• According to it, principal fibers play a major role in supporting
tooth and transmitting forces to bone. When forces are applied
to tooth, principal fibers unfold and straighten and then
transmit the forces to alveolar bone, causing elastic
deformation of socket. Finally when the alveolar bone has
reached its limit, the load is transmitted to the basal bone.

135. VISCOELASTIC THEORY
• According to it, the fluid movement largely controls the
displacement of the tooth, with fibers playing a secondary
role.
• When forces are transmitted to the tooth, the extracellular
fluid is pushed from periodontal ligament into marrow spaces
through the cribriform plate.
• After depletion of tissue fluids, the bundle fibers absorb the
shock and tighten. This leads to blood vessel stenosis – arterial
back pressure – ballooning of vessels – passage of blood into the
tissues- replenishes the tissue fluids.

136. Transmission of Occlusal forces to the bone
• Arrangement of the principal fibers is similar to a
suspension bridge.
• When axial force is applied displacement of root
into the alveolus occurs.
• Oblique fibers alter their wavy, untensed
pattern;assume their full length; and sustain the
major part of the axial force.
• When a horizotal or tipping force is applied; two
phases of tooth movement occur.
• 1st is with in the confines of the periodontal ligament
and 2nd produces a displacement of the facial and
lingual bony plates.

137. • In areas of tension, the principal fiber bundles are taut rather than
wavy.
• In area of pressure, the fibers are compressed, the tooth is
displaced and a corresponding distortion of bone exists in the
direction of root movement.

138. FORMATIVE & REMODELLING FUNCTION
• Periodontal ligament and alveolar bone cells are exposed to
physical forces in response to mastication, parafunction, speech,
and orthodontic tooth movement.
• Cells of the PDL are involved in the formation and resorption of
alveolar bone and cementum, which occur in physiologic tooth
movement, in the accommodation of periodontium to occlusal
forces and in the repair of injuries.

139. • The periodontal ligament is constantly undergoing remodeling.
Old cells and fibers are broken down and replaced by new ones,
and mitotic activity can be observed in the fibroblasts and
endothelial cells.
• PDL has the ability to adapt to rapidly changing applied force and
can maintain its width at constant dimensions throughout its
lifetime. These are the important measures of periodontal
ligament homeostasis.

140. • PDL is highly vascularized tissue, it supplies the nutrition to
the cementum, bone, and gingiva by blood vessels and also
provides lymphatic drainage.
• PDL is supplied with sensory nerve fibers capable of
transmitting tactile, pressure and pain sensation.
• Nerve bundles divide into single myelinated fibers, which
later change into non-myelinated and end into one of the 4
type of neural transmission.
NUTRITIONAL AND SENSORY FUNCTION

141. 4 types of neural transmission are-
• Free endings- tree like
configuration, carry pain
sensation.
• Ruffini-like mechanoreceptors-
located in apical area.
• Coiled Meissners corpuscles
mechanoreceptor- located in the
mid-root regions.
• Spindle like pressure and
vibration ending- located in the
apex and surrounded by fibrous
capsule.

142. HOMEOSTATIC MECHANISM
• Cells of PDL have capacity to resorb & synthesise extracellular
substanceof CT,of ligament,alveolar bone & cementum..
• The resorption and synthesis are controlled procedures.
• Higher rate of collagen turnover.
• If there is a long term damage of periodontal ligament, which is
not repaired, the bone is deposited in the periodontal space.
• This results in obliteration of space and ankylosis between bone
and the tooth.
• The quality of tissue changes if balance between synthesis and
resorption is disturbed.
142

143. • If there is deprivation of Vit. C which are essential for collagen
synthesis, resorption of collagen will continue.
• So there is progressive destruction and loss of extra cellular
substance of ligament.
• This occurs more on bone side of ligament.
• Hence, loss of attachment between bone and tooth and at last, loss
of tooth.
143

144. Various molecules-maintain width of unmineralised PDL
• Msx2-prevents osteogenic differentiation of PDL fibroblasts by
repressing Runx transcriptional activity.
• Balance between osteopontin & bone sialoprotein.
• Matrix Gla protein –inhibitor of mineralisation- in PDL.
• RGD- cementum attachment protein.
• TGF-β downregulate osteoblastic differentiation of PDL.
• Prostaglandins-produced by pdl-inhibit mineralised bone nodule
formation & prevent mineralisation of PDL.

145. • Trauma from occlusion- when occlusal forces exceed the adaptive
capacity of the tissue, tissue injury results. The resultant inury is
termed “trauma from occlusion”.
• TFO refferred to tissue injury not the occlusal forces.
• Occlusion that produces such injury is called Traumatic occlusion.
• Types-
• A) depending upon onset and duration- Acute and Chronic
• B) depending upon cause- primary and secondery
• Acute TFO- occurs due to abrupt change in occlusal force.
Trauma from occlusion-

146. • Causes tooth pain, sensitivity to percussion , increases tooth
mobility.
• In advance condition – causes periodontal necrosis, periodontal
abscess.
• Chronic TFO-
• Most common than acute
• Occurs due to gradual changes in occlusion produce by tooth wear,
drifting movement, and extrusion of teeth combined with
parafunctional habits such as bruxism.

147. • Primary TFO- due to change in the
occulsal forces
• It’s a tissue injury in which tooth
with normal periodontium with
normal height of bone.
Ex- 1) insertion of high filling
2) prosthetic replacement
3) drifting movement or
extrusion of teeth in to spaces of
missing teeth.
4) orthodontic movement.

148. • Secondary TFO-
• Due to reduce ability of tissue
to resist the occlusal forces
by bone loss and reduce
periodontal attachment area-
• 1) Normal periodontium with
reduce height of bone
• 2) Marginal periodontium with
reduce height of bone.

149. Changes on pressure side
• Compression in direction of tooth movement.
• Increase in vascularity-due to increase in capillary
blood supply(helps in mobilisation of fibroblasts &
osteoclasts).
• Osteoclasts-bone resorbing cells-line along socket wall
on pressure side.
• Change in orientation of bony trabeculae-usually
parallel to long axis to teeth become horizontally
oriented.
• Osteoclasts –start resorbing bone.
• Force within physiologic limits-resorption in alveolar
plate immediately adjacent to ligament-FRONTAL
RESORPTION.

150. Changes on tension side
• PDL gets stretched.
• PDL space widened.
• Raised vascularity-mobilisation of
fibroblasts & osteoblasts.
• Osteoid laid down by osteoblasts.

151. TISSUE RESPONSE TO INCREASE OCCLUSAL FORCES-
• Stages of tissue response
• Stage 1 – Injury
• Stage 2 – Repair
• Stage 3 – Adaptive remolding of the periodontium.
• Stage 1-
• Tissue injury is produced by excessive occlusal forces injury like
bone loss, widening of PDL, vessel injury etc.
• Tilting of tooth, rotation of tooth.

152. • Stages II Repair-
• Damaged tissue are removed and new CT cells and fibers, bone and
cementum are formed to restore the injured periodontium.
• Histological Changes-
• When bone is resorbed by excessive occlusal forces. Body reinforce
the thinned bony trabeculae with new bone. This attempt to
compensate lost bone is called buttressing bone formation.
• It characteristic process associated with TFO also occurs when
bone is destroyed by inflammation or osteolytic tumors.
• buttressing bone formation occurs in the jaw is called Central
buttresing. In which endosteal cells deposite new bone.
• If occurs on the bone surface called peripheral buttersing mainly
occurs on lingual and facial surface of alveolar plate.
• Depending on severity peripheral buttresing produce shelf like
thickening of alveolar margin called lipping.

153. • Stage III-
• Periodntium remodeled to create structural relationship.
• Causes- thickening of PDL, angular defect with no pocket formation,
loose teeth, and increase vascularization.
• Radiological signs-
 Increases width of periodontal space with thicking of lamina dura.
 Vertical destruction of interdental septum.
 Radiolucence and condensation of alveolar bone.
 Root resorption.

154. Following extreme force application Changes
• Crushing & total compression of PDL.
• On pressure side-occlusion of blood vessels-PDL deprived of nutritional
supply-regressive changes-HYALINISATION.
• Bone cannot resorb in frontal portion only but resorbs in adjacent marrow
spaces & in alveolar plate below,behind & above hyalinised area-
UNDERMINING/REARWARD RESORBTION
• On tension side-PDL gets overstretched- leading to tearing of blood vessels
& ischaemia.
• Extreme forces-increase in osteoclastic activity-tooth loosened in socket.

155. HYALINIZATION
• It’s a form of tissue degeneration characterized by
formation of a clear, eosinophilic homogenous substance.
• Hyalinization of PDL denotes a compressed and locally
degenerated periodontal ligament.
• Hyalinization is a irreversible process.
• But Hyalinization of PDL is reversible process.

156. Extreme forces applied
Root closely approximates the lamina dura
Total compression of PDL
Occlusion of the blood vessels
Reduce or limited the nutrition supply
Degenerative changes (Hyalinization)

157. • CHANGES OBSERVED DURING FORMATION OF
HYALINIZATION ZONES ARE-
• Gradual shrinkage of periodontal ligament fibers.
• The cellular structures become indistinct.
• The compressed collagenous fibers gradual unite into
a more or less cell free mass.
• Changes also occurs in the ground substance.
• Breakdown of the blood vessel walls leading to spilling
of their contents.

158. • Osteoclasts are formed in marrow spaces and adjacent
areas of the inner bone surface after a period of 20-30
hours.
• The presence of a hyalinization zone indicated that the
ligament is non-function and bone resorption cannot
occur.
• The tooth is hence not capable of further movement
until the local damaged tissue removed and the adjacent
alveolar bone wall resorbs.

159. • The elimination of hyalinization tissue-
a) Resorption of the alveolar bone by osteoclasts
differentiating in the peripheral intact periodontal
membrane and in adjacent marrow spaces.
b) Invasion of cells and blood vessels from the periphery
of the compressed zone by which the necrotic tissue is
removed. Cells eliminate the unwanted fibrous tissue by
enzymatic and phagocytosis action.

160. PERIODONTAL LIGAMENT HEALING
• Process similar to normal wound healing in other
tissues.
• New fibroblasts from perivascular progenitor cells
from adjacent normal PDL.
• Presence of fibrin & fibronectin network-migration of
fibroblasts to site.
• New collagen fibers laid down rapidly-without
functional orientation or attachment to adjacent hard
tissue.
• Reorganisation of initial collagen matrix into oriented
principal fiber bundles.

161. PERIODONTAL LIGAMENT REGENERATION
PRE-REQUISITES
• After removal of inflamed tissue-root surface must be debrided
of contaminants.(interfere with cell attachment).
• Gingival epithelial cells must be prevented from gaining access
to root surface.
• Conditions favoring growth of PDL fibroblasts over gingival
fibroblasts must be created.(use of resorbable membranes to
exclude gingival tissue contact root surface)..
• Geometric nature of lesion-prognosis.(poor for horizontal
attachment loss).

162. EFFECT OF AGING ON PDL
Changes in PDL reported with aging include:-
• Decreased number of fibroblast
• Decreased organic matrix production
• Decrease in number of collagen fibers
• Reduced mitotic activity of PDL cells & reduction in metabolic
rate
• Increased amount of elastic fibers
• Width of PDL will decrease if tooth is unopposed & increase in
excessive occlusal loading

163. SYSTEMIC FACTORS:-
• Connective tissue disorder – Ehlers-danlos syndrome, Scurvy
• Metabolic disorders - Diabetes mellitus
•
• Leukocyte defects - Chediak Higashi
• Hematological disorders - Leukemia
•
• Dermatologic disorders - Papillion Lefevre syndrome
•
• Chromosomal disorders - Down’s syndrome

164. LOCAL FACTORS:-
• Chronic Periodontitis
• Necrotizing ulcerative periodontitis
• Aggressive periodontitis
• Trauma from occlusion

165. CONNECTIVE TISSUE
DISORDER-
EHLERS DANLOS SYNDROME-
• It’s a rare genetic disorders affecting humans caused by a defect in
collagen synthesis.
• Depending on the individual mutation, the severity of the syndrome
can vary from mild to life-threatening
•

166. • Excessive joint mobility, skin hyper
extensibility, easy bruising & peculiar
scarring after skin wounds
• 10 variants have been described the
mode of inheritance of
• 4 types is autosomal
dominant(I,II,III,VIII)
• 3 types are autosomal recessive
(IV,VI,VII)
• other 3 types are x-linked

167. EFFECT ON PDL-
• Gingival bleeding, marked periodontal destruction
• Patient with Type IV, VII, IX ehler danlos syndrome have
been found to be susceptible to rapidly progressive
periodontitis
• No evidence of Type III procollagen or collagen was
detected with indirect immunofluorescence. It is suggested
that an inherited collagen abnormality in a ligament and
tendon probably explains both the destruction of PDL

168. SCURVY-
• A deficiency disease resulting from deficiency of vitamin c which is
required for collagen synthesis in humans.
• Clinical features include Pallor, Sunken eyes, Non stopping diarrhea
• Hemorrhagic lesions into muscles of extremities, joints & nail beds,
delayed wound healing
• Gingivitis with enlarged hemorrhagic bluish red gingiva. Its a classical
signs of vitamin C deficiency

169. Changes in supporting periodontal tissues have been documented
extensively in experimental animals
• Vit C deficiency alone does not cause periodontal destruction,
local bacterial factors are required for increased probing depth
& attachment loss to occur
• Acute vitamin C deficiency results in hemorrhage in periodontal
ligament, osteoporosis of alveolar bone & excessive tooth
mobility

170. Leukocyte defects-
Chediak Higashi syndrome-
• It is a rare disease that affects the production of cells organelles.
• It affects mostly the melanocytes, platelets, phagocytes.
• Causes partial albinism, mild bleeding disorders & recurrent
bacterial infections
• Aggressive periodontitis has been described in these patients.

171. Hematological disorders-
Leukemia-
• Leukemia are malignant neoplasia of WBC precursors
characterized by:-
• Diffuse replacement of bone marrow with proliferating
leukemic cells.
• Abnormal numbers & forms of immature WBCs in
circulating blood.
• Wide spread infiltrates in liver, spleen & lymph nodes &
other body sites.

172. • Leukemic cells can infiltrate the gingiva & cause leukemic
gingival enlargement.
• Gingival hemorrhage is a common finding in leukemic patient
even in absence clinically detectable gingivitis
• Periodontal ligament & alveolar bone may also be involved in
acute & sub acute leukemia
• PDL may be infiltrated by mature & immature leukocyte
• oral ulceration & infections are common findings

173. Dermatologic disorders-
Papillion Lefevre syndrome (PLS)-
• It is an autosomal recessive inherited disease characterized by
diffuse palmar-plantar keratosis
• Primary teeth are affected from 2nd year are all prematurely
exfoliated by 6th year
• Permanent dentition erupt normally but within a few years these
teeth are lost.

174. • Periodontal involvement consists of early inflammatory changes leading to bone
loss & exfoliation of teeth
• Patients with this disease show destructive periodontal disease
Microscopic changes include:-
• Marked chronic inflammation of lateral wall of periodontal pocket
• Plasma cell infiltrate
• Considerable osteoclastic activity with lack of osteoblastic activity
• Extremely thin cementum
• Spirochetes zone in apical area of periodontal pocket as well as
spirochetes adherence to cementum
• Micro colony formation of mycoplasma species
• Cathepsin C an enzymatic protein

175. Chromosomal disorders-
Down’s syndrome-
• A congenital disease resulting from trisomy of chromosome 21
• It is characterized by growth retardation & mental deficiency
• Severity of periodontal destruction exceeds that explainable by
local factors alone.
• Periodontal findings include deep Periodontal pockets associated
with substantial plaque accumulation

176. • Commonest clinical presentation is mobility of lower incisors with
advanced bone loss.
• Acute necrotizing lesions are frequent findings
• 2 factors have been proposed for periodontal destruction:-
-A reduced resistance to infection b/c of poor circulation &
-Defect in T cell maturation & polymorphonuclear leukocyte
chemotaxis.

177. SCLERODERMA
• Derived from the Greek words “sklerosis,” meaning hardness,
and “derma,” meaning skin, scleroderma literally means hard skin.
• a symptom of a group of diseases that involve the abnormal
growth of connective tissue, which supports the skin and
internal organs.
• In other forms, however, the problem goes much deeper,
affecting blood vessels and internal organs, such as the heart,
lungs, and kidneys.
• Scleroderma is called both a rheumatic disease and a connective
tissue disease. The term rheumatic disease refers to a group of
conditions characterized by inflammation or pain in the muscles,
joints, or fibrous tissue.

178. • The most common radiographic finding in patients with systemic
sclerosis is widening of the periodontal ligament Space .
• The most likely explanation seems to be an increase in the
collagen synthesis in the periodontal ligament, which is the
hallmark of this disease.
• Increased collagen synthesis causes an increase in the thickness
and space occupied by the
periodontal ligament.
• Microscopic examination also reveals excessive collagen
deposition.
• This increase in the volume of the periodontal ligament exerts
additional pressure on both tooth and alveolar bone.
• Further, cementum is more resistant to resorption than bone, as
bone is richly vascularized and cementum is avascular.

179. • Therefore, the degenerative changes caused by altered blood
flow, which is related to an increase
in the pressure exerted by the periodontal ligament, affect
bone more readily than cementum.
• Thus this increased volume of periodontal ligament is
accommodated at the expense of alveolar bone without
affecting tooth mobility.

180. • The increased susceptibility to periodontal diseases can be
explained by both pressure ischemia and obliterative
vasculopathy, which causes atrophy of the periodontal ligament
and, at a later stage, mobility of the involved teeth.

181. • The increase in the widths were found to be
more pronounced in the posterior teeth
than in the anterior teeth,the fact that the
teeth bearing more masticatory force have
wider periodontal ligament spaces than
those bearing less force

182. LOCAL
CHRONIC PERIODONTITIS
• An infectious disease resulting in inflamation within supporting tissues
of teeth,progressive attachment loss & bone loss.
• Most prevalent form of periodontitis which can be localized or generalized
• Clinical findings include supragingival & sub gingival plaque accumulation,
gingival inflammation
• Loss of gingival stippling, blunted or rolled gingival margins & flattened or
cratered papillae are also seen

183. • Periodontal findings include pocket formation, loss of
periodontal attachment, loss of alveolar bone & occasional
suppuration.
• With increasing age attachment or bone loss become more
prevalent & severe.
• pattern of bone loss –horizontal or vertical.
• Can be associated with local predisposing factors (e.g. tooth
related or iatrogenic factors)
• Attachment & bone loss are associated with increase in
pathogenic & virulent organisms, these include:-
Porphyromonas Gingivalis
Tannerila Forsythia
Treponema Denticola

184. • In chronic periodontitis the collagenous activity is caused by MMP-8
from neutrophils
• CYTOKINES
• Periodontal pathogens might mediate connective tissue degradation in
periodontal disease by the ability of antigens from their cell walls to
stimulate cytokine production by circulating mononuclear phagocytes
• These cytokines & prostaglandins could in turn induce metalloproteinase
synthesis by resident gingival cells thereby initiating degradation of
ligament attachment & increase in bone resorption

185. NECROTISING ULCERATIVE PERIODONTITIS-
• Extension of necrotizing ulcerative gingivitis into periodontal
structures ,leading to loss of attachment & bone loss
• Cases with NUP presents a clinical picture of necrosis & ulceration
of coronal portion of interdental papillae & gingival margin.
• Painful bright red gingiva that bleeds easily

186. • Deep interdental osseous craters, with absence of pocket
formation are seen
• Advanced lesions of NUP leads to severe bone loss, tooth
mobility & tooth loss
• Microscopically surface biofilm composed of a mixed microbial
flora with different morphotypes & a subsurface flora with
dense aggregation of spirochetes is seen.

187. AGGRESSIVE PERIODONTITIS-
• Characterised by rapid loss of attachment & bone loss occuring in an
otherwise clinically healthy patient with the amount of microbial deposits
inconsistent with disease severity & familial aggregation of diseased
individuals.
• Aggressive periodontitis generally affects systemically healthy individuals
less than 30 years old although patients beyond 30 years may also be
affected)
• It describes 3 of the diseases formerly classified as early onset
periodontitis namely:-
 Localized aggressive periodontitis
 Generalized aggressive periodontitis
 Rapidly progressive periodontitis

188. MECH OF DESTRUCTION
Numerous studies have shown the association between Aggressive
periodontitis & A. Actinomycetemcomitans.
A. Actinomycetemcomitans produces a variety of factors that could
increase its virulence & damage the tissues of host. These
are:-
• Leukotoxin
• Chemotaxis inhibition factors
• Surface associated material (which stimulate bone
resorption)
• Proteases that degrade immunoglobulins
• Collagenase
• Extracellular outer membrane vesicles
• Factors affecting immune response
• Factors damaging host cells

189. SURFACE ASSOCIATED MATERIAL-
• Proteins associated with the outer surfaces of putative
periodontal pathogens are potent inducers of bone resorption &
tissue pathology
• This capsular or surface-associated material has been shown to
stimulate the production of PGE2 & collagenase from bone cells
• COLLAGENASE-
• This bacteria produces a collagenolytic proteinase that can
attack collagen
• In LAP the predominant collagenase found in tissues & crevicular
fluid is MMP-1 & elevated levels TIMP-1 are present

190. LOCALIZED AGGRESSIVE PERIODONTITIS
• Usually has an age of onset at puberty
• Destruction of PDL, loss of attachment, presence of deep
periodontal pockets in absence of signs of clinical inflammation
• Amount of plaque that is present is minimal, forms thin biofilm &
rarely mineralizes to form calculus.
• Vertical loss of alveolar bone around the first molars & incisors
is seen
• Elevated levels of A. Actinomycetemcomitans & in some cases of
P. gingivalis

191. GENERALIZED AGGRESSIVE PERIODONTITIS-
• GAP is characterized by generalized periodontal attachment loss
affecting at least 3 permanent teeth other than first molars &
incisors
• Individuals affected with GAP produce poor antibody response to
pathogens present
• Patients with GAP often have small amounts of bacterial plaque
associated with affected teeth

192. • P. Gingivalis, A. Actinomycetemcomitans & Tannerella Forsythia
are frequently detected in plaque
• In GAP 2 types of stages are seen
Destructive Stage-
• Severely acutely inflamed tissue often proliferating, ulcerated &
fiery red
• Bleeding occurring spontaneously or on slight provocation
• Suppuration is also seen
• Rapid loss of PDL & alveolar bone

193. Periods of quiescence-
• Gingival tissue may appear pink, free of inflammation &
occasionally with some degrees of stippling
• Deep pockets as demonstrated by probing
• Bone level remains stationary
• Patients with GAP may have systemic manifestation such as
weight loss, mental depression & general malaise

194. Rapidly progressive periodontitis-
• Rapidly progressive periodontitis falls under the general category of
early onset periodontitis.
• Destructive lesions are generalized throughout the dentition in a
patient between 14-35 years of age
• Patients demonstrates a less than expected amount of etiology factors
(plaque and calculus) for the amount of periodontal destruction.